AICF and DIC in Liver Cirrhosis: Expressions of a Hypercoagulable State

Abstract

Liver cirrhosis is associated with a large spectrum of he-mostatic abnormalities that may contribute to abnormal microvascular bleeding (1). These include thrombocytopenia, platelet dysfunction, prolonged coagulation screening tests (APTT, PT, TT), decreased coagulation zymogens and co-factors, abnormal coagulation factors (hypocarboxylated factors X, IX, VII, II, dysfibrinogen), decreased natural anticoagulants (antithrombin III, protein C, protein S) and shortened euglobulin clot lysis time or dilute whole blood clot lysis time reflecting increased fibrinolysis (1). The mechanisms involved in these abnormalities are complex and incompletely understood. Thrombocytopenia is thought to be largely due to increased pooling of platelets in an enlarged spleen (hypersplenism), with decreased hepatic production of thrombopoietin as a possible contributor. Decreased coagulation zymogens, cofactors, and anticoagulants have been attributed to decreased synthesis and, to a lesser degree, increased third-spacing (e.g., ascites). Hyper-fibrinolysis appears to result largely from impaired clearance of plasminogen activators by the diseased liver. Because of the striking similarity between the hemostatic abnormalities seen in liver cirrhosis and those observed in disseminated intravascular coagulation (DIC), also called consumption coagulopathy, there has been a long and continued debate as to whether DIC is a common feature of, and an important contributor to, hemostatic failure in liver cirrhosis (2, 3, 4, 5, 6). The notion of a consumptive coagulopathy in liver cirrhosis was supported by earlier observations (7, 8, 9, 10, 11) that survival of radiolabeled platelets, fibrinogen, and plasminogen was shortened in some patients with liver cirrhosis, and, more importantly, shortened survival of fibrinogen, but not that of platelets or plasminogen, could be prolonged with administration of heparin (7, 8, 9, 10) and antithrombin III (ATIII) (11).