The presence of cirrhosis poses an increased risk of both thrombosis and bleeding in individuals with chronic liver disease. This duality is a result of a dynamic disequilibrium between procoagulant and anticoagulant states in individuals with cirrhosis. The mechanism of this imbalance in cirrhosis remains unclear. It is known that the progression of cirrhosis leads to decreased synthetic function and a concurrent lack of natural anticoagulants. Other proposed mechanisms contributing to this hemostatic imbalance include decreased platelet production, increased platelet destruction from hypersplenism, decreased synthesis of Vitamin K-dependent and independent clotting factors and anticoagulant factors, and alterations in purinergic signaling pathways.Given the current state of flux in our understanding of bleeding and thrombophilia in cirrhosis, the recommendations for treatment of these conditions are still evolving.We provide a current update on the proposed pathophysiology of altered hemostasis and thrombophilia in cirrhosis. We discuss recent studies in portal vein thrombosis (PVT) and venous thromboembolism (VTE), which are the common thrombotic consequences of cirrhosis, resulting in substantive morbidity and mortality. To address these, we discuss new prophylactic interventions and current treatment options to manage the heightened risk of thrombosis in cirrhosis, while limiting hemorrhagic complications.

No abstract

No abstract

No abstract