Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. The severity of illness ranges from asymptomatic elevations of serum muscle enzymes to life-threatening cases associated with severe electrolyte imbalances, acute renal failure, disseminated intravascular coagulation, and death.

The classic presentation of rhabdomyolysis includes myalgias, pigmenturia due to myoglobinuria, and elevated serum muscle enzymes. The most commonly measured enzyme is serum creatinine kinase (CK), which is typically greater than 10,000 IU/L. It should be noted that serum CK levels may remain elevated in the absence of myoglobinuria since myoglobin is cleared from the serum more rapidly than CK. Since serum and/or urine myoglobin levels often take at least hours (if not days) to obtain results, these should not be relied upon to make the diagnosis. Rhabdomyolysis can be reliably diagnosed with the combination of the urine dipstick that is positive for heme (because of urine myoglobin) and urine microscopy showing an absence of red blood cells. Other abnormal electrolyte findings include hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis.

Rhabdomyolysis has many varied etiologies, which are difficult to categorize. Direct mechanical injury resulting in rhabdomyolysis can be caused by trauma, electrocutions, prolonged immobilization, ischemic limb injury, and crush injuries. Other cases can be caused by heatstroke and exertional rhabdomyolysis following vigorous exercise (e.g., strong-man triathlons). In addition, rhabdomyolysis can be caused by drugs and toxins, which can exert either direct myotoxicity (e.g., statins) or cause indirect muscle damage (e.g., alcohol or cocaine). Infections, inflammatory disorders, endocrine, and metabolic etiologies are also included in the long list of differential diagnoses. Genetic causes must be considered if no other cause is readily apparent.