Mechanism and clinical management strategies of rebalanced hemostasis in severe liver disease

Severe liver disease is frequently accompanied by prolonged prothrombin time or international normalized ratio， thrombocytopenia， and abnormal fibrinogen level， which have traditionally been interpreted as hypocoagulability and a bleeding tendency. Recent studies have shown that hemostatic abnormalities in liver disease do not simply result from deficiency of procoagulant factors， but represent a fragile rebalanced hemostatic state shaped by multiple mechanisms including parallel reductions in procoagulant factors and natural anticoagulants， platelet and fibrinolytic abnormalities， imbalance of the von Willebrand factor/a disintegrin and metalloproteinase with a thrombospondin type 1 motif member 13 axis， and endothelial activation. This article reviews the key mechanisms of rebalanced hemostasis in severe liver disease， the limitations of conventional coagulation markers， coagulation features across different disease states， and their implications for clinical management. Clinical decision-making should shift from correcting abnormal laboratory values to identifying destabilization of the inflammation-endothelium-coagulation-fibrinolysis network， with individualized assessment based on disease stage and the risk of bleeding/thrombosis.