The term rhabdomyolysis is used to describe the breakdown or disintegration of striated muscle. Almost independent of the miscellaneous initial events, the pathogenesis follows a common final pathway with intracellular calcium accumulation and the depletion of ATP.
Many clinical features of rhabdomyolysis are nonspecific, and the course of the disease varies depending on the underlying condition. As some complications of rhabdomyolysis can be quite severe (such as hyperkalemia, cardiac arrest and acute renal failure), early recognition and prompt management of this condition are pivotal for a successful outcome.
Almost half of all patients with rhabdomyolysis present with the following triad of symptoms: myalgias, weakness and typical brown-red colored urine due to the presence of myoglobin. A large number of patients presenting with calf pain or muscle swelling have their diagnosis confounded by other conditions, most notably deep venous thrombosis.
Non-specific systemic symptoms, such as fever, abdominal pain, malaise and nausea and may also be observed. Proper assessment of symptoms can be hampered in patients with altered mental status, electrolyte imbalance or uremic encephalopathy. The transaminases tend to be increased, which can lead to the condition being confused with acute liver injury.
Physical examination may reveal signs of dehydration, such as decreased skin turgor, delayed capillary refill and dry mucous membranes. If trauma has occurred, the overlying skin is often bruised or discolored. With the development of a compartment syndrome, the affected area is painful with specific sensory and motor deficits.
The most common complication is acute renal failure due to acute tubular necrosis as a result of mechanical obstruction by myoglobin (in particular if serum creatine kinase levels are higher than 16.000 IU/l). Mortality rate is approximately 10% and even higher in patients with acute renal failure.
First screening of rhabdomyolysis can be performed with a urine dipstick test. The orthotoluidine portion of the dipstick turns blue in the presence of hemoglobin or myoglobin; therefore it can be used as a surrogate marker for myoglobin if there are no red blood cells in freshly spun sediment of urine.
The most sensitive laboratory test for detecting rhabdomyolysis is serum creatine kinase level. As muscle cells disintegrate and release creatine kinase into plasma, the degree of its elevation shows a direct correlation with the degree of muscle necrosis.
Other muscle markers can also be employed. Aldolase is a glycolytic pathway enzyme that is found in high concentration in skeletal muscle (but also liver and the brain), and together with creatine kinase is highly suggestive of muscle injury. An increase in levels of carbonic anhydrase III is specific for skeletal muscle injury, as it is not present in myocardium.
On the other hand, determining levels of myoglobin (skeletal muscle protein involved in oxidative metabolism) appears to be less sensitive tests for establishing the correct diagnosis, as it is rapidly and unpredictably eliminated by hepatic metabolism.
Finally, directed laboratory testing aimed at uncovering the underlying cause of rhabdomyolysis is crucial. Such diagnostic evaluations may include toxicologic testing, bacteriologic and viral tests, genetic analysis, muscle biopsy and forearm ischemic test.