• R A Pedowitz, J Fridén, and L E Thornell.
• Department of Anatomy, University of Umeå, Sweden.
• J. Surg. Res. 1992 Mar 1;52(3):243-50.

AbstractThe pathophysiology of skeletal muscle injury induced by compression beneath pneumatic tourniquets is poorly understood. Tourniquet hemostasis was induced in rabbit hindlimbs for 2 hr with a cuff inflation pressure of either 125 mm Hg (n = 5) or 350 mm Hg (n = 5). Skeletal muscle biopsies, taken 2 days later from tissue beneath and distal to the tourniquet, were frozen and analyzed using enzyme- and immunohistochemical techniques. In the 350 mm Hg tourniquet group, four of 10 thigh muscle samples demonstrated significant regional necrosis (mean 37.3% of the total cross-sectional area). Regional necrosis was not observed in thigh muscles of the 125 mm Hg tourniquet group or in any of the ischemic leg muscles. A topographic pattern of necrosis consistent with the arterial distribution of skeletal muscle suggested pathogenic events during the reperfusion period, such as granulocyte-mediated superoxide radical formation. Extremely large and rounded fibers (histochemically identified as Type IIB fibers) were observed in compressed thigh muscles, indicating differential fiber sensitivity to tourniquet compression and ischemia. The present study demonstrated significant skeletal muscle necrosis after a 2 hr tourniquet applied at a clinically relevant cuff inflation pressure. Recent studies of systemic changes associated with limb "ischemia" should be reassessed in consideration of the confounding effects of tissue compression induced beneath pneumatic tourniquets.

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