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Correspondence  |   June 2003
Neuroprotective and Antiepileptic Activities of Ketamine in Nerve Agent Poisoning: In Reply
Author Notes
  • Post-Anesthesia Care Unit, Tel Aviv Sourasky Medical Center.
Article Information
Correspondence
Correspondence   |   June 2003
Neuroprotective and Antiepileptic Activities of Ketamine in Nerve Agent Poisoning: In Reply
Anesthesiology 6 2003, Vol.98, 1517. doi:
Anesthesiology 6 2003, Vol.98, 1517. doi:
In Reply:—
We read with interest the letter of Mion et al.  regarding our review article. The issue that the authors raise, i.e.  , our report of experimental data indicating a potential dangerous reaction to ketamine (prolonged apnea and respiratory distress) when animals were exposed to sulfur mustard, is theoretical, at least in part. As reviewers, we could do no more than collect and present the specific experimental model and the related results at face value. The clinical aspects of the possible use of ketamine in nonconventionally intoxicated patients is problematic on several fronts. First, because ketamine potentially generates undesirable side effects per se  that additively affect target-organs of nerve agents (e.g.  , central nervous system: hallucinations; respiratory system: increased secretions), such potentiation may lead to unacceptable neurologic conditions. Second, ketamine has never been accepted clinically as a safe drug to control epileptic episodes, although its potential has been shown in animal models. Indeed, Mion et al.’  s use of the word “may” is entirely appropriate in illustrating a potential but not contemporary use of ketamine as an antiseizure drug because of its NMDA-antagonistic properties. In the clinical setting, following the American, Israeli, and European protocols of antinerve agent protection, however, benzodiazepines are the only  proven drugs to effectively control seizures while scopolamine, another weak NMDA-receptor antagonist, is the drug used to antagonize organophosphates’ central effects. We indeed discussed in our review article the notion brought up by Mion et al.  that “…ketamine [is] suitable for induction and maintenance of anesthesia in patients exposed to organophosphorous compounds.”1 Importantly, this reference used by the authors is inappropriate and extrapolative, because the article by Sheth et al.  dealt with neither anesthesia nor organophosphorous compounds.
Finally, the concise explanation of the NMDA receptors-ketamine interactions in the central nervous system was appropriate, considering the scope of our review.
Reference
Reference
Sheth RD, Gidal BE: Refractory status epilepticus: Response to ketamine. Neurology 1998; 51: 1765–6Sheth, RD Gidal, BE