Snapshot A 73-year-old man with chronic obstructive pulmonary disease, coronary artery disease, and hypertension is admitted to the intensive care unity for septic shock due to a left lower lobe pneumonia and treated with fluid resuscitation, pressors, and antibiotics. Liver function tests demonstrated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) over 1,000 U/L. Toxicology and viral hepatitis screening tests are negative. Introduction Clinical definition acute hepatic injury secondary to hypoperfusion Epidemiology Risk factors ischemia and shock respiratory failure heart failure etiology Pathogenesis hypoperfusion to the liver leading to acute hepatocellular injury most commonly from global hypoperfusion less commonly from hepatic artery thrombosis due to dual blood supply may occur with coexisting portal vein thrombosis Presentation Symptoms weakness fatigue mental confusion (from cerebral hypoperfusion, not hepatic encephalopathy) Physical exam hypotension tachycardia Studies Diagnostic testing diagnostic approach test for hepatocellular injury evaluate for concomitant end-organ hypoperfusion rule out viral and toxin etiologies laboratory studies liver function tests rapid increase in AST and ALT to 25-250x normal limit peak at 1-3 days after hypoperfusion event and normalize within 1-2 weeks moderate increase in bilirubin and alkaline phosphatase coagulation studies normal PT and PTT chemistries normal albumin rapid increase in creatinine is supportive of global hypoperfusion Differential Acetaminophen toxicity distinguishing factor elevated serum paracetamol Acute viral hepatitis distinguishing factor positive hepatitis viral screening Treatment Management approach hemodynamic support and resuscitation treat underlying etiology Complications Liver failure