Liver Disease

Liver Disease is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

Liver disease can impair hemostasis (see Figure 20-1) due to a reduction in coagulation factor production by hepatocytes, with the exception of vWF and factor VIII. Cholestasis, which leads to impaired vitamin K absorption, can also contribute because of decreased production of Factors II, VII, IX, and X. Patients who have stable liver disease typically only have a mild coagulopathy, though decompensated liver disease will worsen the coagulopathy severity. Liver disease may produce other hemostatic complications that include thrombocytopenia due to splenic sequestration, DIC, hyperfibrinolysis. Infection, renal insufficiency, and vasomotor dysfunction may also disrupt the fragile balance of procoagulant and anticoagulant activities.1 Although PT/INR and aPTT prolongations imply an increased risk of bleeding, they do not reflect concurrent reductions in protein C and protein S.

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General Principles

Liver disease can impair hemostasis (see Figure 20-1) due to a reduction in coagulation factor production by hepatocytes, with the exception of vWF and factor VIII. Cholestasis, which leads to impaired vitamin K absorption, can also contribute because of decreased production of Factors II, VII, IX, and X. Patients who have stable liver disease typically only have a mild coagulopathy, though decompensated liver disease will worsen the coagulopathy severity. Liver disease may produce other hemostatic complications that include thrombocytopenia due to splenic sequestration, DIC, hyperfibrinolysis. Infection, renal insufficiency, and vasomotor dysfunction may also disrupt the fragile balance of procoagulant and anticoagulant activities.1 Although PT/INR and aPTT prolongations imply an increased risk of bleeding, they do not reflect concurrent reductions in protein C and protein S.

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