Rhabdomyolysis

Excerpt

Rhabdomyolysis refers to the dissolution of skeletal muscle and is characterized by leakage of muscle cell contents, myoglobin, sarcoplasmic proteins, and electrolytes into the extracellular fluid and circulation. The word rhabdomyolysis is derived from the Greek words rhabdos (rod-like/striated), mys (muscle), and lysin (release). The most common causes of rhabdomyolysis are crush injuries secondary to trauma or immobilization, extreme physical exertion, metabolic myopathies, viral illness, and electrolyte disorders.

The common symptoms and signs are muscle weakness, pain, myalgias, and local swelling. Rhabdomyolysis may be associated with dark reddish-colored urine due to myoglobinuria. Clinically, rhabdomyolysis can range from mild elevation in creatinine phosphokinase to medical emergencies like compartment syndrome, intravascular fluid depletion, disseminated intravascular coagulation, pigment-induced acute kidney injury (AKI), and cardiac arrhythmias.

Laboratory diagnosis of rhabdomyolysis is based on elevations of serum creatine phosphokinase (CPK), the most sensitive laboratory evaluation of muscle injury; there is no specific established diagnostic serum level of CPK. Many clinicians use 3 to 5 times the upper limit of normal values of 100 to 400 U/L (approximately 1000 U/liter) for diagnosis. However, the elevation of CPK levels does not determine the severity of muscle damage and renal injury.

Rhabdomyolysis is a major cause of AKI. If identified early, the prognosis of AKI from rhabdomyolysis is relatively benign. Alternative causes for AKI, like dehydration, sepsis, and pharmaceutical-induced adverse effects, should always be considered. Seizures, alcohol use, drugs, and a prolonged bedridden state are common causes of nontraumatic rhabdomyolysis. Other rare causes of rhabdomyolysis include Haff disease, mushroom poisonings, and genetic disorders.

Recognition of rhabdomyolysis can be traced back to the time when the Israelites experienced rhabdomyolysis-like symptoms after consumption of quail during their departure from Egypt. This myolysis resulted from consuming quails that ate poisonous plants (to which the quails are not susceptible) during the spring migration. A similar clinical presentation has also been reported from the Mediterranean region after consuming robins, chaffinches, and skylarks, as these birds are also not susceptible to the active alkaloids from hemlock and other poisonous herbs. In more recent times, war, earthquakes, and other man-made and natural disasters have resulted in crush injuries. In 1943, Bywaters and Stead identified myoglobin as the offending agent for brown urine acute tubular necrosis through animal experiments.