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Bilirubin 9.3 mg/dL (Direct 4.3 mg/dL, Indirect 3.5 mg/dL). CT scan of the abdomen and pelvis showed hepatomegaly with a normal biliary tree. The EBV viral capsid antigen (VCA) IgM was positive at .160 u/ML. Patient underwent a liver biopsy on hospital day 3 which showed sinusoidal patterns of inflammation and an in-situ hybridization study confirmed the diagnosis of EBV hepatitis. She was started on Solumedrol 1 mg/kg with improvement of symptoms and resolution of hepatic and hemolytic anemia lab abnormalities. Discussion: Hepatic involvement due to Epstein-Barr virus infection can be common but is typically subclinical or mild in presentation with only 5% of patients presenting with jaundice. The pathological manifestations can be extensive, as patients can also present with hemolytic anemia, specifically cold agglutinin autoimmune hemolytic anemia. The pathogenesis is believed to be due to EBV IgM antibodies cross reacting with RBC antigens. The pathogenesis of cholestasis in EBV hepatitis involves direct damage of hepatic cells by autoantibody free radical activation and the inflammation of bile ducts. The majority of cases are self-resolving; however, antivirals such as ganciclovir in conjunction with corticosteroids can provide benefit in severe cases. Due to the high global prevalence of Epstein-Barr virus, healthcare professionals should be aware of the diagnosis, management and complications of hepatic manifestations. Introduction:We present a case of acute on chronic liver failure in a patient on chronic Augmentin and total parenteral nutrition (TPN). We highlight the mechanisms and key findings of liver injury associated with intestinal failure and Augmentin, which are relevant for evaluating the risks and benefits of such therapies. Case Description/Methods: A 49-year-old woman with a history of cervical cancer treated with chemoradiation complicated by vaginal stenosis with reconstructive surgery complicated by short gut syndrome with chronic TPN dependency and chronic pelvic infections on Augmentin suppression therapy presented with hyperbilirubinemia and acute renal failure. Initial laboratory results include bilirubin 29.4 (predominantly direct), mildly elevated liver enzymes, normal alkaline phosphatase, INR 1.6, and creatinine 3.64. Her TPN and Augmentin were held. Evaluation for autoimmune markers and acute viral hepatitis serologies were negative. Genetic testing showed heterozygous C282Y mutation. Urinary copper was high with low serum ceruloplasmin, however ophthalmology exam was not concerning for Wilson's disease. Abdominopelvic non-contrast CT showed new abdominopelvic ascites. Liver biopsy revealed cholestatic hepatitis and cirrhosis. Her presentation was likely secondary to acute Augmentin hepatotoxicity in the setting of chronic intestinal-failure associated liver disease (IFALD). The patient ultimately expired due to septic shock. Discussion: Augmentin is a known cause of DILI, with clavulanic acid established as the causative agent. Onset occurs days to months following use and liver...