Methadone Toxicity with Electrocardiographic Sodium Channel Blockade Changes in a Pediatric Patient Post-cardiopulmonary Arrest: a Case Report

Abstract

Background: Cardiopulmonary arrest in the pediatric population due to methadone toxicity is not commonly reported. Severe methadone toxicity often involves respiratory depression with reports of orthostatic hypotension, due to vasodilation, and QTc prolongation.<br /> Case presentation: A pair of toddler siblings presented in cardiopulmonary arrest due to methadone ingestion. They were successfully resuscitated with no significant neurobehavioral deficits despite a suspected prolonged “downtime." After return of spontaneous circulation, the older sibling, a four-year old male, had electrocardiographs (ECGs) that were suggestive of sodium channel blockade. These changes were reversed following bicarbonate therapy. The two-year old child's ECGs did not show such changes.<br /> Discussion: There is no prior clinical literature on sodium channel blockade in methadone toxicity. The older sibling's ECG findings and response to bicarbonate therapy appeared to be consistent with sodium channel blockade. There have been preclinical data that suggest methadone cardiotoxicity may involve cardiac sodium channels. Pharmacogenetic variations could also explain how these effects may selectively manifest.<br /> Conclusion: Physicians should be aware of the possible toxicologic causes of cardiopulmonary arrest in the pediatric population. Pharmacogenetic variations may contribute to different clinical manifestations in methadone cardiotoxicity.