Objective: To review the management of hepatic encephalopathy (HE), including lifestyle modifying strategies and pharmacological interventions. Data Sources: A literature search of PubMed through March 2016 was conducted utilizing the keywords hepatic encephalopathy, ammonia, and cirrhosis. All published articles evaluating treatments for HE were considered. Study Selection and Data Extraction: Available English-language data from reviews, abstracts, presentations, and clinical trials of the treatment of HE in humans were reviewed; relevant clinical data were selected and included. Data Synthesis: HE is a prevalent complication of portal hypertension and cirrhosis that results in altered mental status and neuropsychiatric impairment. Although the pathogenesis has not been elucidated, numerous treatment options exist. This review will explore the role of dietary interventions and supplements, including use of zinc, acetyl-l-carnitine, and probiotics, in the management of HE. Additionally, the use of various ammonia-lowering agents will be evaluated. The nonabsorbable disaccharides represent first-line therapies for the management and prophylaxis of HE; rifaximin use has been demonstrated to be effective for both treatment and prophylaxis of HE symptoms, with use relegated to those patients who fail to respond to or tolerate the nonabsorbable disaccharides. In light of toxicities associated with the use of neomycin and metronidazole, recent guidelines recommend both as alternatives for the treatment of HE, with the use of vancomycin discouraged. Conclusion: Although numerous treatment options are available, management of HE remains a clinical challenge. Additional research is needed to explore the pathogenesis and better understand the role of pharmacotherapy in managing this condition.

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Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare, acute, but serious cutaneous adverse reactions, associated with exposure to drugs and can result in significant morbidity and mortality. The incidence of SJS ranges from 1.2 to 6 per million per year, with fatality in up to 5% of cases, while TEN affects 0.4 to 1.2 per million per year with mortality in up to 30% of patients. 1-3 SJS and TEN are rare variants of severe, adverse cutaneous drug reactions characterized by extensive painful erythematous macules, eventually evolving to epidermal detachment and mucous membrane erosions resulting from massive apoptosis of epithelial cells. Distinguishing features of SJS and TEN from other morbilliform drug rashes is based on the manifestation of skin lesions and the extent of epidermal detachment. 4,5 SJS/ TEN are differentiated by the extent of epidermal detachment. SJS involves <10% body surface area detachment, while TEN is characterized by extensive involvement of >30% body surface area. 4,5 The exact pathophysiological mechanism has not been fully elucidated, but it is believed to be a delayed hypersensitivity reaction mediated by T1 helper cells. The reaction typically occurs 4 to 28 days after initiation of the offending drug, although the highest risk of developing SJS and TEN occurs in the first 2 months after exposure to the drug on a continuous basis. Both SJS and TEN may present with prodromal symptoms lasting up to 1 week, such as fever, sore throat, coughing, myalgia, and arthralgia. Following this period, cutaneous manifestations appear as discrete maculopapular rash, similar to a morbilliform rash. 4,5 Mucosal involvement is present in nearly all of the patients, whereas ocular and visceral involvement occurs less frequently. 4,5