S3372 Ketamine-Induced Biliary Injury: A Potential Precursor to Vanishing Bile Duct Syndrome

Introduction: Vanishing bile duct syndrome (VBDS), a rare cholestatic disorder characterized by irreversible loss of intrahepatic bile ducts. Commonly associated with autoimmune diseases, infections, and DILI, it remains a diagnostic challenge. Ketamine-induced cholangiopathy, though primarily described in chronic abuse or intensive care unit sedation, has emerged as a potential contributor. However, its association with VBDS is not well established. We present a case of biopsy-confirmed VBDS with imaging resembling primary sclerosing cholangitis (PSC), in a patient with prior ketamine exposure, raising the possibility of a causal link. Case Description/Methods: A 56-year-old woman with no history of alcohol use presented with progressive jaundice and episodes of altered mental status. Her medical history included herpes simplex virus encephalitis, during which she required intubation and brief ketamine sedation. Months later, she developed acute cholestatic liver injury. Laboratory testing revealed hyperbilirubinemia, elevated alkaline phosphatase, and transaminases. MRCP revealed intrahepatic bile duct dilation with beading. Liver biopsy demonstrated ductopenia, consistent with VBDS and sclerosing cholangitis. Endoscopic retrograde cholangiopancreatography (ERCP) showed multifocal ductal irregularities suggestive of a PSC-like pattern. However, autoimmune serologies were negative, and the patient had no history of inflammatory bowel disease. She was treated with ursodeoxycholic acid, corticosteroids, and symptomatic measures, but continued to deteriorate. Her course was complicated by recurrent episodes of bacteremia, vertebral compression fractures, sacral wounds, and intrapulmonary shunting. Liver transplant evaluation was deferred due to poor functional status. She ultimately succumbed to complications of liver failure and sepsis. Discussion: This case illustrates a potential continuum from ketamine-induced cholangiopathy to VBDS. Ketamine has been increasingly recognized as a cause of secondary sclerosing cholangitis, particularly in chronic abuse or intensive care unit settings. Proposed mechanisms include direct cholangiocyte toxicity, increased bile viscosity, and biliary ischemia, leading to progressive ductal injury and loss. Although PSC was initially considered based on cholangiographic features, the absence of autoimmune markers or IBD, coupled with the temporal relationship to ketamine exposure, supports secondary cholangiopathy. The subsequent development of VBDS, suggests ketamine may trigger a progressive biliary injury culminating in irreversible ductopenia.