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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
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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
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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
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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