Treatment of hepatic encephalopathy

Abstract

Hepatic encephalopathy (HE) is predominantly induced by a portosystemic shunt as a complication of excessive portal hypertension. Initial treatments for HE involve the identification and improvement of the causal triggers, such as infection, constipation, dehydration, and gastrointestinal bleeding. A majority of the pharmacotherapies are aimed at decreasing the production of ammonia. Lactulose alters gastrointestinal pH by favoring lactobacilli over urease-containing bacteria and enhances the production of nonabsorbable ammonia. Furthermore, these laxatives enhance fecal nitrogen excretion. Although neomycin was the first antibiotic to be effective in the treatment of HE, its use has been limited because of ototoxicity and nephrotoxicity. Recently, rifaximin, a minimally absorbable oral antibiotic, which is available in many countries, has been used in lactulose resistance encephalopathy. When used in conjunction with lactulose, rifaximin has been shown to reduce recurrent encephalopathy and hospitalization. Supplementation of branched-chain amino acids is also beneficial for patients with HE because of their stimulatory effect on ammonia detoxification to glutamine. Balloon-occluded retrograde transvenous obliteration is recommended for patients with refractory HE especially caused by portosystemic shunt. Liver transplantation is eventually performed in patients who are resistant to the abovementioned pharmacological and interventional therapies.