We read with interest the paper by de Tymowski et al.1 describing the factors and outcomes of burn-associated cholestasis. This retrospective study described 111 patients (52%) with burn-associated cholestasis among 214 patients who had suffered severe burn injuries. The authors suggested that increased levels of total bilirubin ≥2x the upper limit of normal (ULN) with or without an increase in serum alkaline phosphatase (ALP) ≥1.5x the ULN or gamma-glutamyltransferase (GGT) ≥3x the ULN was associated with poorer survival at 90 days. Of the 74 patients alive at the time of discharge from the intensive care unit (ICU), 38 had cholestasis. As the authors describe, biliary lesions in severe burn injuries may be related to hypoxic hepatitis or hypovolemic shock. We report the case of a 29-year-old man admitted to our ICU for burns following a road traffic accident. On Day 17 after admission, he developed icteric cholestasis: aspartate aminotransferase: 79 UI/L, alanine aminotransferase: 69 UI/L, GGT: 551 UI/L, ALP: 332 UI/L, prothrombin time: 62%, total bilirubin: 27 μmol/L. Bilirubin increased to more than 25x the ULN over a 3-month period. Viral hepatitis, autoimmune hepatitis, obstructive jaundice, and alcoholic hepatitis were ruled out. A liver biopsy showed cholangitis without fibrosis or steatosis, and magnetic resonance cholangiography was normal. The only potentially incriminating drug was ketamine administered for analgesia (between 200 mg and 400 mg daily for more than 3 months). When ketamine was stopped, icteric cholestasis gradually improved over several months. Ketamine is a commonly used dissociative anesthetic that antagonizes the N-methyl-d-aspartate (NMDA) receptor. At subanesthetic doses it has strong analgesic properties that can be beneficial for neuropathic pain resistant to conventional therapies.