S3239 When the Bile Speaks: Isolated Hyperbilirubinemia as a Marker of Sepsis

Introduction: As the leading cause of morbidity and mortality in hospitalized patients, sepsis imposes a significant financial burden on healthcare costs. Hepatic involvement, particularly cholestasis, can occur early in sepsis. Isolated hyperbilirubinemia- without marked transaminitis- may be a subtle sign of sepsis-induced cholestasis. This case highlights the diagnostic value of isolated hyperbilirubinemia in a patient with undifferentiated altered mental status. Case Description/Methods: A 69-year-old man with congestive heart failure and end stage renal disease on hemodialysis presented with altered mental status. Despite normal vital signs, physical exam revealed scleral icterus and a non-tender distended abdomen with fluid wave. Labs were notable for AST 47, ALT 44, ALP 105, total bilirubin 10.5 (direct bilirubin 7.5, indirect bilirubin 2.9), PT 20.3, and INR 1.73. Abdominal imaging, including ultrasound and magnetic resonance cholangiopancreatography (MRCP) revealed nodular liver with ascites, normal gallbladder, and no biliary obstruction. Paracentesis demonstrated fluid with SAAG of 1.4 and ascitic protein of 3.4, suggesting ascites is likely due to heart failure. Viral, autoimmune, and metabolic workup for cirrhosis was negative. Two blood cultures grew Staphylococcus epidermidis, likely from the patient's permcath, which was subsequently removed. A new catheter was placed for dialysis, and vancomycin was started. The patient’s mental status and bilirubin levels gradually normalized with treatment. Discussion: Sepsis impairs bile transport via inflammatory cytokines, altered hepatocyte transporters, and microvascular dysfunction, resulting in intrahepatic cholestasis. This can present with marked hyperbilirubinemia out of proportion to transaminase elevation, mimicking other intrahepatic or extrahepatic cholestatic processes. In this case, the absence of intrinsic liver disease or biliary obstruction and clinical improvement with infection control support a diagnosis of sepsis-induced cholestasis. Studies show increased mortality with sepsis-induced hyperbilirubinemia, suggesting its diagnostic and prognostic value. Thus, recognizing this pattern and distinguishing it from other causes in a timely manner is essential. Management includes antibiotics and source control. While the benefit of ursodeoxycholic acid remains unclear in this setting, corticosteroids may assist liver recovery but are not routinely recommended. Further research is needed to develop targeted treatments for this hepatobiliary complication of sepsis.