[Diagnostics and treatment of hepatic encephalopathy]

Hepatic encephalopathy (HE) comprises a broad range of potentially reversible neuropsychiatric disturbances in patients with liver dysfunctions after exclusion of other neurological and/or metabolic causes. Impaired liver function may be due to acute hepatic failure, portal-systemic bypass without hepatocellular disease, or liver cirrhosis with portal hypertension. The insufficient hepatic detoxification results in accumulation of neurotoxic agents, in particular ammonia, which causes neurological disturbances by astrocyte swelling. Besides, inflammatory cytokines and reactive oxygen species appear to play a crucial role in the pathogenesis of HE. Several predisposing factors may favour the development of HE, including gastrointestinal haemorrhages, hypovolaemia, and infections. Clinical findings range from minimal alterations of neurocognitive functions, only detected by psychometric tests, to confusion and coma. In general, diagnosis is based on clinical findings. Measurement of serum ammonia has no validated role in HE diagnosis. Visually evoked potentials (P300 wave) and critical flicker frequency analysis are objective and sensitive techniques for detection of minimal HE. Avoidance or correction of predisposing factors remains paramount in the treatment of HE. Non-absorbable disaccharids, such as lactulose and lactitol, and antimicrobial drugs, such as neomycin, are used to lower the increased ammonia levels. The efficacy of these treatment options, however, remains questionable. Thanks to its favourable adverse events profile and the beneficial effects on clinical signs of HE, as proven by several studies, the antimicrobial agent rifaximin is a promising drug in the treatment of HE. The present study aims to give a practical overview of diagnosis and treatment of HE.