Rebalanced hemostasis in the hepatopathic patient

Abstract

Hepatic dysfunction alters both the procoagulant sphere (reducing the levels of procoagulant and antifibrinolytic factors) and the anticoagulant (by decreasing the anticoagulant and fibrinolytic factors). That is, it can predispose both to bleeding and thrombosis. Even more complex, liver disease is associated with thrombocytopenia, among others, splenomegaly, and platelet dysfunction by predisposing to a defective platelet-endothelium interaction and decreasing the synthesis of thromboxane A2 in the platelet membrane, thereby altering platelet activation.

Therefore, an unstable equilibrium occurs in the liver patient, which has been called “rebalanced” hemostasis at the level of primary, secondary, and fibrinolysis hemostasis. Its clinical translation is that the hepatic patient is more exposed to both acute bleeding episodes and thrombosis.