Study objective: We sought to characterize the clinical manifestations, outcome, and etiology of inadvertent ketamine overdose in the emergency department.
Methods: We investigated cases of inadvertent ketamine overdose in children seen in the ED solicited through electronic mail subscription lists or reported to the Institute for Safe Medication Practices. The clinical manifestations, outcome, and reported cause for each case are described.
Results: We identified 9 cases of inadvertent ketamine overdose in children treated in the ED. Patients received either 5 (n=3), 10(n=5), or 100 (n=1) times the intended dose, either by the intramuscular (n=5) or intravenous (n=4) route. All 9 experienced prolonged sedation (3 to 24 hours). Four experienced brief respiratory depression shortly after administration, and assisted ventilation was performed in 2. Two children without respiratory difficulty or hypoxemia were intubated by their physicians as a precaution. In 5 children, the dosing error was not discovered until late in the sedation, often when the child was not waking at the expected time. No adverse outcomes were noted, and all children were normal neurologically on discharge and longer-term follow-up if available.
Conclusion: No adverse outcomes were noted in 9 healthy children treated in the ED who inadvertently received 5 to 100 times the intended dose of ketamine. Toxicity manifested as prolonged sedation in all 9 and brief respiratory depression in 4. The margin of safety in ketamine overdose may be wide, although less common and more serious outcomes cannot be excluded by this small, self-reported sample.
Original Articles
Ketamine-Induced Exacerbation of Psychotic Symptoms and Cognitive Impairment in Neuroleptic-Free Schizophrenics
Author links open overlay panelAnil K.Malhotra, M.DaDebra A.Pinals, M.DaCaleb M.Adler, M.DaIgorElman, M.DaAllanClifton, B.AaDavidPickar, M.DaAlanBreier, M.Da
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https://doi.org/10.1016/S0893-133X(97)00036-5Get rights and content
Abstract
The N-methyl-d-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia. We administered subanesthetic doses of the NMDA receptor antagonist ketamine in a double-blind, placebo–controlled design to 13 neuroleptic-free schizophrenic patients to investigate if schizophrenics will experience an exacerbation of psychotic symptoms and cognitive impairments with ketamine. We also examined whether schizophrenics experienced quantitative or qualitative differences in ketamine response in comparison to normal controls. Schizophrenics experienced a brief ketamine-induced exacerbation of positive and negative symptoms with further decrements in recall and recognition memory. They also displayed greater ketamine-induced impairments in free recall than normals. Qualitative differences included auditory hallucinations and paranoia in patients but not in normals. These data indicate that ketamine is associated with exacerbation of core psychotic and cognitive symptoms in schizophrenia. Moreover, ketamine may differentially affect cognition in schizophrenics in comparison to normal controls.
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