18. Hepatic Encephalopathy

  1. Eugene R. Schiff MD, MACP, FRCP3,
  2. Willis C. Maddrey MD, MACP, FRCP4 and
  3. Michael F. Sorrell MD, FACP5
  1. Ravi K. Prakash MD, MRCP(UK)1 and
  2. Kevin D. Mullen MD2

Published Online: 31 OCT 2011

DOI: 10.1002/9781119950509.ch18

Schiff's Diseases of the Liver, Eleventh Edition

Schiff's Diseases of the Liver, Eleventh Edition

How to Cite

Prakash, R. K. and Mullen, K. D. (2011) Hepatic Encephalopathy, in Schiff's Diseases of the Liver, Eleventh Edition (eds E. R. Schiff, W. C. Maddrey and M. F. Sorrell), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781119950509.ch18

Editor Information

  1. 3

    Center for Liver Diseases and Schiff Liver Institute, University of Miami Miller School of Medicine, Miami, FL, USA

  2. 4

    Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA

  3. 5

    University of Nebraska College of Medicine, Omaha, NE, USA

Author Information

  1. 1

    Division of Gastroenterology, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH, USA

  2. 2

    Division of Gastroenterology, MetroHealth Medical Center, Cleveland, OH, USA

Publication History

  1. Published Online: 31 OCT 2011
  2. Published Print: 9 DEC 2011

ISBN Information

Print ISBN: 9780470654682

Online ISBN: 9781119950509



  • Hepatic encephalopathy;
  • minimal hepatic encephalopathy;
  • overt hepatic encephalopathy;
  • covert hepatic encephalopathy;
  • ammonia;
  • GABA (γ-aminobutyric acid);
  • endogenous benzodiazepines;
  • astrocytes;
  • glutamine;
  • intestinal glutaminase;
  • West Haven criteria;
  • psychometric hepatic encephalopathy score;
  • inhibitory control test;
  • critical flicker fusion frequency test;
  • cerebral edema;
  • lactulose;
  • rifaximin


Hepatic encephalopathy (HE) is a serious complication of cirrhosis and involves a broad range of neurologic and neuropsychiatric impairments. Ammonia is mainly implicated in the pathogenesis of HE. It is now well established that some degree of cerebral edema is present in all grades of HE. The first major effort to standardize nomenclature was performed by the Hepatic Encephalopathy Consensus Group at the World Congress Meeting in Vienna, 1998. Adoption of these criteria has been a key factor in enhancing research projects in this field over the last decade. Terminology continues to evolve and change in this field. Subclinical hepatic encephalopathy was changed to minimal hepatic encephalopathy in 1998 and was defined as an entity that is seen in cirrhotic patients with an abnormality only in specific psychometric tests. A number of studies have shown impaired quality of life, poor driving and navigational skills, and increased risk of developing overt HE in the presence of minimal HE. The principles of treating HE has remain unchanged in the last 30 years. These are to provide supportive care to the patient, look for concomitant causes for encephalopathy, identify and treat precipitating factors, and initiate empirical treatment. There are now two medications that are Food and Drug Administration approved for the treatment of overt HE.