One of the most serious complications of chronic or
fulminant liver failure is
hepatic encephalopathy (HE), associated most commonly with
cirrhosis. In the presence of chronic
liver disease, HE is a sign of decompensation, while in
fulminant liver failure its development represents a worrying sign and usually indicates that
transplantation will be required. Despite the significance of HE in the course of
liver disease, the progress in development of new therapeutic options has been unremarkable over the last 20 years. An up-to-date review regarding HE, including both research and review articles. HE is a serious and progressive, but potentially reversible, disorder with a wide spectrum of neuropsychiatric abnormalities and motor disturbances that ranges from mild alteration of cognitive and motor function to
coma and death. Although a clear pathogenesis is yet to be determined, elevated
ammonia in serum and the central nervous system is the mainstay for pathogenesis and treatment of HE. Management includes early diagnosis and prompt treatment of precipitating factors. Clinical trials and extensive clinical experience have established the efficacy of diverse substances in HE treatment. Novel
therapies with clinical promise include:
L-ornithine L-aspartate,
sodium benzoate,
phenylacetate,
AST-120, and the molecular adsorbent recirculating system. Eventually,
liver transplantation is often the most successful long-term
therapy for HE.