Liver transplantation is frequently complicated by hemostatic defects associated with end-stage liver disease, surgical bleeding, and the grafted organ recovering from ischemia and reperfusion injury. Management of hemostatic defects in patients undergoing liver transplantation, therefore, requires a thorough understanding of pathophysiology of coagulation, clinically relevant assessment of coagulation, and the selection of rational treatment modes.
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Pathophysiology of Coagulation in End-state Liver DiseaseHemostasis, a vital homeostatic function, is the process by which blood in a liquid state is transformed into a solid state, then back to a liquid state. The vascular endothelium, platelets, and coagulation proteins participate, simultaneously and interdependently, in 5 equally important phases, namely the vascular phase, the platelet phase, the fibrin formation phase, the fibrin polymerization phase, and the fibrinolysis phase. Liver disease affects all 5 phases of coagulation. 1 The vascular phase of coagulation is impaired by peripheral vasodilation, development of numerous collateral vessels, reduced vascular constrictive response and elasticity, and decreased interaction between vessel walls and platelets, and is seen as prolonged bleeding time. 2 The platelet phase is also significantly affected in most patients. Thrombocytopenia is observed in up to 70%, 3 and is caused by splenomegaly, shortened platelet survival, platelet consumption, sequestration of platelets in the regenerating liver, the folic acid deficiency in alcoholic liver disease, and toxic effects of alcohol on megakaryocytes. Platelet dysfunction is also revealed by the prolonged bleeding time in the presence of adequate platelet count and diminished clot retraction. 4 The coagulation cascade is affected at all levels, because production of most proteins involved in coagulation is 17
