A 62-year-old man with a past medical history of hepatitis C, liver cirrhosis, end-stage renal disease, and cerebrovascular accident was admitted to the medical wards with hepatic encephalopathy. Therapy with lactulose was initiated and resulted in resolution of the encephalopathy. On hospital day 3, the patient again became encephalopathic, less responsive, and developed hypotension. The primary team bolused the patient with 250 mL of 5% albumin, and a critical care medicine consultation was requested. At the time of evaluation the patient was awake but not following commands. Vital signs were BP of 75/45 mm Hg, pulse rate of 84/min, respiratory rate of 22/min, and temperature of 37.1°C. His finger stick was 180 mg/dL, and oxygen saturation was 99% on room air. Lungs were clear to auscultation bilaterally, and cardiac examination was unremarkable. The abdomen was distended and resonant, and there was no evidence of pedal edema. There were no overt signs of GI bleeding (hematemesis or melena). A sepsis workup sent on admission (blood cultures and urinalysis) was negative. Chest radiography was grossly clear (Fig 1). Laboratory specimens drawn 5 h prior to the evaluation were significant for a drop in hematocrit level from 37.2% to 28.6%. Arterial blood gas results at the time of evaluation showed the following values: pH 7.45; Pco2, 32 mm Hg; Po2, 101 mm Hg; potassium, 6.8 mEq/L; hematocrit, 26.3%; and lactic acid, 14 mM. The intensivist team prepared for intubation to protect the airway in the setting of worsening mental status and shock. Per report, the patient had not eaten since the prior day.