Hepatic encephalopathy (HE) (synonyms: hepatic encephalopathy; hepatoencephalopathy; hepatoportal encephalopathy; minimal hepatic encephalopathy; portosystemic encephalopathy (PSE); ICD-10-GM K72.7-: Hepatic encephalopathy and coma hepaticum) describes central nervous system (CNS) dysfunction due to acute or chronic liver disease. Often underlying hepatic encephalopathy is chronic liver disease such as cirrhosis (liver shrinkage). Liver disease results in retention (retention) of neurotoxic substances (substances toxic to the nervous system) in the blood, especially ammonia – the detoxification function of the liver is inadequate. Neurological-psychiatric abnormalities are the result.
22-74% of patients with liver cirrhosis already have “minimal hepatic encephalopathy” (synonym: latent (hidden) hepatic encephalopathy) (see under “Classification”). The incidence (frequency of new cases) for hepatic cirrhosis is approximately 250 cases per 100,000 population per year (in Europe and the United States).
Course and prognosis: Hepatic encephalopathy is potentially reversible (reversible) with adequate therapy. The focus is on treatment of the underlying disease. In addition, hepatic encephalopathy is treated symptomatically. Symptoms range from mild mood swings or poor concentration to hepatic coma (coma hepaticum). Even in the latent stage of the disease (“minimal hepatic encephalopathy”), affected individuals are impaired in their ability to work, drive, and ultimately in their quality of life. Clinically manifest hepatic encephalopathy often occurs episodically. Each episode leads to deterioration in psychometric performance, a decline in quality of life, and an increase in mortality risk (risk of death). A chronic-progressive (permanently progressive) course is rarely seen. A fulminant (sudden, rapid and severe) course is also possible, e.g. in the context of acute liver failure. In this case, the affected person may fall into a coma within a few days.
