The obesity epidemic has prompted remarkable changes in the proportion of obese children who are referred for habitual snoring. However, the contribution of obesity to adenotonsillar hypertrophy remains undefined.
In our study, 206 nonobese habitually snoring children with polysomnographically diagnosed obstructive sleep apnea (OSA) were matched for age, gender, ethnicity, and obstructive apnea-hypopnea index (OAHI) to 206 obese children. Size estimates of tonsils and adenoids, and Mallampati class scores were obtained, and allowed for the assessment of potential relationships between anatomic factors and obesity in pediatric OSA.
The mean OAHI for the two groups was approximately 10.0 episodes/h total sleep time. There was a modest association between adenotonsillar size and OAHI in nonobese children (r = 0.22; p < 0.001) but not in obese children. The mean (± SEM) adenotonsillar size was larger in nonobese children (3.85 ± 0.16 vs 3.01 ± 0.14, respectively; p < 0.0001), and conversely Mallampati class scores were significantly higher in obese children (p < 0.0001).
The magnitude of adenotonsillar hypertrophy required for any given magnitude of OAHI is more likely to be smaller in obese children compared to nonobese children. Increased Mallampati scores in obese children suggest that soft-tissue changes and potentially fat deposition in the upper airway may play a significant role in the global differences in tonsillar and adenoidal size among obese and nonobese children with OSA.