title: [Hepatic encephalopathy].
abstract: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome, which can develop in acute and chronic liver disease. It is functional in nature and potentially reversible. Signs of neurodepression characterize HE in chronic liver disease, whereas neuroexcitatory symptoms may prevail in fulminant hepatic failure. Manifest HE is graded into four severity stages, which range from mild personality changes to deep coma, and is distinguished from subclinical (latent) HE. Diagnosis of manifest HE is made on the basis of clinical symptoms, whereas psychometric or neurophysiological tests are required for detection of subclinical HE. However, the frequently employed paper-pencil tests are not sensitive enough to diagnose subclinical HE. A promising alternative is determination of critical flicker frequency (CFF), which picks up low grade HE as a continuum, but requires cooperation of the patient. HE is now seen as the clinical manifestation of a chronic low grade cerebral edema, which triggers alterations in astrocyte function with consequences for glioneuronal communication. Ammonia, inflammatory cytokines, benzodiazepines and electrolyte disturbances can trigger or aggravate glial swelling. This may explain why a variety of heterogenous conditions can precipitate episodes of HE, such as infections, drugs, trauma, bleeding etc. Diagnosis and rigorous treatment of these precipitating factors is the most important therapeutic measure, which is supported by dietary and drug treatment.
authors.affiliation: Klinik für Gastroenterologie, Hepatologie und Infektiologie, Heinrich-Heine-Universität Düsseldorf. haeussin@uni-duesseldorf.de
authors.forename: D
authors.initials: D
authors.lastname: Häussinger
mesh_terms: D001253:Astrocytes / Q000502:physiology; D001921:Brain / Q000503:physiopathology; D002450:Cell Communication / Q000502:physiology; D003937:Diagnosis, Differential; D006501:Hepatic Encephalopathy / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D019965:Neurocognitive Disorders / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D009474:Neurons / Q000502:physiology; D011379:Prognosis; D012307:Risk Factors