Splenomegaly, hypersplenism and coagulation abnormalities in liver disease

Splenomegaly is a frequent finding in patients with liver disease. It is us ually asymptomatic but may cause hypersplenism. Thrombocytopenia is the mos t frequent manifestation of hypersplenism and may contribute to portal hype rtension related bleeding. A number of therapies are available for treating thrombocytopenia due to hypersplenism including splenectomy, partial splen ectomy, partial splenic embolization, TIPS etc. None is entirely satisfacto ry. Hypersplenism usually improves following liver transplantation. Therapy with cytokines such as thrombopoietin may offer hope for the future. Patie nts with liver disease also have abnormalities in coagulation. This is not surprising as all coagulation proteins (except for von willebrand factor vW F) and most inhibitors of coagulation are synthesized in the liver. Genetic or acquired abnormalities of coagulation may predispose to thrombosis of t he hepatic or portal veins with significant clinical sequelae. An understan ding of the mechanisms involved in coagulation and thrombosis is valuable i n choosing from the increasing treatment options available. These include c lotting factors, haemeostatic drugs and newer therapies such as recombinant factor VIIa. Splenic artery aneurysms are the most common visceral artery aneurysms in man. Rupture is frequently catastrophic. These aneurysms are b eing increasingly recognized in liver transplant patients and require treat ment before or during transplant surgery.