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Key Features

  • Impaired hepatic function leads to decreased synthesis of clotting factors, including factors II, VII, V, IX, and fibrinogen, whereas factor VIII levels may be elevated in spite of depressed levels of other coagulation factors

  • Can predispose patients to bleeding or thrombosis, so caution and experience are needed for optimal management

Clinical Findings

  • Bleeding at any site from coagulopathy

  • Oozing at venipuncture sites from excessive fibrinolysis

  • Clinical signs of liver disease

  • No response to vitamin K

  • Disseminated intravascular coagulation (DIC) may occur in end-stage liver disease

Diagnosis

  • The PT (and with advanced disease, the aPTT) is typically prolonged and corrects on mixing with normal plasma

  • A normal factor V level, in spite of decreases in the activity of factors II, VII, IX, and X, however, suggests vitamin K deficiency rather than liver disease

  • Qualitative and quantitative deficiencies of fibrinogen also are prevalent among patients with advanced liver disease, typically leading to a prolonged PT, thrombin time, and reptilase time

Treatment

  • Hemostatic treatment usually not required until bleeding complications occur

  • Infusion of fresh frozen plasma may be considered if active bleeding is present and the aPTT and PT are markedly prolonged; however, the effect is transient and concern for volume overload may limit infusions

  • Patients with bleeding and a fibrinogen level consistently < 80–100 mg/dL should receive cryoprecipitate

  • Liver transplantation, if feasible, results in production of coagulation factors at normal levels

  • The use of recombinant human activated factor VII in patients with bleeding varices is controversial, although some patient subgroups may experience benefit

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