Rhabdomyolysis secondary to drug overdose and prolonged coma.
Recent research has contributed to the understanding of nontraumatic rhabdomyolysis. In cases associated with coma, the pathophysiology is secondary to local pressure necrosis caused by compression from the patient's own body. The local pressure results in an edema-ischemia cycle concluding with compartmental tamponade and muscle breakdown. Myoglobin released by the damaged muscle indirectly induces the acute renal failure via its breakdown product, ferrihemate, which poisons renal tubular cells. Uric acid nephropathy may also play a role. Radionuclide scanning has assumed a significant role as a diagnostic tool to determine the extent of soft tissue injury. Early volume expansion and administration of sodium bicarbonate and mannitol are recommended as prophylaxis against renal failure. Fasciotomy appears to have a role both in the prevention of limb damage and in the diminution of the systemic toxic effects produced by muscle breakdown.
D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology; D000328:Adult; D003128:Coma / Q000150:complications*; D006801:Humans; D006996:Hypocalcemia / Q000503:physiopathology; D008297:Male; D008635:Mescaline / Q000506:poisoning*; D008691:Methadone / Q000506:poisoning*; D009211:Myoglobin / Q000378:metabolism; D009212:Myoglobinuria / Q000150:complications / Q000209:etiology* / Q000503:physiopathology; D011187:Posture
D009211:Myoglobin; D008635:Mescaline; D008691:Methadone