Bleeding in Acute and Chronic Liver Disease

Abstract

Liver disease can present both with indolent or rapidly progressive disease. The liver plays a crucial role in regulating hemostasis through protein production, and different pathophysiological mechanisms form an underlying basis for bleeding in both acute and chronic liver disease. Acute liver failure features both synthetic dysfunction and high consumption. Chronic liver disease more frequently exhibits findings of synthetic dysfunction and vitamin K deficiency though can also include hyperfibrinolysis. Due to decreased liver production of both procoagulants and anticoagulants, synthetic dysfunction can create a precariously balanced hemostasis, and the predisposition toward bleeding may not be as prominent as some laboratory parameters may suggest. In liver disease, most laboratory measures of coagulation including prothrombin time (PT)/international normalized ratio (INR) are poor predictors of bleeding risk as they only effectively measure presence or loss of procoagulant factors of the extrinsic pathway. Viscoelastic testing such as ROTEM™ and TEG™ may be able to better model the in vivo clotting process and may help guide use of blood components and factor concentrates. Though rare, bleeding events in both chronic and acute liver disease can be catastrophic. Management of coagulopathy is essential both to prevent spontaneous bleeding and to protect patients when undergoing high-risk procedures, especially in the setting of acute bleeding. In the setting of variceal or upper gastrointestinal bleeds, medications such as octreotide, thrombopoietin agonists, and proton pump inhibitors may be needed as well. Invasive endoscopic treatments may be needed to treat gastrointestinal bleeds and varices either prophylactically or reactively. Interventional radiology, surgical procedures, and liver transplant can be considered in selected cases. Patients with acute and chronic liver disease present a complicated balance of coagulation, and careful monitoring is required to optimize outcomes. Vitamin K, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrates, recombinant activated factor VII, platelets, and anti-fibrinolytics may be considered depending on the etiology and volume constrictions.