8/10/2019 Causes of Rhabdomyolysis
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Causes of rhabdomyolysis
Causes of rhabdomyolysisAuthor
Marc L Miller, MD
Section EditorsIra N Targoff, MD
Jeremy M Shefner, MD, PhD
Deputy Editor
Paul L Romain, MDDisclosures
All topics are updated as new evidence becomes available and
ourpeer review processis
complete.
Literature review current through: Oct 2012. | This topic last
updated: Jun 12, 2012.
INTRODUCTION
Rhabdomyolysis is a syndrome characterized by muscle necrosis
and therelease of intracellular muscle constituents into the
circulation. Creatine kinase (CK) levels are
typically markedly elevated, and muscle pain and myoglobinuria
may be present. The severity of
illness ranges from asymptomatic elevations in serum muscle
enzymes to life-threatening diseaseassociated with extreme enzyme
elevations, electrolyte imbalances, and acute kidney injury.
The causes of rhabdomyolysis will be reviewed here. The clinical
manifestations and diagnosisof rhabdomyolysis; the clinical
features and diagnosis of acute kidney injury due to
rhabdomyolysis; the management of patients with rhabdomyolysis,
including methods to prevent
acute kidney injury and related metabolic complications; and the
prevention and management of
acute compartment syndrome are discussed in detail separately.
(See"Clinical manifestations
and diagnosis of rhabdomyolysis"and"Clinical features and
diagnosis of heme pigment-inducedacute kidney injury (acute renal
failure)"and"Prevention and treatment of heme pigment-
induced acute kidney injury (acute renal
failure)"and"Crush-related acute kidney injury (acuterenal
failure)"and"Acute compartment syndrome of the extremities".)
PATHOPHYSIOLOGYThe clinical manifestations and complications of
rhabdomyolysisresult from muscle cell death, which may be triggered
by any of a variety of initiating events.
The final common pathway for injury is an increase in
intracellular free ionized cytoplasmic and
mitochondrial calcium. This may be caused by depletion of ATP,
the cellular source of energy,
and/or by direct injury and rupture of the plasma membrane
[1,2]. The latter pathway of injuryalso results in ATP
depletion.
The increased intracellular calcium leads to activation of
proteases, increased skeletal musclecell contractility,
mitochondrial dysfunction, and the production of reactive oxygen
species,
resulting in skeletal muscle cell death [1]. ATP depletion
causes dysfunction of the Na/K-
ATPase and Ca2+
ATPase pumps that are essential to maintaining integrity of the
myocyte. ATPdepletion leads to myocyte injury and the release of
intracellular muscle constituents, including
creatine kinase and other muscle enzymes, myoglobin, and various
electrolytes.
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