Abstract

The syndrome was first described by British physician Eric Bywaters in patients during the 1941 London Blitz. It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products notably myoglobin, potassium and phosphorus that are the products of rhabdomyolysis. Recently, similar condition was described in epileptic patients either due to severe attack of fits or following a toxicity induced by anti-epileptic medications. The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin. These systemic effects are caused by a rhabdomyolysis. In addition to tissue directly suffering the crush mechanism, down stream tissue is subject to ischemia-reperfusion injury of the appendicular musculoskeletal system. Without proper preparation, the patient, with pain control, may be cheerful before extrication, but die shortly thereafter. This sudden decompensation is called the "smiling death". A case report 28 year old male with history of epilepsy. he suddenly felt down into ground with attack of seizure activity followed by myalgia and muscle weakness. On presentation he was breathlessness hypertensive, lung congestion with low urine output (10 ml of dark red urine/day). Investigations revealed normal sonographic kidneys, high serum creatinine 8.22 mg/dl, serum creatine kinase (CK total) of 420,700 u/l (normal 30-200u/l), hyponatremia 128 mmol/l, hyperkalemia of 5.7 mmol/l, hyperuricemia uric acid 9.0 mg/dl, metabolic acidosis; serum bicarbonate was 15 mmol/l, hyperphosphatemia 8 mg/dl, hypocalcemia 6.2 mg/dl and positive myoglobin in urine. Supportive hemodialysis session was indicated for normalization of metabolic profile, adjustment of fluid overload, removal of myoglobin toxic burden, sevelamer was added to control hyperphosphatemia. Daily, hemodialysis was done for 4 consecutive days.clinically improved with serum creatinine, BUN and creatine kinase dropped to normal levels with normalization of electrolyte and uric acid, So Hemodialysis stopped. However, after days of improvement of serum creatinine it start to increase again by around 200 mg/dl per day, with maintaining of normal renal function. Clinically, patient complained of severe right thigh pain, hypotonia related to right thigh muscles with oedema of whole right leg up to inguinal region, with difficulity of walking. Doppler u/s of arterial and venous system of the lower limbs was normal, normal nerve conduction. Muscle biopsy was done under anesthesia, methylprednisolone was initiated 60 mg iv per day. On next day, a dramatic improvement of the patient clinical condition, he was walking with no pain. The muscles of the right thigh regained its normal tone and the oedema disappeared. The biopsy results came later and showed multifocal necrotic muscle fibers, myophagocytosis, up regulation of MHC-I in absence of inflammatory infiltrates. In view of this, patient was discharged on maintenance oral prednisolone 40 mg daily with gradual tapering of the dose over 15 days. After two months, his serum creatinine 0.8 mg/dl, normal serum creatine kinase. we report a rare case of crush syndrome after combined trauma and possible toxic effect from antiepileptic medications with good outcome after careful stepwise management.

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