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  • Associated with crush injuries to muscle, immobility, drug toxicities, and hypothermia.

  • Usually markedly elevated muscle enzymes.


Rhabdomyolysis is a syndrome of acute necrosis of skeletal muscle associated with myoglobinuria and markedly elevated creatine kinase levels. Acute tubular necrosis is a common complication of rhabdomyolysis and is due to the toxic effects of filtering excessive quantities of myoglobin in the setting of hypovolemia (see Acute Tubular Necrosis in Chapter 22-06). Experimental models of severe rhabdomyolysis in which blood volume and pressure are maintained ordinarily are not associated with acute tubular necrosis. Many patients in whom rhabdomyolysis develops are volume-contracted and, therefore, oliguric renal failure is encountered routinely. Compartment syndrome, disseminated intravascular coagulation, and cardiac arrhythmias are serious but less common complications of rhabdomyolysis.

Rhabdomyolysis is a common complication of severe crush injuries to muscle. Cocaine use and alcohol intoxication, particularly in the setting of prolonged immobility and exposure hypothermia, are leading causes of hospital admissions for rhabdomyolysis. Use of statins is another important cause of rhabdomyolysis. The presence of compromised kidney and liver function, diabetes mellitus, and hypothyroidism as well as concomitant use of other medications increase the risk of rhabdomyolysis in patients taking statins. The cytochrome P450 liver enzymes metabolize all statins except for pravastatin and rosuvastatin. Drugs that block the action of cytochrome P450 include protease inhibitors, erythromycin, itraconazole, clarithromycin, diltiazem, and verapamil. Use of these drugs concomitantly with the statins (but not pravastatin or rosuvastatin) can increase the risk of development of rhabdomyolysis. The likelihood of rhabdomyolysis also increases when statins are used with niacin and fibric acids (gemfibrozil, clofibrate, and fenofibrate). Rhabdomyolysis is an uncommon complication of polymyositis, dermatomyositis, and the myopathy of hypothyroidism, despite the high levels of creatine kinase often seen in these conditions.

Often there is little evidence for muscle injury on clinical assessment of the patients with rhabdomyolysis—specifically, myalgias and weakness are usually absent. The first clue to muscle necrosis in such individuals may be a urinary dipstick testing positive for “blood” (actually myoglobin) in the absence of red cells in the sediment. This myoglobinuria results in a false-positive reading for hemoglobin. Urine tests for myoglobin are insensitive, however, and are positive in only 25% of patients with rhabdomyolysis. Such an abnormality should prompt determination of the serum creatine kinase level, which invariably is elevated (usually markedly so). Other commonly encountered laboratory abnormalities in rhabdomyolysis include elevated serum levels of AST, ALT, and lactate dehydrogenase (due to release of these enzymes from skeletal muscle), hyperkalemia, and hypocalcemia. The massive acute elevations of muscle enzymes peak quickly and usually resolve within days once the inciting injury has been removed.


Vigorous fluid resuscitation (eg, 4–6 L/day but often more in the setting of severe crush injuries) is indicated. Urine alkalinization (to minimize precipitation of myoglobin within tubules) has been recommended to reduce kidney ...

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