Extract

Case Presentation

A 48-year-old male with no significant past medical history came to the emergency department (ED) because of sudden onset of diffuse myalgia especially in the legs, chest and back. It was associated with mild diaphoresis. Symptoms started acutely as he was driving back home from his work as a cab driver. He denied fever, new medications, recreational drug use, recent illness, significant physical exertion and trauma. Vital signs on admission were: temperature, 98.2 F; pulse, 90/min; blood pressure, 148/88 mm Hg; and SaO2, 98% on room air. Physical examination was significant for tenderness in the thighs and shoulder area, without weakness. The patient was passing dark brown coloured urine in the ED. Electrocardiogram showed normal sinus rhythm, without irregularities. His laboratory testing showed normal haemoglobin and white cell count. Urinalysis was positive with 4+ haemoglobin, but minimal grouped red blood cells. Urine toxicology screen was negative. Creatinine Phosphokinase (CPK) was 16192 IU/l (normal 41–85) on admission and peaked at >160,000, 40 h later. Serum myoglobin was elevated as well > 4000 ng/ml, on admission. (Such high values are rarely seen, except in cases of crush injuries.) Diagnosis of rhabdomyolysis was made, but the etiology was unknown. He was started on intravenous normal saline at a rate of 200 cc/h, with strict monitoring of urine output. His urine output was maintained around 2–3 ml/kg/h. Labs done 4 h later revealed hyperkalemia and elevation of serum creatinine, consistent with acute kidney injury due to tubular toxicity (ATN) of myoglobin. His myalgias lasted for about 10–12 h, and then resolved. CPK and myoglobin started to improve on day 4. The acute kidney injury was likely ATN, due to myoglobulinuria, and creatinine increased rapidly to 3.0 mg/dl within 48 h, peaked at 3.6 mg/dl on day 5, and then started improving. Rheumatologic work up including Anti-nuclear antibody was negative. His mother had been hospitalized the month prior, for weakness secondary to rhabdomyolysis, which led to renal failure. Her hospital course was complicated by intracranial haemorrhage and expiration. She had eaten buffalo fish before she was admitted. Our patient, had taken out soup fish from the freezer one month later which was made from the same fish, and ingested it. Diagnosis of Haff disease was established on basis of compatible history, laboratory findings, and in consultation with Center for Disease Control. Patient was discharged on day 6, asymptomatic, and improving renal function.

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