Liver Disease and Hemostatic (Dys)function

Cirrhosis presents with decreased procoagulant factors as a consequence of the impaired synthetic capacity of the liver. This was taken as evidence to explain the abnormalities of the coagulation tests prothrombin time (PT) and activated partial thromboplastin time (aPTT) and the bleeding events that occur in these patients. It was for long time (and probably is still) common practice to test patients with the PT and to treat those with predefined (but arbitrary) cutoff values with plasma or prohemostatic agents to prevent or stop bleeding. However, anticoagulant factors that contrast the procoagulants are also decreased in cirrhosis. It was therefore postulated that the coagulation balance (i.e., the net result between the action of pro- and anticoagulants) is somewhat rebalanced. Subsequent studies supported this view showing that plasma from cirrhotic patients generates normal amounts of thrombin. In addition, primary hemostasis (i.e., platelet-vessel wall interaction) is rebalanced notwithstanding cirrhosis present with thrombocytopenia. It was shown that increased levels of the adhesive protein von Willebrand factor (a typical feature of cirrhosis) compensate for the low number (function) of platelets. The earlier considerations have been instrumental to help dismantle the old paradigms of cirrhosis as the epitome of the acquired hemorrhagic coagulopathies and the traditional coagulation tests PT and aPTT as suitable predictors of bleeding risk. The demise of the old paradigms and the rise of the new one may have important practical implications for the management of patients with cirrhosis and will be discussed in this chapter.