Intramuscular Pressures with Limb Compression: Clarification of the Pathogenesis of the Drug-Induced Muscle-Compartment Syndrome

Charles A. Owen, Scott J. Mubarak, Alan R. Hargens, Ladd Rutherford, Lawrence P. Garetto, Wayne H. Akeson

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Abstract

To study muscle necrosis due to prolonged limb compression, we measured intramuscular pressure by inserting wick catheters into 10 volar forearms and 10 anterior tibial compartments of adult volunteers. We then placed the subjects in positions in which victims of drug overdose are commonly found. Intramuscular pressures in the area of direct compression on hard surfaces ranged from 26 to 240 mm Hg, and averaged 101 mm Hg. Most remarkable was a mean pressure of 180 mm Hg on compression of the forearm by the rib cage. These pressures are sufficient to cause muscle and capillary ischemia and necrosis by local obstruction of the circulation. This local injury by limb compression may produce edema sufficient to start compartment tamponade and consequent muscle-compartment and crush syndromes. (N Engl J Med 300:1169–1172, 1979) CRUSH syndrome is the systemic manifestation of muscle necrosis and consists of myoglobinuric renal failure, shock, acidosis and hyperkalemia. Since the description by Bywaters and Beall in 1941,1 numerous articles have linked limb compression, muscle-compartment syndrome and crush syndrome. Compression of a limb may initiate muscle-compartment syndromes in one or more extremities and produce the systemic manifestations of crush syndrome. The severity of the syndrome depends on the amount of muscle damage.2 The syndrome was first seen among casualties who had been buried under debris during the London Blitz of December, 1940.1 Currently, the most common cause of the syndrome.

Original languageEnglish (US)
Pages (from-to)1169-1172
Number of pages4
JournalNew England Journal of Medicine
Volume300
Issue number21
DOIs
StatePublished - May 24 1979

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  • Medicine(all)

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