Apnea and Oxygen Desaturations in Children Treated with Opioids after Adenotonsillectomy for Obstructive Sleep Apnea Syndrome
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BACKGROUND: Recent case reports have alerted the medical community of fatality in children receiving codeine after tonsillectomy and/or adenoidectomy for obstructive sleep apnea syndrome. OBJECTIVE: The objective of this study was to compare the rates of oxygen desaturation before and after adenotonsillectomy in children with obstructive sleep apnea syndrome (OSAS), and to examine the relationship between cytochrome P450 2D6 (CYP2D6) genotype and respiratory events. STUDY DESIGN: This was a prospective observational study. METHODS: Twenty-six children with OSAS (mean age 78 months, range 1.8-17 years) who underwent adenotonsillectomy were studied. CYP2D6 genotype was characterized in 21 of these children. The primary endpoints of the study were the change in the rate of desaturation and in the nadir oxygen saturation values before and in the first 24 hours after surgery as measured by pulse oximetry. RESULTS: Twenty-two children received codeine and four were managed with hydrocodone. There was no post-operative improvement in the mean rate of desaturation (1.84 ± 1.45/hour pre-operative vs 2.97 ± 3.3/hour post-operative; p = 0.119; 95% CI -2.56, 0.313), or the post-operative nadir of oxygen saturation (85.2 ± 5.8% pre-operative vs 84.0 ± 6.8% post-operative; p = 0.632; 95% CI -3.00, 4.84) on the night after surgery. Prior to surgery, six children had an oxygen saturation nadir <80%, while post-surgery, the number increased to eight children. Ten children improved their parameters after surgery. CYP2D6 genotype by itself did not predict the changes in desaturation or nadir. CONCLUSION: Post-operative use of opioids following OSAS may not be safe for all children. It is conceivable that if the child is among the significant proportion that experiences increased oxygen desaturations, the CNS depressing effects of codeine or hydrocodone and their respectively potent morphine or hydromorphone metabolites can further compromise respiratory drive. Larger studies are needed to investigate the potential contribution of CYP2D6 genotype.
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