Hemostasis abnormalities in cirrhosis

Abstract

The long-lasting paradigm of cirrhosis as the epitome of the acquired hemorrhagic coagulopathies has been challenged by evidence from the literature. This article reviews the mechanisms responsible for regulation of hemostasis in the light of the evidence provided within the last few years. Numerous studies have evaluated the mechanisms responsible for regulation of primary hemostasis, coagulation and fibrinolysis which were thought to be severely impaired in cirrhosis and were considered responsible for the abnormalities of the prothrombin time and the bleeding events observed in these patients. These evaluations have been performed by newer laboratory tests under experimental conditions that mimic closely the condition operating in vivo. Cirrhosis presents with thrombocytopenia and decreased levels of both pro- and anticoagulants. Notable exceptions are factor VIII and von Willebrand factor (VWF) which are increased. Thrombocytopenia (unless very severe) is no longer considered a bleeding risk as platelets from cirrhosis display normal adhesiveness in a flowing system that is mainly supported by the increased levels of VWF. Patients with cirrhosis generate normal amounts of thrombin that is mainly supported by the concomitant deficiency of pro- and anticoagulants that restores the balance between these two opposing drivers.