Nouveautés dans l'encéphalopathie hépatique : de l'encéphalopathie hépatique minimale à l'encéphalopathie hépatique clinique

Hepatic encephalopathy (HE) is a diffuse brain dysfunction caused by acute or chronic liver insufficiency and/or portosystemic shunt. Its pathophysiology is complex and multifactorial, with a synergistic involvement of hyperammonemia due to the lack of liver detoxification, neuro-inflammation related to modification of the gut microbiome, blood-brain barrier alterations causing various degree of cerebral edema and neurotransmitters impairment (especially GABA and glutamate). The clinical presentation includes a wide spectrum of non-specific symptoms, from subtle neurocognitive defects with normal neurologic examination, so-called minimal HE to deep coma, with various degrees of altered state of vigilance in between, so-called overt HE. HE represents a major prognosis factor in cirrhotic patients with an increased mortality and an altered quality of life. To date, there is no definite gold standard or even a specific clinical or paraclinical diagnostic test. Therefore, even though frequent, the diagnosis is not always easy, and one should carefully seek for the exclusion of other causes of brain dysfunction. The diagnosis relies on the combination of information about past medical history, psychometric tests for minimal HE, blood ammonemia, electroencephalogram and MRI with spectroscopy. New treatments for HE are under development; secondary prophylaxis relies on the association of non-absorbable disaccharides (lactulose) and non-absorbable antibiotics (rifaximin). Ammonemia scavengers are currently studied. Fecal transplantation is one of many promising treatment strategies that has been proposed. At the end liver transplantation can represent the only alternative.