Coagulopathy in cirrhosis - The role of the platelet in hemostasis

摘要

Cirrhotic patients are at increased risk of bleeding, particularly gastrointestinal bleeding, as a consequence of portal hypertension and/or coagulopathy attributed to liver synthetic dysfunction. Paradoxically, they are also at risk of thrombosis, predominantly in the splanchnic circulation, especially when platelet counts are increased by transfusion or drug therapy, A major problem in clinical practice is the inadequacy of coagulation tests, which do not predict bleeding or thrombotic events, but may result in the inappropriate administration of therapies (e.g., plasma transfusions prior to procedures). Additionally, these tests cannot provide information on the dynamic interaction between the coagulation and anticoagulation pathways. Evidence is mounting to highlight the central role of the platelet, of which the quantitative and qualitative properties may determine the dynamic hemostatic forces in cirrhosis. Cirrhotic thrombocytopenia and platelet dysfunction are multifactorial with many simultaneous contributions. Portal hypertension leads to splenic pooling, sequestering platelets from the circulation. Portosystemic shunting and gut barrier disruption result in endotoxaemia with systemic immune activation, antiplatelet antibody production, aberrant fibronolysis, and activation of coagulation with platelet consumption. Cirrhosis and decreased functional liver mass result in lower thrombopoetin levels and platelet underproduction.