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The K-Hole Collapse: A Systematic Review of Multi-Organ Somatotoxicity and Management Strategies in Chronic Ketamine Misuse

Wiktoria Podlasiewicz, Aleksandra Majewska, Leon Miller, Gabriela Augustynowicz, Klaudia Dziuba, Wiktoria Michalska, Karolina Gaweł, Emilia Dedio, Aleksandra Kozik, Weronika Matera

Quality in Sport September 18, 2026 DOI: 10.12775/qs.2026.74.75172 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Esketamine Ketamine
Key findings The authors argue that chronic recreational ketamine misuse causes severe multi-organ toxicity, including permanent cognitive deficits, ketamine-induced uropathy with hydronephrosis, "ketamine cramps" from sphincter of Oddi dyskinesia, cardiac remodeling and fibrosis, and hypercapnic respiratory failure. They contend that absolute abstinence is the cornerstone of management, and that no established pharmacotherapy exists for ketamine cravings, creating a therapeutic gap.

Abstract

Ketamine is a psychoactive substance and an N-methyl-D-aspartate (NMDA) receptor antagonist, commonly used in anesthesiology, psychiatry, and emergency medicine. Its unique dissociative properties have led to a significant global increase in recreational misuse, particularly among young adults in nightlife environments. While the medical applications of ketamine demonstrate a favorable safety profile, its uncontrolled, chronic consumption poses severe toxicological risks. The primary mechanism of action of ketamine relies on blocking NMDA receptors, which leads to a secondary glutamate surge and localized neurotoxicity. This study aims to systematically evaluate the multi-organ manifestations, clinical complications, and management strategies associated with ketamine misuse. The article was developed using the "PubMed" and "Google Scholar" databases, with a particular emphasis on articles published after 2021. Chronic recreational ketamine misuse induces severe somatotoxic and neuropsychiatric injuries, including permanent cognitive and executive deficits, ketamine-induced uropathy (KIU) with secondary hydronephrosis, and excruciating gastrointestinal episodes ("ketamine cramps") triggered by sphincter of Oddi dyskinesia. Recent reports also highlight significant structural cardiac remodeling, myocardial fibrosis, and the risk of hypercapnic respiratory failure during acute, high-dose intoxications. Multidisciplinary treatment requires absolute abstinence as the cornerstone of therapy, combined with targeted pharmacotherapy, symptomatic clinical stabilization, and psychotherapy. Due to a therapeutic gap resulting from the lack of established pharmacological treatments to reduce ketamine cravings, further clinical trials are essential to improve patient recovery during detox and long-term rehabilitation.

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