Semin Liver Dis 2003; 23(3): 259-270
DOI: 10.1055/s-2003-42644
Copyright © 2003 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Pathogenesis of Hepatic Encephalopathy in Acute Liver Failure

Javier Vaquero1,2 , Chuhan Chung2 , Michael E. Cahill2 , Andres T. Blei2
  • 1Post-doctoral Research Fellow Department of Medicine Lakeside Veterans Administration Medical Center Northwestern University Feinberg School of Medicine Chicago, Illinois
  • 2Section of Hepatology, Department of Medicine, Lakeside Veterans Administration Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois
Further Information

Publication History

Publication Date:
02 October 2003 (online)

Preview

ABSTRACT

Hepatic encephalopathy (HE) in acute liver injury signifies a serious prognosis. Brain edema and intracranial hypertension are major causes of death in this syndrome. Comparison of HE in acute liver failure (ALF) with that of cirrhosis allows recognition of important differences and similarities. A key role for ammonia in the pathogenesis of both HE and brain edema is now firmly supported by clinical and experimental data. Additional factors, such as infection, products of the necrotic liver, and synergistic toxins, may contribute to an altered mental state. A low plasma osmolarity, high temperature, and both high and low arterial pressure may affect brain water content. A combined derangement of cellular osmolarity coupled with cerebral hyperemia can explain the development of brain edema in ALF. Increasingly, study of the mechanisms responsible for brain swelling provides critical information for understanding the pathogenesis of HE.

REFERENCES