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Essentials of Diagnosis
Elevated creatine kinase (CK) levels greater than five times upper limit of normal.
Muscle pain, tenderness, or weakness.
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GENERAL CONSIDERATIONS
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Rhabdomyolysis is a clinical disorder characterized by skeletal muscle breakdown and release of intracellular contents (myoglobin, electrolytes, intracellular enzymes) into the circulation. Approximately 26,000 cases occur annually in the United States. The common clinical presentation includes muscle pain, weakness, tea- or dark-colored urine (myoglobinuria), and elevation of creatine kinase (CK) greater than five times upper limit of normal. Myoglobin is readily filtered by the glomerulus, and in high levels it can lead to renal tubular injury and acute kidney injury (AKI). The severity of illness ranges from asymptomatic elevations in CK to life-threatening electrolyte imbalances, intravascular volume depletion, and complications from AKI.
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Table 11–1 lists common causes of rhabdomyolysis.
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The manifestations of rhabdomyolysis are a result of muscle cell death. The mechanisms involved include direct muscle injury (trauma) or muscle adenosine triphosphate (ATP) depletion. Trauma leading to muscle compression has been described in several situations. Crush injuries sustained in earthquakes and accidents are a common cause of rhabdomyolysis. Similar prolonged muscle compression is seen during prolonged surgical procedures as well as vascular occlusion (tourniquet use). Effects of muscle compression are also evident in prolonged immobilization, resulting in limb compression. Normal individuals are noted to have developed rhabdomyolysis following intense physical exertion. Several cases of rhabdomyolysis have been noted in extreme conditioning programs involving repetitive, high-intensity exercise. Studies have demonstrated that these participants have concomitant significant fluid losses and elevation of body temperature. Sickle cell trait has also been associated with a significantly high risk of exertional rhabdomyolysis. Besides direct muscle injury, decreased muscle energy stores are thought to be contributory to development of rhabdomyolysis. Injury threshold is also lowered in strenuous activity in physically untrained individuals, during fasting states and extremely hot conditions. Certain pathologic states including grand mal seizures and delirium tremens can lead to rhabdomyolysis in normal individuals.
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Recurrent episodes of rhabdomyolysis usually reflect an underlying inherited defect in muscle metabolism. The mechanism of muscle breakdown is assumed to be insufficient ATP in the muscle cells. These genetic defects include disorders of ...