Case Report
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 14, 2017; 23(2): 373-376
Published online Jan 14, 2017. doi: 10.3748/wjg.v23.i2.373
Posterior reversible encephalopathy syndrome in alcoholic hepatitis: Hepatic encephalopathy a common theme
Elizabeth S John, Ramy Sedhom, Ishita Dalal, Ranita Sharma
Elizabeth S John, Ramy Sedhom, Ishita Dalal, Ranita Sharma, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ 08901, United States
Author contributions: All authors took care of the patient medically; John ES drafted the report; Sedhom R, Dalal I and Sharma R made critical appraisals of the report.
Informed consent statement: Informed consent was acquired from the patient.
Conflict-of-interest statement: None of the authors have any financial disclosures or conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Elizabeth S John, MD, Department of Medicine, Rutgers Robert Wood Johnson Medical School, 1 Robert Wood Johnson Place, MEB 492, New Brunswick, NJ 08901, United States. elizabethjohn17@gmail.com
Telephone: +1-973-5926116
Received: July 22, 2016
Peer-review started: July 25, 2016
First decision: August 22, 2016
Revised: September 6, 2016
Accepted: October 10, 2016
Article in press: October 10, 2016
Published online: January 14, 2017
Core Tip

Core tip: Posterior reversible encephalopathy syndrome (PRES) has been described in a number of settings, but not in the setting of severe alcoholic hepatitis, as is presented in this case report. There are clear molecular relationships between ammonia, which is detoxified to glutamine in the brain, causing astrocytic swelling, cerebral edema, and vasogenic edema. This vasogenic edema is a pivotal component of PRES and accounts for one of the major hypotheses of the syndrome. Thus, though a clear connection between hyperammonemia and PRES has never been documented, there is a theoretical relationship.