Impaired liver function due to cirrhosis or other causes leads to decreased synthesis of clotting factors, including factors II, V, VII, IX, X, and fibrinogen; whereas factor VIII levels, largely made in endothelial cells, may be elevated despite depressed levels of other coagulation factors. The PT (and with advanced disease, the aPTT) is typically prolonged and usually 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.
The coagulopathy of liver disease usually does not require hemostatic treatment unless bleeding occurs. Infusion of FFP 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 below 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. The coagulopathy of liver disease can predispose to bleeding or thrombosis, so caution and experience are needed for optimal management.