Extremity Tourniquets

Skin

Trauma to the skin can be caused by pressure necrosis due to inadequate padding between the skin and tourniquet or friction burns due to movement of a poorly applied tourniquet. Obese patients with redundant upper extremity skin folds are at increased risk for skin injury. Skin preparation solutions may soak into the padding under the tourniquet, resulting in full-thickness chemical burns.

Muscle

Myocytes are very sensitive to compression and ischemia. Injury is more severe with lengthy tourniquet inflation or high pressure. Usually, injury is greatest beneath the tourniquet. Associated ischemia, edema, and microvascular congestion cause the post-tourniquet syndrome. This includes stiffness, pallor, and weakness (not paralysis), with subjective extremity numbness. Rhabdomyolysis may occur if the tourniquet is inflated for a prolonged period of time under high pressure. Compartment syndrome may occur after tourniquet deflation as a result of edema and reperfusion hyperemia.

Peripheral Nerves

Mechanical pressure compresses nerves directly beneath the tourniquet cuff, and shear forces at the proximal and distal edges of the cuff also cause nerve injury ranging from paresthesia to complete paralysis. Distal ischemia plays a lesser role. The contribution of tourniquet time to the development of nerve injury is unclear, and paralysis has been reported with as little as 30 minutes of tourniquet inflation. Lower extremity nerve injury usually involves the sciatic nerve. The upper extremity appears to be more commonly associated with tourniquet related nerve injury than the lower extremity, with radial nerve injury more frequently observed than either ulnar or median nerve injury. When tourniquet-related nerve injury occurs in the lower extremity, the sciatic nerve is the most likely to be affected.

Localized nerve injuries tend to be neuropraxic injuries, with structural damage limited to the myelin sheath surrounding individual axons, without injury to the axon itself. Neuropraxic injuries tend to be self-limiting, with an excellent prognosis for complete recovery within a period of several days to weeks. In contrast, axonotmetic injuries involve damage to the axon itself, resulting in loss of signaling function once electrical excitability is lost and depolarization can no longer occur. These injuries take longer to recover as the axon must regenerate along the connective tissue highway, and some injuries may not completely recover. Rarely, a permanent nerve deficit occurs ( Table 55.1 ).

Vasculature

Arteries and veins, especially prosthetic grafts (e.g., arteriovenous fistulas, arterial bypass grafts), are susceptible to traumatic injury from mechanical compression. Although direct arterial injury is rare (0.03% to 0.14% incidence), fractured atherosclerotic plaque may cause localized thrombosis or embolize distally to cause ischemia. Although deep venous thrombosis (DVT) is a known and common complication of lower limb surgery, tourniquets bear no relation to deep venous stasis and thrombus formation. Rather, systemic hypercoagulability is due to catecholamine release and platelet aggregation caused by tourniquet-related or surgical pain. In contrast, active bleeding after tourniquet release may be aggravated by ischemia-caused tissue plasminogen activator release and fibrinolysis.