[Pathophysiological mechanisms of coagulation dysfunction associated with liver disease].

Coagulation abnormalities associated with liver diseases easily lead to spontaneous and secondary bleeding, which is associated with hemodynamic changes, reduced synthesis of coagulation factors, liver disease-related thrombocytopenia, and pharmacological interventions. On the other hand, patients with liver disease also have a hypercoagulable state, making them prone to portal vein thrombosis, which is associated with hemodynamic changes, reduced synthesis of anticoagulants, abnormal vascular intima structure, inflammation, and pharmacological treatment. Additionally, patients with liver disease are at an intertwined risk of bleeding and thrombosis and are in a fragile state of hemostasis rebalancing for an extended period. Genetic factors and diagnostic and therapeutic procedures further challenge the management of coagulation function in patients with liver disease. This article discusses the mechanisms of coagulation abnormalities from the perspectives of both bleeding and thrombosis, providing assistance for dynamically managing and rebalancing the hemostasis in patients with liver disease.