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For further information, see CMDT Part 16-09: Acquired Disorders of Coagulation

KEY FEATURES

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

  • Clinical signs of advanced liver disease

DIAGNOSIS

  • The prothrombin time (PT) (and with advanced disease, the activated partial thromboplastin time [aPTT]) is typically prolonged and corrects on mixing with normal plasma

  • A normal factor V level, with decreased activity of factors II, VII, IX, and X, 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 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 benefit

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