Rhabdomyolysis is often diagnosed on the basis of creatine kinase levels at least five times the upper limit of normal. According to recommendations by the American College of Cardiology; the American Heart Association; and the National Heart, Lung, and Blood Institute, for rhabdomyolysis occurring in patients on lipid-lowering therapy, rhabdomyolysis is defined as a creatine kinase level more than 10 times the upper limit of normal. Levels are often considerably higher.
Recurrent cases of rhabdomyolysis without any precipitating trauma or exertion should raise suspicion of a genetic defect in metabolism. Defects in glycogen, lipid, mitochondria, and purine metabolism can cause rhabdomyolysis. Muscle biopsies should be obtained in these patients, with appropriate staining for diagnosis.
The mechanism of muscle cell destruction is direct injury to the muscle cell membrane, depletion of cellular energy due to hypoxia, or electrolyte disturbances that affect the sodium/potassium pump in the cell. Muscle injury results in leakage of extracellular calcium into the intracellular space, which eventually leads to muscle cell death and necrosis. Once cellular necrosis occurs, cellular products, such as myoglobin, potassium, and creatine kinase, escape into the blood. Acute renal failure can result from massive deposition of muscle enzymes and myoglobin in the renal tubules. Previous studies have suggested that acute renal failure can result from hypovolemia and aciduria.
Rhabdomyolysis can occur at any age but is more frequent in individuals older than 60 years or younger than 10 years. The risk for rhabdomyolysis is higher in those with a body mass index > 40 kg/m2. Patients with sickle cell anemia may be at higher risk for exertional rhabdomyolysis.
The most common symptoms are muscle weakness, myalgia, and dark-colored urine. Severe cases of rhabdomyolysis can cause oliguria or even anuria. Cardiovascular symptoms can include cardiac arrhythmias or cardiac arrest; these often stem from severe electrolyte abnormalities. Hypokalemia during strenuous physical activity can increase the risk for rhabdomyolysis, owing to low potassium levels restricting muscle vasodilation. Asymptomatic elevations in creatine kinase levels can also occur. Myoglobulinemia and myoglobinuria may occur after strenuous physical activity.
The diagnosis is established by checking serum creatine kinase levels. Urinalysis may reveal pigmented granular casts and a dark reddish-brown supernatant. Urine dipstick reveals positive results for blood but no red cells, owing to the presence of myoglobin. Serum creatinine levels may be elevated. Other causes of dark tea-colored urine include hemoglobinuria, porphyria, bile pigments, food (eg, beets), and drugs (eg, rifampin, chloroquine).
Complications of acute rhabdomyolysis include multiple electrolyte abnormalities (eg, hypocalcemia, hypercalcemia, hyperphosphatemia, hyperkalemia). The latter may require treatment. The most serious complication is acute renal failure. A large retrospective cohort study suggested that morbidity and mortality often depends on the underlying cause of rhabdomyolysis, with higher rates of in-hospital mortality or requirement of renal replacement therapy in patients with compartment syndrome, sepsis, neuroleptic malignant syndrome, cardiac arrest, and certain surgeries.
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