• Parikshit Duriseti, Rishi Mamtani, Nicolaos E Madias, and James A Strom.
• Department of Medicine, St. Elizabeth's Medical Center, Boston, MA, United States; Department of Medicine, Tufts University School of Medicine, Boston, MA, United States. Electronic address: duriseti.parikshit@mayo.edu.
• Am. J. Med. Sci. 2021 Aug 1; 362 (2): 207-210.

AbstractHepatic encephalopathy (HE) includes cognitive, psychiatric and neuromotor abnormalities observed from brain dysfunction secondary to liver disease and/or porto-systemic shunting. HE can have a wide range of clinical manifestations ranging from trivial lack of awareness, decreased attention span, personality changes to confusion, seizures, coma, and death. The onset of HE in cirrhosis is a poor prognostic factor. While HE has a complex pathogenesis which is not completely understood, hyperammonemia plays an important role in neurotoxicity and brain dysfunction. Alkalemia facilitates the conversion of NH4+ to NH3, which is free to cross the blood-brain barrier exacerbating HE. Prompt recognition and correction of underlying risk factors is central to the management of HE.Copyright © 2020 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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