Abstract

CRITICAL BLEEDING can be defined as lifethreatening, catastrophic bleeding that continues despite standard surgical or medical management. Its primary cause is a failure of the coagulation system to produce a stable fibrin plug at the site of vascular injury. The key to obtaining hemostasis is the generation of thrombin at the site of vascular disruption. This will activate platelets and convert fibrinogen to fibrin, which can be stabilized via the thrombin-activated fibrinolysis inhibitor (TAFI) pathway. The complexing of tissue factor, exposed by endovascular disruption, and factor VII is now thought to be the initiating event of this process. Although severe perioperative bleeding in cardiac surgery is multifactorial in origin, failure of thrombin generation is known to be a main cause. Therefore, in late 2001 we introduced into our clinical practice the hemostatic agent, recombinant factor VIIa (rFVIIa; NovoSeven , Novo Nordisk, Bagsvaerd, Denmark), which since 19882 has proven effective in other perioperative settings. rFVIIa exerts its hemostatic effect by enhancing thrombin generation on the surface of activated platelets.

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