Ketamine-Related Deaths Registered in Scotland 2013–2024
Amira Guirguis, John Martin Corkery, Fabrizio Schifano
Clinical Neuropsychopharmacology and Addiction January 4, 2026 DOI: 10.53941/cna.2026.100001 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Sample size | 88 |
| Population | Decedents in Scotland where ketamine was implicated in death, 2013–2024 |
| Duration | 2013–2024 |
| Topics | Ketamine Esketamine |
| Keywords | Polysubstance dependence Public health Accidental Epidemiology Cause of death Environmental health |
| Key findings | Scottish ketamine-related deaths increased twentyfold over a decade, with most deaths accidental and involving polysubstance use, particularly opioids and benzodiazepines. |
Abstract
Background: Ketamine, a dissociative anaesthetic and non-competitive NMDA receptor antagonist, has legitimate medical applications. However, rising illicit use across the United Kingdom (UK) has been accompanied by growing reports of toxicity, dependence, and deaths. These have led to renewed policy discussions. Rationale and
Aim: Previous national studies have reported ketamine-related deaths elsewhere in the UK, but not in Scotland. This study examined all Scottish deaths (2013–2024) where ketamine was implicated, to provide a comprehensive evidence base for UK-wide policy discussions.
Methods: Data were derived from anonymised National Records of Scotland records. All cases where ketamine was implicated in death were identified. Descriptive and comparative analyses were undertaken by year, sex, age, manner, and substances co-implicated.
Results: Eighty-eight deaths were identified (≈0.5% of cases), with a steady increase over time. Most decedents were male (81.8%); mean age was 35 years. Most (84%) were accidental and involved polysubstance use—typically opioids (58%), stimulants (55%), benzodiazepines (48%), gabapentinoids (25%), and alcohol (22%). Acute drug use was the principal cause of death in 85% of cases.
Discussion: The marked upward trend parallels that observed elsewhere in the UK. Polysubstance involvement, especially combinations of ketamine with opioids or benzodiazepines, substantially increases fatal risk through additive central nervous system depression. These findings reinforce the need for clearer public health messaging, targeted harm-reduction interventions, and careful monitoring of misuse, prescribing and diversion trends.
Conclusions: Scottish ketamine-related deaths increased twentyfold in a decade. Most are preventable, highlighting the need for continued targeted education, intervention, and epidemiological monitoring.
Comparable studies
Other observational and cohort studies on ketamine, most cited first.
| Study | Year | Design | Participants |
|---|---|---|---|
| Taming the Ketamine Tiger Volunteers from a prison population | 2010 | Observational study | n = 20 |
| Increased spontaneous MEG signal diversity for psychoactive doses of ketamine, LSD and psilocybin Humans | 2017 | Observational study | |
| Disruption of Frontal–Parietal Communication by Ketamine, Propofol, and Sevoflurane Surgical patients undergoing induction of anesthesia with intravenous ketamine | 2013 | Observational cohort | n = 30 |
| Do the dissociative side effects of ketamine mediate its antidepressant effects? Treatment-resistant inpatients with major depressive disorder or bipolar disorder | 2014 | Observational cohort | n = 108 |
| Concomitant BDNF and sleep slow wave changes indicate ketamine-induced plasticity in major depressive disorder Patients with treatment-resistant major depressive disorder | 2012 | Observational cohort | n = 30 |