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For further information, see CMDT Part 14-09: Acquired Disorders of Coagulation

Key Features

  • Impaired hepatic function leads to decreased synthesis of clotting factors, including factors II, VII, V, IX, X, and fibrinogen

  • Factor VIII levels, largely made in endothelial cells, may be elevated despite 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


  • 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


  • Hemostatic treatment usually not required unless bleeding complications occur

  • Infusion of fresh frozen plasma may be considered if active bleeding is present and the aPTT and PT are 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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