Rhabdomyolysis
From NPPAWIKI
Contents |
Background
Rhabdomyolysis was first described in the victims of crush injury following the 1940-1941 London, England, bombing raids of World War II. Since then, multiple etiologies of rhabdomyolysis have been discovered.
Natural History
Most cases of rhabdomyolysis develop as a result of muscle injury or strain, or other external causes (such as medication or intoxication). However, the cause is not always obvious. Pain, tenderness, weakness and edema of the affected muscles may be present. If the swelling is very rapid (i.e., sudden released of significant pressure on the tissues), hypotension and shock may ensue. Other symptoms are nonspecific and result either from the consequences of the breakdown of muscle tissue, or from the original condition that caused the muscle breakdown.
Pathophysiology
Rhabdomyolysis is the breakdown of muscle fibers with leakage of potentially toxic intracellular contents into the systemic circulation. The overall mortality rate for patients with rhabdomyolysis is approximately 5%; however, the mortality rate of any single patient is dependent upon the underlying etiology and any existing comorbidities.
The final common pathway of rhabdomyolysis is most likely to be a disturbance in myocyte calcium homeostasis. In the United States, rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure.
Clinical Aspects of Rhabdomyolysis
Incidence is higher in males than in females, especially in the subgroups of trauma and inherited enzyme deficiencies. Rhabdomyolysis may occur in infants, toddlers, and adolescents who have inherited enzyme deficiencies of carbohydrate or lipid metabolism or who have inherited myopathies, such as Duchenne muscular dystrophy and malignant hyperthermia.
Clinical sequelae of rhabdomyolysis include the following: (a) Hypovolemia (sequestration of plasma water within injured myocytes); (b) Hyperkalemia (release of cellular potassium into the systemic circulation); (c) Metabolic acidosis (release of cellular phosphate and sulfate); (d) Acute renal failure (nephrotoxic effects of liberated myocyte components); and (e) Disseminated intravascular coagulation (DIC).
Notes & References
[1] Visweswaran P, Guntupalli J. Rhabdomyolysis. Crit Care Clin. 1999;15:415-428.
Credits & Notices
Authors-contributors to this page (listed alphabetically, last name, first & middle initial only, no institutional affiliations, no scientific titles):
Stawicki SP
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