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medical_problem | A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th鈥75th percentile) and weighed 55 kg (50th鈥75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5鈥3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4鈥48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm 脳2.2 cm脳2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.
| What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 16 years old.
The concentration of creatinine is 0.57 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.8 cm, which is 162.8 cm * 1 m / 100 cm = 1.628 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.628 m * 1.628 m) = 20.752 kg/m^2.The patient's BMI is 20.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 54.918 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 54.918 * 0.85) / (0.57 * 72) = 141.042 mL/min. Hence, the patient's creatinine clearance is 141.042 mL/min. | 141.042 |
medical_problem | A 56-year-old man was admitted to the renal unit of the tertiary university hospital with symptoms of polyuria with nocturia, and polydipsia with severe thirst for the past 2 months. Initially, the patient visited a local clinic and was diagnosed as type 2 DM with a fasting blood sugar, 150mg/dL. Despite being controlled hyperglycemia with an oral hypoglycemic agent, he continued drinking daily more than 8 L of cold water (about 10 bottles of refrigerated water, 750 ml capacity) and passed large amounts of urine frequently. He had no specific history including head trauma or mental disorder, and denied any pertinent family history. The patient showed no signs of systemic illness such as fever or arthralgia, or neurologic symptoms involving the central nervous system. He has been working as a gardener with 176 cm in height and 68 kg in weight (71 kg before this event). The physical examination was unremarkable with blood pressure of 132/70 mmHg, pulse rate of 80/min, respiratory rate of 16/min, and temperature of 36.8鈩. In the laboratory findings, his white blood cell count was 9,700/mm3; hemoglobin, 13.4 g/dL; platelet, 376脳103/mm3; sodium, 140 mEq/L; potassium, 3.8 mEq/L; blood urea nitrogen (BUN), 12 mg/dL; creatinine, 1.0 mg/dL and osmolality 295 mOsm/kg water. HbA1c was 7.2% and post-prandial glucose was checked around 180mg/dl with fasting blood sugar of 140 mg/dL. In urine analysis, the urine pH was 6.0; specific gravity 1.006; albumin (-); glucose (-); WBC 0-4/HPF; RBC 0-2/HPF, and osmolality 140mOsm/kg water. Fluid intake and output in 24 hours recorded 9 L in oral water intake from water containers and 11.7 L in urine output. In hormone assays, ACTH was 25.2 pg/mL (reference value, 6.0-76.0 pg/mL), prolactin 8 碌g/L (reference value, 0-15 碌g/L), cortisol 9.8 碌g/dL (referencel value, 5-25 碌g/dL), hGH 2.26 ng/mL (reference value, 0.5-17 ng/mL), and TSH 0.99 碌U/mL (reference value, 0.5-4.7 碌U/mL). Also, angiotensin converting enzyme (ACE) activity was within normal range (reference value, <40 U/L).
On hospital day 5, the patient underwent a water deprivation test according to the method of Miller-Moses test because of persistent polydipsia and polyuria despite blood glucose control. The results are shown in . During dehydration, the patient lost 3kg (4.4% of body weight), and urine osmolality remained hypotonic below 130 mOsm/kg. Basal ADH level was 5.18 pg/dL, and the repeat ADH level following the stimulation by water deprivation was 3.95 pg/dL, which revealed no increment despite the increased serum osmolality up to 300 mOsm/kg from the baseline levels of 285 to 295 mOsm/kg. One puff (5 碌g) of desmopressin nasal spray resulted in the increase of urine osmolality to 266 mOsm/kg (>100% increase from the baseline level, 126 mOsm/kg) and in the marked reduction of urine output from 200-410 ml/hr to 44-60 ml/hr. These results were compatible with CDI,, whose causes would be mostly idiopathic because of normal findings in hypothalamus and hypophysis in magnetic resonance imaging (MRI) scan of sella ().
On discharge (hospital day 9), the dose of desmopressin nasal spray (minirin nasal spray庐) was adjusted to 1 puff per 12 hrs (10 碌g/day), and urine output was markedly reduced to below 2-3 L/day with no more intense thirst. Also, DM was controlled with fasting blood sugar below 115 mg/dL by metformin (novamet GR庐 500mg bid) and American Diabetes Association (ADA) recommended diet. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 56 years old.
The concentration of creatinine is 1.0 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.76 m * 1.76 m) = 21.952 kg/m^2.The patient's BMI is 22.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 68.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 56) * 68.0 * 1) / (1.0 * 72) = 79.333 mL/min. Hence, the patient's creatinine clearance is 79.333 mL/min. | 79.333 |
medical_problem | In 2008, a 59-year-old Japanese woman was admitted for evaluation of renal disease. RA had been diagnosed at another hospital in 1972 when she presented with bilateral arthropathy of the hands, knees, ankles, and feet. Treatment was started with a combination of a gold preparation and nonsteroidal anti-inflammatory drugs (NSAIDs), but was not been effective. Prednisolone (PSL; 15 mg daily) and bucillamine (BUC; 200 mg daily) were started in 1987, but her disease remained active. Methotrexate (MTX; 5 mg daily) was started in 1995 but was discontinued because of nausea. In 2002, urinary protein was found to be positive by a dipstick urine test, and BUC was stopped. Then treatment was continued with PSL (5 mg/day) and loxoprofen (50 mg/day). However, urinary protein excretion increased in 2007, and serum creatinine (Cre) was elevated to 1.96 mg/dL.
On admission, the patient was 154.2 cm tall and weighed 44.0 kg, with a blood pressure of 128/60 mmHg and temperature of 36.4 掳C. Physical examination did not reveal any abnormalities of the heart and lungs. The joints of her hands, knees, ankles, and feet showed bilateral swelling and deformity. In addition, the lower extremities were edematous. Her cervical spine was unstable, with flexion causing numbness in the upper limbs.
Laboratory findings were as follows: serum Cre was 4.2 mg/dL, the estimated glomerular filtration rate (eGFR) was 9.3 mL/min/1.73m3, C-reactive protein (CRP) was 0.9 mg/dL, and SAA was 43.2. In addition, rheumatoid factor (RF) was positive at 59 U/mL (normal: < 10), and cyclic citrullinated peptide (CCP) antibodies were positive at 218.5 (normal < 4.5). 24-hour urinary protein excretion was 6.5 g, and the urine sediment contained 1 鈥 5 red cells per high-power field (HPF). The disease activity score (DAS)-CRP was 7.1. Radiographs showed deformation of the finger and foot joints as well as atlantoaxial joint subluxation. Renal biopsy was performed for evaluation of her kidney disease.
Renal biopsy
Light microscopic examination of a biopsy specimen containing 4 glomeruli revealed global sclerosis in all 4. There was severe tubular atrophy, and tubulointerstitial fibrosis occupied ~ 95% of the entire renal cortex. All 4 glomeruli contained multinodular structures of amorphous material with a PAM-positive border. This material was positive for Congo-red and amyloid A, but was negative for 魏 and 位 chains, 尾-2 microglobulin, and transthyretin (). Electron microscopy showed randomly arranged fibrils measuring 8 鈥 12 nm in diameter corresponding to the amyloid deposits (f). AA amyloidosis was diagnosed from these findings. In addition to the glomeruli, amyloid deposits were mainly observed in the interlobular artery walls and tubulointerstitium (e). Endoscopic biopsy of the stomach, duodenum, and colon revealed AA-positive deposits in the small arteries and tissues of the submucosal layer (a).
Clinical course
PSL was discontinued, and administration of a soluble tumor necrosis factor (TNF) receptor inhibitor (etanercept; 25 mg every 2 weeks) was started in May 2008, but it was not effective. By September 2008, Cre was increased to 6.0 mg/dL. She underwent surgery to prepare an arteriovenous fistula for hemodialysis. Etanercept was discontinued, and a humanized anti-interleukin-6 receptor antibody (tocilizumab; 8 mg/kg = 360 mg/month) was started in February 2009. After 3 months, her CRP decreased to 0.0 mg/dL, and the DAS28-CRP sore was 2.12. After 2 years of tocilizumab therapy, urinary protein excretion was decreased to 1.1 g/day, and Cre was 4.0 mg/dL. Subsequently, Cre remained in the range of 4.5 鈥 5.0 mg/dL until December 2017. While Cre increased to 7.1 mg/dL after initiation of treatment with denosumab (a human monoclonal antibody that binds to receptor activator of NF魏B ligand) for osteoporosis in October 2018, it remained at 7.0 mg/dL in June 2019 ().
Gastroduodenal biopsy was performed in May 2013 and May 2017. On both occasions, no amyloid deposits were detected in the submucosal blood vessels (b).
| What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 59 years old.
The concentration of creatinine is 1.96 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.2 cm, which is 154.2 cm * 1 m / 100 cm = 1.542 m. The patient's weight is 44.0 kg. The patient's bmi is therefore 44.0 kg / (1.542 m * 1.542 m) = 18.505 kg/m^2.The patient's BMI is 18.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 44.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 59) * 44.0 * 0.85) / (1.96 * 72) = 21.467 mL/min. Hence, the patient's creatinine clearance is 21.467 mL/min. | 21.467 |
medical_problem | A 34-year-old man was admitted for evaluation of worsening pedal edema. He was apparently healthy until four years back, when he developed edema of both feet and nonpruritic macular skin rash involving both lower limbs. Subsequently, he was detected to have hypertension, proteinuria and mild renal failure (6 months ago). He had no history of arthralgia, Raynaud's phenomenon, paraesthesia or gastrointestinal hemorrhage.
Six weeks prior to admission in our centre, he developed weakness of left upper and lower limbs with slurring of speech and was hospitalized elsewhere. A computerized tomographic scan of head had revealed an infarct in the right middle cerebral artery territory and he was treated with aspirin, statins, and antihypertensives. He made a complete recovery but was detected to have renal failure and was referred to us for further evaluation.
He weighed 74 kg and had a height of 174 cm. He had pallor and bilateral pitting pedal edema. There was no skin rash or lymphadenopathy. Blood pressure was 140/90 mmHg. Examination of cardiovascular system, respiratory system, and abdomen was normal. There were no neurological deficits.
Investigations revealed hemoglobin of 8.79 gm/dL, platelet count of 112000/mm3, total WBC count of 7960/mm3 - with a normal differential count, ESR of 40 mm at end of first hour. Urinalysis showed protein ++++, 6-8 RBCs/HPF; and 24 hour urine protein was 4420 mg. Blood urea was 72 mg/dL and serum creatinine was 3.1 mg/dL with normal serum levels of electrolytes. Liver function tests, PT and aPTT were normal. Serum albumin was 3.6 gm%, serum globulin 3.8 g/dL and serum cholesterol 240 mg/dL. Serum protein electrophoresis was normal. Blood and urine cultures were sterile. HBsAg, antihepatitis C virus (HCV) and HIV antibodies were negative VDRL, cANCA, pANCA, antiphospholipid antibodies, ANA, antids DNA were negative. Serum homocysteine [12 碌mol/L] was normal and serum complement levels were reduced (C3:70 mg/dL, C4:18 mg/dL). Serum cryoglobulin assay was positive. On PAGE electrophoresis, the mobility was suggestive of mixed cryoglobulins. HCV RNA was negative in serum [polymerase chain reaction (PCR)]. Qualitative analysis for HCV RNA [by reverse transcriptase-PCR (RT-PCR)] in the cryoprecipitate was negative []. Doppler study of extra cranial carotid and vertebral vessels was normal. Ultra sonogram of abdomen, ECG, and echocardiogram were normal. Bone marrow examination was normal. X-rays of chest, skull spine, and pelvis were normal. Kidney biopsy showed lobular accentuation of glomeruli with mesangial proliferation, mild endocapillary proliferation, and double contour of glomerular basement membrane on light microscopy. Intracapillary eosinophilic PAS positive hyaline deposits were noted []. Interstitium showed mononuclear infiltrates. Immunofluorescence showed mesangial and capillary granular positivity for C3 IgG and IgM.
| What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 34 years old.
The concentration of creatinine is 3.1 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.74 m * 1.74 m) = 24.442 kg/m^2.The patient's BMI is 24.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 69.559 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 34) * 69.559 * 1) / (3.1 * 72) = 33.034 mL/min. Hence, the patient's creatinine clearance is 33.034 mL/min. | 33.034 |
medical_problem | A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient鈥檚 pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, 纬-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/渭l, erythrocytes 5.00 脳 106/渭l, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 脳 103/渭l.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient鈥檚 thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient鈥檚 physical size, which would ensure appropriate training. We palpated the patient鈥檚 quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient鈥檚 feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, 尾-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20鈥40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient鈥檚 voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient鈥檚 comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 卤 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A 渭Tas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3鈥5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0鈥135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process.
| What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 67 years old.
The concentration of creatinine is 0.56 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.57 m * 1.57 m) = 25.153 kg/m^2.The patient's BMI is 25.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.811 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (61.811 (in inches) - 60) = 49.665 kg.
Hence, the patient's IBW is 49.665 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 49.665 kg + 0.4 * (62.0 kg - 49.665 kg) = 54.599 kg. The patient's adjusted body weight is 54.599 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 54.599 * 0.85) / (0.56 * 72) = 84.025 mL/min. Hence, the patient's creatinine clearance is 84.025 mL/min. | 84.025 |
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