EM1908G "Hemostasis in Liver Failure: A Tendency to Bleed or Clot?" (IM GR-082319)

Clinicians often regard patients with advanced liver disease as prone to bleeding. Today’s discussion will explore recent data which redefine the magnitude of the bleeding diathesis in patients with advanced cirrhosis and acute liver failure (ALF), and will explore mechanisms of “re-balanced hemostasis,” a relatively new concept in which patients re-establish a neutral state of hemostasis by compensatory mechanisms. Bleeding complications of portal hypertension will not be considered, since they occur as a consequence of hydrostatic pressure and wall tension within blood vessels rather than defective hemostasis.

Although the INR detects deficiencies in liver-derived, pro-hemostatic factors, it provides unreliable information to estimate bleeding risk in patients with liver disease. Thus, the concept of “autoanticoagulation,” the notion that patients with liver failure are prone to bleed and protected from venous thromboembolism by virtue of elevated INR, has been strongly refuted. The platelet count, however, is a more accurate predictor of bleeding complications, and in vitro and clinical studies suggest that a platelet count of >60x109/L is sufficient to support thrombin generation at the 90th percentile of normal, which may be a goal of correction.

The general mechanism of re-balanced hemostasis in liver disease can be at least partially explained by 2 important concepts: (1) liver-derived pro- and anti-coagulant proteins are decreased in parallel, and (2) endothelial-derived hemostatic factors (factor VIII and vonWillebrand factor) are released in response to systemic inflammation, and compensate (perhaps over-compensate) for deficient liver-derived pro-hemostatic factors and platelets, respectively.

Target Audience

UT Southwestern faculty, fellows, residents and medical students, community physicians, nurse clinicians, physician assistants and nurses.

Learning Objectives

At the conclusion of this activity, the participant should be able to:

  • Better understand the risk of bleeding and thrombosis in patients with acute and chronic liver failure, the mechanisms that contribute to the relatively low risk, and how to better assess this risk.
  • Comprehend that the long-held practice of injudicious transfusion of plasma and platelets may be doing harm to patients with liver failure.
  • Appreciate new indications for repletion of pro-hemostatic factors, and the remaining questions which require further study.
Course summary
Available credit: 
  • 1.00 AMA
Course opens: 
Course expires: 

R. Todd Stravitz, M.D.
Professor, Department of Internal Medicine
Division of Gastroenterology, Hepatology and Nutrition
Virginia Commonwealth University Medical Center
Burton Combes Memorial Lecturer

Available Credit

  • 1.00 AMA


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