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Obesity increases the risk for persisting obstructive sleep apnea after treatment in children
Louise M O'Brien1, Sinthu Sitha, Louise A Baur
1Division of Pediatric Sleep Medicine and Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, School of Medicine, 571 S. Preston Street Suite 321, Louisville, KY 40202, USA.
Insights
Childhood obesity significantly increases the risk of persistent obstructive sleep apnea (OSA) after adenotonsillectomy. Obese children are more likely to have ongoing OSA symptoms post-treatment.
Area of Science:
- Pediatric Pulmonology
- Sleep Medicine
- Obesity Research
Background:
- Obstructive sleep apnea (OSA) is a common condition in children.
- Obesity is a known risk factor for OSA, but its impact on treatment outcomes requires further evaluation.
Purpose of the Study:
- To assess how obesity at diagnosis affects treatment success in pediatric obstructive sleep apnea (OSA).
Main Methods:
- Retrospective analysis of 69 children with diagnostic and follow-up polysomnography data.
- Obesity defined as BMI z-score > 2; OSA defined as respiratory disturbance index (RDI) >= 5.
- Outcomes assessed post-adenotonsillectomy.
Main Results:
- Obese children had significantly higher post-treatment RDI compared to non-obese children (10.7 vs. 3.7, p=0.01).
- Disease resolution rates were lower in obese children (45%) versus non-obese (77.5%, p=0.011).
- Obesity was associated with a 4.2-fold increased odds of persistent OSA post-treatment (adjusted OR 3.7, p=0.016).
Conclusions:
- Childhood obesity at diagnosis is a significant predictor of persistent OSA after adenotonsillectomy.
- This risk persists irrespective of the initial severity of OSA.
- Weight management may be crucial for improving treatment outcomes in obese children with OSA.
Objective:
To evaluate the impact of obesity at diagnosis on treatment outcomes in paediatric obstructive sleep apnea (OSA).
Methods:
Children were included if they had both diagnostic and follow-up studies for OSA. Anthropological and polysomnographic data were collected at the time of both studies. Polysomnograms were scored using standard criteria and OSA was defined as a respiratory disturbance index (RDI) >or=5. Obesity was defined as a body mass index standard deviation (z-)score (BMIsds) greater than 2, adjusted for age and gender.
Results:
For 69 children (49 males), mean age was 7.1+/-4.2 years and 29 (42%) children were obese. There was no significant difference in RDI between obese and non-obese children at diagnostic study. Following adenotonsillectomy the obese children had a significantly higher mean RDI (10.7+/-15.6 versus 3.7+/-4.3; p=0.01). Disease resolution occurred in 77.5% of non-obese compared to 45% of obese children (p=0.011). The odds ratio (OR) for persistent OSA in obese compared to non-obese children was 4.2 (95% CI: 1.5-11.9; p=0.005). Using initial RDI as a covariate, these data show that obesity in children has an adjusted OR for persistent OSA after adenotonsillectomy 3.7 (95% CI: 1.3-10.8, p=0.016).
Conclusion:
For children, obesity at the time of diagnosis is a major risk for persisting OSA after treatment, regardless of the severity of initial disease.
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