Ketamine: friend or foe?

The risks of using ketamine as treatment in appropriately selected patients is small, but repeated administration might be associated with the danger of dependency and complications in vulnerable individuals.1 3 4 Proposed mechanisms by which ketamine may exert its therapeutic effects in addiction include augmentation of neuroplasticity, interruption of related functional neural networks and blocking reconsolidation of drug-related memories.1 There is an on-going international debate regarding the ideal legislation for this drug.1 Ketamine is currently classified as a schedule III controlled substance.2 Long-term ketamine misuse can produce toxicity in the urological and hepatobiliary tracts and cause neurocognitive impairment. Emerging evidence suggests that ketamine abuse is associated with hepatic parenchymal injury, cholangiopathy, cholestasis and biliary dilatation.2 5 Negative psychological effects include blunted affect, dissociation, paranoia and cognitive decline.2 Habitual use of ketamine affects prefrontal dopaminergic transmission, which is involved in working memory and executive function.4 A strong association between ketamine abuse and upper gastrointestinal tract (GIT) symptoms has been reported.5 Most patients who abuse ketamine develop upper GI symptoms years prior to uropathy-related symptoms, which is prevalent in up to 100% of people using more than 5 g daily.6 A high index of suspicion for abuse should be retained when assessing patients with chronic upper GI symptoms to allow early detection and enable appropriate intervention.5 The cachexia observed in this patient could have been related to upper GIT disease and the associated malnutrition, biliary dysfunction and acute kidney injury.2 The exact pathophysiological mechanism by which ketamine produces upper GI, urological and hepatobiliary toxicity remains unknown.5 Its NMDA antagonist effect may affect gastric motility. Side-effects associated with ketamine use in depression: a systematic review.