Diagnosis of hepatic encephalopathy

Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric symptom that co-occurs with various diseases such as acute hepatic failure and liver cirrhosis. Ammonia, which induces brain edema, is the main cause of HE. In the case of zinc or branched-chain amino acid deficiency, hyperammonemia is intensified. Recently, intestinal dysbiosis was revealed to induce intracranial neuroinflammatory responses in a cirrhotic mouse model in which the dysbiosis is similar to that observed in human subjects with cirrhosis. For the precise diagnosis of HE including minimal HE, a combination of quantitative neuropsychological and electrophysiological tests is necessary, but the diagnosis is highly complicated; computer-assisted neuropsychological tests are useful in this regard. While minimal HE could interfere with a patient’s quality of life and prognosis, it should be considered as a potential candidate for overt HE and therapeutic intervention. In a prospective study, hyponatremia in a cirrhotic subject was associated with increased mortality and not only affected brain function but also predisposed the patient to HE. The improvement of serum sodium concentration by the administration of vaptans might therefore improve HE.