Ischemia/reperfusion injury in microvascular surgery

Early microscopic evidence for endothelial damage in arterial microanastomoses

“…Several components in the connective tissue of vessel wall are thrombogenic, especially collagen and tissue factors. The damaged endothelium and the exposed connective tissue elements initiate the extrinsic pathway of thrombosis, leading to thrombin formation, platelet accumulation and thrombosis at the anastomotic site [2].…”

“…These events are responsible for the reduction or absence of flow in the downstream microcirculation and for the onset of the no-reflow phenomenon [3]. Shutdown of the microcirculation is manifested as flap ischemia [2]. In addition, other factors can play a role in the pathogenesis of the no-reflow phenomenon.…”

“…Although the success rate of revascularized tissue transfer approaches 90-97%, the key to success is to avoid thrombus formation at the microanastomoses site. Thrombosis of the arterial microanastomoses is the major reason for flap complications [2]. This situation can occur rapidly at the site of anastomosis or its development may be delayed resulting in secondary ischemia.…”

“…The usual cause for flap failure is a technical problem occurring during the microanastomosis. Moreover, it is well known that thrombogenicity at the anastomotic site is maximal over the first 30 min after reperfusion [2]. The damaged endothelial cells and the exposed connective tissue play an important role in the molecular and cellular mechanisms of coagulation and thrombosis [3,6].…”

“…The damaged endothelial cells and the exposed connective tissue play an important role in the molecular and cellular mechanisms of coagulation and thrombosis [3,6]. The release of cytokines from endothelial cells and the exposure of plasma proteins and platelets to subintimal collagen can trigger vascular thrombosis [2]. For these reasons the early events at the microanastomotic site are crucial for flap success.…”