Hepatic encephalopathy is a complex and potentially reversible neuropsychiatric syndrome complicating acute or chronic liver disease. Clinical manifestations are multiple and varied, ranging from minimal neurological changes to coma.
Ammonia is the main toxic substance involved in the pathogenesis of hepatic encephalopathy, although other mechanisms, such as modifications of the blood-brain barrier, disruptions in neurotransmission and abnormalities in GABAergic and benzodiazepine pathways may also play a role.
The identification and treatment of precipitating factors is crucial in the management of patients with hepatic encephalopathy. Current treatments are based on reducing intestinal ammonia load by agents such as antibiotics or disaccharides, although their efficacy is yet to be clearly established.