[Hepatic encephalopathy]

Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome which develops during chronic or acute liver disease. It is functional in nature and potentially reversible and symptoms range from subtle personality changes to deep coma. Diagnosis of manifest HE is made on a clinical basis, whereas psychometric tests are required to diagnose subclinical HE (SHE). Paper-pencil tests are frequently used for diagnosing SHE, but they may be inferior to measurements of critical flicker frequency, which pick minimal and low grade manifest HE as a continuum. Pathogenetically, HE is seen as clinical manifestation of low grade chronic cerebral edema, which is accompanied by alterations in glioneuronal communication. Different factors such as ammonia, inflammatory cytokines, benzodiazepines and electrolyte imbalances may precipitate or aggravate glia edema, thereby explaining precipitation of HE episodes by a variety of unrelated factors. Recognition and rigorous treatment of these precipitating factors is the most important measure in HE therapy, which may be augmented by dietary and medical approaches.