Hepatic encephalopathy: from pathophysiology to treatment

Digestion. 2006:73 Suppl 1:86-93. doi: 10.1159/000089783. Epub 2006 Feb 8.


Hepatic encephalopathy (HE) is a neuropsychiatric syndrome due to hepatic dysfunction and porto-systemic shunting of the intestinal blood. Cirrhosis is the most frequent liver disease causing HE. On most occasions, HE appears due to a superimposed precipitating factor (gastrointestinal bleeding, infections, renal and electrolyte disturbances, etc.). Ammonia produced in colon by intestinal bacteria is the main toxic substance implicated in the pathogenesis of HE. Other mechanisms, such as changes in the GABA-benzodiazepine system, accumulation of manganese into the basal ganglia of the brain, changes in blood-brain barrier and neurotransmission disturbances are also present. Clinical manifestations of HE may vary widely, from minimal neurologic changes, only detected with specific tests, to deep coma. Treatment of HE should be directed to controlling the precipitating factors, as well as therapies aimed at correcting the above-mentioned pathophysiological changes, mainly reduction of blood ammonia levels. Artificial liver support systems may play a role in the future. Liver transplantation should be evaluated as a definitive therapy in all cases of HE.

Publication types

  • Review

MeSH terms

  • Ammonia / metabolism
  • Anti-Bacterial Agents / therapeutic use
  • Antipsychotic Agents / therapeutic use
  • Brain / metabolism
  • Brain / physiopathology
  • Hepatic Encephalopathy / etiology*
  • Hepatic Encephalopathy / therapy
  • Humans
  • Neurotransmitter Agents / metabolism
  • Portasystemic Shunt, Transjugular Intrahepatic
  • Receptors, GABA-A / metabolism
  • Synaptic Transmission*
  • Treatment Outcome


  • Anti-Bacterial Agents
  • Antipsychotic Agents
  • Neurotransmitter Agents
  • Receptors, GABA-A
  • Ammonia