Tourniquet-induced neuromuscular injury. A recent review of rabbit and clinical experiments.

A rabbit model was developed which facilitates controlled, experimental studies of tissue injury beneath and distal to a pneumatic tourniquet. Non-uniform tissue deformation was observed beneath inflated tourniquets; such patterns were not predicted by previous mathematical models. Two hours was a time threshold for tourniquet compression injury; depending upon the cuff inflation pressure, greater muscle injury was induced beneath the tourniquet than distal to it. A topographic pattern of necrosis was observed after two hours of tourniquet compression, which may relate to the microvascular anatomy of skeletal muscle and to pathogenic events during tissue reperfusion. With a four hour total tourniquet time, skeletal muscle injury beneath the cuff was significantly decreased by hourly, ten minute reperfusion intervals. A reperfusion interval after two hours of 350 mmHg cuff inflation tended to exacerbate muscle injury. Physiologic and morphologic nerve abnormalities were induced by a two hour, 350 mmHg tourniquet. Axonal degeneration may correlate with EMG changes after clinical tourniquet application. Paranodal myelin invagination is probably not an important mechanism of injury at clinically relevant tourniquet inflation pressures. Wide cuffs, limb shaped cuffs, and direct determination of the minimal necessary inflation pressure facilitated the use of lower tourniquet pressures in extremity surgery. In conclusion, tourniquet application, at clinically relevant cuff inflation pressures and durations, induces greater neuromuscular injury beneath the tourniquet than distal to it. Investigators of systemic effects of limb ischemia should be aware of compression injury induced by pneumatic tourniquet models. Surgeons must weigh the advantages of a bloodless field against the disadvantages of tourniquet-induced neuromuscular injury.