Liver Disease
GENERAL PRINCIPLES
Liver disease can impair hemostasis (see Figure 20-1) due to a reduction in synthesis of most coagulation factors. Cholestasis, which leads to impaired vitamin K absorption, can also impair hemostasis because of decreased production of Factors II, VII, IX, and X.
Patients who have stable liver disease typically have a mild coagulopathy. Liver disease may produce other hemostatic complications that include thrombocytopenia due to splenic sequestration, DIC, and hyperfibrinolysis. Although PT/INR and aPTT prolongations imply an increased risk of bleeding, they do not reflect concurrent reductions in protein C and protein S nor compensatory increases in factor VIII and vWF.Treatment of Bleeding in Patients With Liver Disease
• Vitamin K replacement may shorten a prolonged PT/INR caused by a vitamin K antagonist (e.g., warfarin), dietary deficiency, or cholestasis, but it does not stop bleeding.
• For patients who have an elevated INR or aPTT, FFP may decrease bleeding, but it may cause volume overload and does not work immediately.
• Prothrombin complex concentrate (e.g., Kcentra 25 IU#8725;kg IV) will work more rapidly than FFP in normalizing an elevated INR during bleeding and requires less volume administration, but it has not undergone extensive testing in patients who have liver disease.44
• Cryoprecipitate, 1.5 units/10 kg body weight, corrects hypofibrinogenemia (lt;100 mg#8725;dL).
• Recombinant factor VIIa does not stop GI bleeding in liver disease and may cause thrombosis.45
• Platelet transfusion or thrombopoietin may decrease transfusion requirements in those with bleeding or undergoing an invasive procedure who have severe thrombocytopenia (lt;50 ? 109#8725;L).
• Antifibrinolytic therapy (e.g., tranexamic acid) can be used with persistent mucosal oozing or puncture wound bleeding.
• Variceal bleeds should be treated as in Chapter 18.