TOURNIQUET-RELATED HYPOTENSION IN VENOUS STASIS ULCER EXCISION

Extremity tourniquets are widely used to achieve bloodless dissection in the surgical field. Excision of venous stasis ulcers (VSU) is aided by tourniquet use because of large dilated veins associated with veno us stasis disease. We present 3 patients with hypotensive shock occurr ing 10 to 15 minutes after tourniquet release after excision of venous stasis ulcers. All patients had long histories of venous stasis chang es and two-thirds had prior histories of deep vein thromboses and pulm onary embolism. Mean tourniquet inflation time was 34 minutes and ther e were electrocardiographic changes in two-thirds of the patients. All patients responded rapidly to standard resuscitation measures and in all 3 postoperative testing for pulmonary embolus and myocardial infar ction was negative. Wound cultures revealed no organisms in 1 patient, mixed Gram-positive cocci in another, and greater than 10(5) Serratia marcescens in the third patient. Although small decreases in blood pr essure and blood pH, and increases in blood lactate, PCO2, and creatin ine phosphokinase, are normally associated with the use of extremity t ourniquets, hypotensive shock has not been reported. The combined effe ct of tourniquet ischemia and venous stasis changes may cause hypotens ive shock by (1) an endotoxic bolus upon tourniquet release, (2) pulmo nary microembolization of platelet, fibrin, and leukocyte aggregates c ausing vasoactive substance release, and (3) synergistic effects of pl atelet-activating factor, a known mediator of endotoxic shock. The unt oward events noted in these patients may be prevented by (1) proximal to distal dissection of the ulcer with initial ligation of large veins , (2) pretreatment with steroids and/or platelet-activating factor ant agonists, and/or (3) slow release of the tourniquet.