Hepatic Encephalopathy, commonly shortened to “HE”, is a potentially reversible disturbance of brain function due to liver failure. HE is characterized by a broad spectrum of symptoms including personality changes, intellectual impairment and a depressed level of consciousness. It appears HE is the result of neurotoxins that accumulate with liver failure. Ammonia, which is usually metabolized by the liver, is a critical neurotoxin in the process of developing HE, but other toxins are also involved. HE is reversible with appropriate medical therapy, but it is a hallmark of advanced, decompensated liver disease.
HE has a variety of symptoms, from very subtle cognitive impairment to full-blown coma. At the mild end of the spectrum, the term minimal encephalopathy refers to patients with cirrhosis who do not show signs cognitive abnormalities, but who show these signs with formal neuropsychological testing. Despite its subtlety, minimal HE is an important diagnosis, as it has been associated with a reduced quality of life as well as impaired driving skill.
By definition, HE is an essential feature of acute liver failure. Although some of the clinical features of HE in acute and chronic liver failure are similar, advanced encephalopathy in acute liver failure is a harbinger for the development of brain swelling (cerebral edema), which is very rare in chronic liver disease.