Rhabdomyolysis (lysis of skeletal muscle cells) is a potentially lethal syndrome with broad spectrum of clinical and biochemical
findings. Rhabdomyolysis is caused by a diverse spectrum of inherited and acquired disorders affecting muscle
membranes, membrane ion channels and muscle energy supply. The commmon final pathophysiological mechanisms
of all causes of rhabdomyolysis is an uncontrolled rise in free intracellular calcium and activation of calcium-dependent
proteases leading to destruction of myofibrils and lysosomal digestion of muscle fiber contents. Recent advances
in molecular genetics and muscle enzyme histochemistry may enable a specific metabolic diagnosis in many patients
with idiopathic recurrent rhabdomyolysis. Muscle weakness, myalgias, pigmenturia (dark, tea-colored urine) are the
main clinical manifestations. Elevated activity of serum creatin kinase is the most sensitive laboratory finding. Fulminant
rhabdomyolysis may be associated with severe metabolic disturbances and involvement of other organ systems.
Cardiac arrest, compartment syndrome, and acute renal failure are the major complications. The prevention of life-threatening
complications of rhabdomyolysis strongly depends on early diagnosis and adequate therapy. The management
of patients in acute phase of rhabdomyolysis is governed by renal and metabolic consequences of myoglobinuria and
requires early vigorous hydration. After the metabolic syndrome has been corrected, triggering factors and predisposing
conditions should be investigated in all cases of rhabdomyolysis. Since the repair mechanism of striated muscle
functions very well, the prognosis of appropriately treated rhabdomyolysis is excellent.