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Rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibers with leakage of muscle contents into the circulation. The most common causes are crush injury, overexertion, alcohol abuse and certain medicines and toxic substances. Several inherited genetic disorders, such as McArdle's disease and Duchenne's muscular dystrophy, are predisposing factors for the syndrome. Clinical features are often nonspecific, and tea-colored urine is usually the first clue to the presence of rhabdomyolysis. Screening may be performed with a urine dipstick in combination with urine microscopy. A positive urine myoglobin test provides supportive evidence. Multiple complications can occur and are classified as early or late. Early complications include severe hyperkalemia that causes cardiac arrhythmia and arrest. The most serious late complication is acute renal failure, which occurs in approximately 15 percent of patients with the syndrome. Early recognition of rhabdomyolysis and prompt management of complications are crucial to a successful outcome. (Am Fam Physician 2002;65:907-12. Copyrigh to 2002 American Academy of Family Physicians.)
habdomyolysis, which literally means striated muscle dissolution or disintegration,1 is a potentially lethal clinical and biochemical syndrome.2 Approximately 26,000 cases of rhabdomyolysis are reported annually in the United States.3 Prompt recognition and early intervention are vital. Full recovery can be expected with early diagnosis and treatment of the many complications that can develop in patients with this syndrome.
Clinical features of rhabdomyolysis may be absent initially, and its most serious complication, acute renal failure, is common. Many patients develop dialysis-dependent acute renal failure associated with the misuse of alcohol or other drugs.4 The nephrotoxicity of myoglobin is decreased by forced alkaline diuresis. Critically ill patients with acute renal failure are also likely to develop multiorgan failure syndrome, with a resultant increase in mortality.5
Pathophysiology
Muscle injury, regardless of mechanism, results in a cascade of events that leads to leakage of extracellular calcium ions into the intracellular space.6 The excess calcium causes a pathologic interaction of actin and myosin that ends in muscle destruction and fiber necrosis (Figure 1).
With muscle injury, large quantities of potassium, phosphate, myoglobin, creatine kinase (CK) and urate leak into the circulation. Under physiologic circumstances, the plasma concentration of myoglobin is very low (0 to 0.003 mg per dL). If more than 100 g of...