Neurol. praxi. 2012;13(4):198-203

Rhabdomyolysis

doc.MUDr.Peter Špalek, PhD.

Centrum pre neuromuskulárne ochorenia, Neurologická klinika SZU, Univerzitná nemocnica Bratislava - Ružinov

Rhabdomyolysis, a syndrome of skeletal muscle breakdown with leakage of muscle contents, is frequently accompanied by myoglobinuria,

and if sufficiently severe, acute renal failure with potentially life-threatening metabolic derangements may ensue. 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 and dark, tea-colored urine are the main clinical

manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The severe life-threatening

conditions of rhabdomyolysis are associated with extreme elevations in creatine kinase, electrolyte imbalance, myoglobinuria,

acute renal failure and disseminated intravascular coagulation. 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.

diagnosis, management.

Keywords: rhabdomyolysis, acquired causes, inherited causes, creatine kinase, myoglobinuria, acute renal failure, clinical manifestation,

Published: July 31, 2012  Show citation