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Abstract Details
Hepatic encephalopathy
Nat Rev Dis Primers. 2022 Jun 23;8(1):43. doi: 10.1038/s41572-022-00366-6.
1Department of Gastroenterology, Hepatology and Infectious Diseases, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. haeussin@uni-duesseldorf.de.
2Department of Hepatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, (Uttar Pradesh), India.
3Laboratory of Neurobiology, Centro de Investigación Principe Felipe, Valencia, Spain.
4Department of Gastroenterology, Hepatology and Infectious Diseases, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
5Liver Failure Group ILDH, Division of Medicine, UCL Medical School, Royal Free Campus, London, UK.
6European Foundation for the Study of Chronic Liver Failure, Barcelona, Spain.
7Department of Gastroenterology, Diabetology and Hepatology, University Hospital Brandenburg an der Havel, Brandenburg Medical School, Brandenburg an der Havel, Germany.
8Department of Translational and Precision Medicine, Universita' degli Studi di Roma - Sapienza, Roma, Italy.
9Department of Medicine, University of Padova, Padova, Italy.
10UCM Digestive Diseases, Virgen del Rocío University Hospital, Institute of Biomedicine of Seville (HUVR/CSIC/US), University of Seville, Seville, Spain.
11Institute of Clinical Neuroscience and Medical Psychology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
12Department of Surgery and Cancer, St. Mary's Hospital Campus, Imperial College London, London, UK.
13Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Abstract
Hepatic encephalopathy (HE) is a prognostically relevant neuropsychiatric syndrome that occurs in the course of acute or chronic liver disease. Besides ascites and variceal bleeding, it is the most serious complication of decompensated liver cirrhosis. Ammonia and inflammation are major triggers for the appearance of HE, which in patients with liver cirrhosis involves pathophysiologically low-grade cerebral oedema with oxidative/nitrosative stress, inflammation and disturbances of oscillatory networks in the brain. Severity classification and diagnostic approaches regarding mild forms of HE are still a matter of debate. Current medical treatment predominantly involves lactulose and rifaximin following rigorous treatment of so-called known HE precipitating factors. New treatments based on an improved pathophysiological understanding are emerging.
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