Management of disordered hemostasis and coagulation in patients with cirrhosis.

Abstract

Introduction The coagulopathy of cirrhosis and portal hypertension is complicated and often challenging to predict. While patients with cirrhosis are clearly prone to bleed, there is often a concurrent paradoxical propensity toward thrombosis. A finely regulated balance between bleeding and thrombosis is maintained in the healthy individual. When vascular breach or injury occurs, the clotting system activates (Fig. 1). In cirrhosis, a more precarious balance exists with heightened sensitivity to exogenous factors. 7 This rebalanced system is maintained by compensatory mechanisms, such as elevated levels of procoagulant factors like von Willebrand factor, FVIII, and reduced levels of anticoagulant factors like protein C. Additionally, a fibrinolysis pathway (not shown) governs clot dissolution, which may be altered in cirrhosis. Factors like infection, renal dysfunction, and endothelial injury can alter this balance. Tests commonly used to predict bleeding such as the prothrombin time/international normalized ratio do not reliably predict bleeding risk in patients with cirrhosis. Other, more global measures are currently under study and available in some centers (e.g., thromboelastography, thrombin generation assay), but there is no single test available today that can accurately predict bleeding or thrombosis tendency in patients with cirrhosis. Management of the bleeding cirrhosis patient is well studied with established clinical guidelines. Treating cirrhosis patients with thrombosis is less defined and clinicians must currently rely on expert recommendation, inference, and extrapolation from data in other patient populations. As our understanding of the intricacies of the coagulation system in cirrhosis develops, new tests and treatments for thrombosis and bleeding will likely emerge.