Rhabdomyolysis is a severe clinical symptom of variable etiology. Acquired factors of exogenous origin such as traumata and endogenous metabolic disturbances have to be separated from
hereditary disease as causative mechanism. Most frequently, exertional stress during
hyperthermia, traumatic damage or
ethanol abuse are observed. Almost independent of the diverse initial events, the pathogenesis follows a common final pathway with intracellular
calcium accumulation and
ATP depletion. Clinical symptoms vary. Seldom, the classical triad of
muscle pain, weakness, and dark urine is observed. Recurrent episodes should raise suspicion of an inherited disorder. Severe complications are
hypovolemia,
electrolyte disorders with
hyperkalemia and
hypocalcemia resulting in life threatening arrhythmias, a
compartment syndrome,
disseminated intravascular coagulation and
acute renal failure, which is frequently oligo-anuric. In combination with often severe underlying disease,
renal failure causes death in 1/5 of the patients. The diagnosis is made with the determination of serum
creatine kinase and the
myoglobin levels in plasma and urine. Therapeutic options are to correct the
hypovolemia with sufficient fluid supply, the prevention of
oliguria using
loop diuretics, alkalinization of the urine, normalization of serum
electrolytes with reduction of hyperkaemia, and
decompression of
compartment syndromes. An underlying disease should be evaluated to initiate specific therapeutical and preventative steps. Avoiding pre-disposing factors by identifying the mechanisms of disease will reduce the occurrence of
rhabdomyolysis with its still high mortality.