The syndrome of rhabdomyolysis: Pathophysiology and diagnosis

George D. Giannoglou, Yiannis S. Chatzizisis, Gesthimani Misirli

Research output: Contribution to journalReview article

139 Scopus citations

Abstract

Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular material into the blood circulation. Its major causes include trauma, ischemia, drugs, toxins, metabolic disorders, and infections. The pathophysiological hallmark of the syndrome is an increase in intracellular free ionized calcium due to either cellular energy depletion, or direct plasma membrane rupture. The increased intracellular calcium activates several proteases, intensifies skeletal muscle cell contractility, induces mitochondrial dysfunction, and increases the production of reactive oxygen species, ultimately resulting in skeletal muscle cell death. Clinically, the syndrome presents with severe muscular pain, weakness and myoglobinuria. Increased myoglobin and creatine phosphokinase as a consequence of muscular cell death are the major laboratory findings, which, in combination with the clinical presentation, lead the clinician to the final diagnosis of the syndrome.

Original languageEnglish (US)
Pages (from-to)90-100
Number of pages11
JournalEuropean Journal of Internal Medicine
Volume18
Issue number2
DOIs
StatePublished - Mar 2007

Keywords

  • Calcium
  • Cell death
  • Diagnosis
  • Energy depletion
  • Rhabdomyolysis

ASJC Scopus subject areas

  • Internal Medicine

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