Management of Hepatic Encephalopathy

Abstract

Hepatic encephalopathy (HE) is a serious and potentially reversible complication of liver disease that can be seen in cirrhosis, portal-systemic bypass, and acute liver failure. Manifestations of HE range from subtle deficits in attention and awareness to more profound disturbances in cognition, behavior, and motor function that may ultimately progress to coma. The West Haven Criteria is the current gold standard classification system for HE. Myriad factors are postulated to be involved in the pathogenesis of HE, particularly neurotoxins including ammonia, which is mostly gut-derived from the metabolism of dietary protein. Although serum ammonia levels do not have diagnostic or prognostic value for HE, pharmacologic therapies are directed at lowering blood ammonia levels and decreasing gut production of nitrogenous substances. The majority of patients with cirrhosis who present with an overt episode of HE will have an inciting factor such as infection or gastrointestinal bleeding that requires thorough evaluation and management to correct the underlying cause. Lactulose is the first-line therapy for the treatment of episodes of overt HE; the addition of rifaximin is recommended following a recurrent episode of HE for secondary prophylaxis. Patients with HE unresponsive to conventional treatment may benefit from alternative therapies such as supplementation with oral branched-chain amino acids; however, the role of adjunctive agents is limited by low-quality evidence. Evaluation for a spontaneous portosystemic shunt, such as a splenorenal shunt, should also be considered in refractory cases. In acute liver failure, the risk of cerebral edema and herniation is correlated with higher levels of blood ammonia. Patients with acute liver failure who develop moderate to severe HE should be managed in an intensive care unit setting in an institution with a liver transplant center.