Bleeding in OLT is related to two different mechanisms. There is no doubt that the extensive surgical trauma plays a critical role in the origin of serious bleeding. However, this bleeding can be aggravated by defects in the hemostasis system. Hemostasis defects can be divided into those present before the operation and secondary to the underlying liver disease and those originating during the operation. Intraoperative defects can be classified according to the three main systems of hemostasis: coagulation, fibrinolysis, and platelet function. Serious problems with coagulation are clearly related to the quality of the graft and are less frequent now since better graft preservation techniques have been introduced. Adequate intraoperative monitoring and substitution therapy with plasma products is also important in controlling coagulation defects. However, problems resulting from hyperfibrinolysis seem to be of clinical importance, especially during the anhepatic stage and after graft reperfusion. While lack of hepatic clearance seems to be an important cause of t-PA increase during the anhepatic stage, enhanced release may be important for the rise after graft reperfusion. There is also evidence that decreased platelet numbers and function, especially after graft reperfusion, play a role. The clinical relevance of this finding remains to be elucidated. Finally, it has recently been demonstrated that antifibrinolytic agents may reduce intraoperative blood loss. However, the effect of aprotinin and other antifibrinolytic agents has still to be confirmed by randomized clinical studies. Future scientific research should focus on the mechanisms underlying the hemostasis defects. It can be expected that these efforts may finally result in a further reduction in the usage of blood products during liver transplantation.