VENOUS ISCHEMIA IN SKIN FLAPS - MICROCIRCULATORY INTRAVASCULAR THROMBOSIS

Although endothelial cell injury and microcirculatory intravascular cl otting have been implicated in the pathophysiology of skin-flap failur e and various hematologically active drugs have been used to improve f lap survival, the basic underlying pathophysiology has not been docume nted previously. In this study of venous ischemia in pig flaps, we foc us on the accumulation and distribution of platelets and fibrinogen in the flap, on the morphologic changes in the flap microcirculation, an d on changes in various coagulation factors in the venous effluent fro m the flap. Bilateral buttock skin flaps and latissimus dorsi myocutan eous flaps were designed and elevated on 12 pigs. All flaps had a prim ary ischemic insult (clamp application to the vascular pedicle) of 2 h ours, followed by 2 hours of reperfusion, and then one side was subjec ted to a 6-hour period of secondary venous ischemia (clamp application to the dominant flap vein). In six animals, radioactively labeled aut ologous platelets and human fibrinogen were injected intravenously hal f an hour before termination of secondary venous ischemia. Flaps were weighed and counted for radioactivity. Flap biopsies and the buffy coa t of venous effluent were processed for electron microscopy. In the ot her six animals, venous effluent was collected before secondary ischem ia, upon immediate reperfusion, and at 4 and 8 hours after termination of secondary ischemia. Venous plasma levels of fibrinogen, von Willeb rand factor, and antithrombin III were measured. Platelet and fibrinog en accumulation was increased in flaps with venous stasis when compare d with control flaps at both time intervals studied; a twofold increas e was seen prior to reperfusion, and a threefold increase was seen fol lowing 4 hours of reperfusion. Venous effluent could not be collected from buttock skin flaps because of slow reflow and clotting in the col lecting system. In comparing the venous effluent of control flaps with that of venous ischemic latissimus dorsi flaps, hematocrit was signif icantly elevated. Blood samples collected for analysis of fibrinogen, antithrombin III, and von Willebrand factor could not be analyzed beca use of postcollection clotting. Electron microscopy showed extravasati on of red blood cells and activated platelets, fibrin, and red blood c ells in distended and partly disrupted capillaries. The venous ischemi a reperfusion injury is associated with thrombosis in the microcircula tion and alterations in consumption of coagulation factors. This study gives physiologic support for potential beneficial effects of treatme nt modalities that aim at counteracting the different components of th rombus formation.