Justin M. Joseph, MD, Margaret Lieberman, MD University of New Mexico, Albuquerque, NM Introduction: This case demonstrates ketamine overuse causing cholestatic liver injury and dilation of the common bile duct. Biliary sphincterotomy failed to improve laboratory values while ketamine use was ongoing. After six months of continued ketamine cessation, liver function testing has significantly improved but biliary dilation persists on imaging.
Case Description/
Methods: A 34-year-old woman engaged in ketamine overuse for over a decade. She had ketamine bladder syndrome. After one year of overuse, she developed a chronically elevated alkaline phosphatase between 1000 and 1500 without associated hyperbilirubinemia. She was asymptomatic. Imaging showed CBD dilation to 16mm. MRCP demonstrated intrahepatic and extrahepatic biliary dilation. EUS demonstrated an absence of choledocholithiasis. Empiric biliary sphincterotomy did not reduce alkaline phosphatase. Liver biopsy demonstrated chronic lymphocytic portal inflammation as well as bile ductular proliferation/reaction. With cessation of ketamine, a 75% reduction in alkaline phosphatase occurred after 6 months, though imaging findings of biliary dilation are unchanged. Discussion: Ketamine is a noncompetitive inhibitor of NMDA receptors that causes dissociation and hallucinations. Overuse causes ketamine bladder syndrome, characterized by urinary obstructive symptoms and renal papillary necrosis.1 Chronic use is also a rare cause of chronic cholestatic injury with imaging findings of intrahepatic and extrahepatic biliary dilation. As in this case, hyperbilirubinemia is often absent. Ketamine is excreted through both the urine and the bile, and hepatic metabolism of ketamine produces a toxic intermediate affecting the biliary epithelial cell. Biopsy findings resemble either chronic biliary obstruction (as in this case) or sclerosing cholangitis.2 This case shows that ketamine cessation should not be delayed as a diagnostic workup takes place. In addition, biliary sphincterotomy and other endoscopic therapies do not address the underlying mechanism of liver injury and are not expected to result in clinical benefit without ketamine cessation.
1 Srirangam S, Mercer J. Ketamine bladder syndrome: an important differential diagnosis when assessing a patient with persistent lower urinary tract symptoms. BMJ Case Rep. 2012 Sep 30;. doi: 10.1136/bcr-2012-006447.
2 LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Ketamine. 2018 Apr 25.
Disclosures: Justin Joseph indicated no relevant financial relationships. Margaret Lieberman indicated no relevant financial relationships.
Justin M. Joseph, MD, Margaret Lieberman, MD. P6002 - Ketamine-Induced Cholestatic Liver Injury and Subsequent Recovery With Cessation, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.
