In Response to van Gorp F. et al
Article Outline
To the Editor:
We read with great interest the recent paper discussing escitalopram overdose.1 Because serotonin syndrome constitutes a well-described set of recognizable symptoms,2 we were most interested in QT prolongation given that it is often asymptomatic but has grave implications. Many patients who ingest citalopram warrant prolonged telemetry monitoring because the QT prolonging effect of the metabolite didesmethylcitalopram can be delayed.3 Since it is unclear if delayed QT prolongation also occurs following escitalopram ingestion, we therefore commend the authors for their effort to investigate the clinical effects of this drug and for attempting to confirm ingestion with quantitative analysis.
However, it should be noted that less than half of the patients had serum confirmation of escitalopram, and the authors consider a reported history of ingestion as a reliable estimate of actual ingestion. Despite the cited publications to support this, there is also considerable evidence to suggest the contrary in both adults and children.4, 5, 6 In fact, the unreliability of history is demonstrated when the authors excluded a patient who reported a large ingestion, but had an inappropriately low serum concentration. Also, because no information is provided as to whether in the patients who where chronically taking escitalopram, measured concentrations might have been more reflective of therapeutic drug monitoring than of overdose. Furthermore, since no patient in this study suffered a death, seizure or cardiac dysrhythmias, the lack of morbidity and mortality raises concerns about the true incidence of actual ingestion or significant exposure in this cohort.
The authors suggested that the risk of torsades de pointes with escitalopram poisoning were similar to citalopram given that 14% of patients were found to have an abnormal QT based on their QT-HR criteria, but we have several concerns with these results. First, it is unclear at which time or how many different QT measurements were made during the admission. Single measurements could potentially miss delayed effects, whereas averaging several measurements could hide significantly abnormal values. It would have also been important to attempt to correlate the serum concentration of escitalopram with the QT interval, and to evaluate for the metabolite most likely responsible for the effect. Regardless, the fact that no patient suffered torsades raises questions about their estimation.
QT prolongation is a dynamic process and future endeavors should concentrate on prospectively collecting consecutive escitalopram ingestions, obtaining serum confirmation of both the parent drug and the metabolite and most importantly obtaining serial ECGs to observe for magnitude and duration of well-described QT effects in relation to drug and metabolite concentrations.
References
- . Clinical and ECG Effects of Escitalopram Overdose. Ann Emerg Med. 2009;54:404–408
- . The serotonin syndrome. N Engl J Med. 2005;352:1112–1120
- . Citalopram overdose: late presentation of torsades de pointes (TdP) with cardiac arrest. J Med Toxicol. 2008;4:101–105
- Unproven ingestion: an unrecognized bias in toxicological case series. Clin Toxicol (Phila). 2007;45:946–949
- Comparison of patient questionnaires and plasma assays in intentional drug overdoses. Basic Clin Pharmacol Toxicol. 2004;95:31–37
- Accuracy of information on substance use recorded in medical charts of patients with intentional drug overdose. Psychiatry Res. 2007;152:73–79
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PII: S0196-0644(09)01442-5
doi:10.1016/j.annemergmed.2009.07.031
© 2010 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.
Refers to article:
- Clinical and ECG Effects of Escitalopram Overdose , 26 June 2009
- In reply
