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Effects of overnight supplemental oxygen in obstructive sleep apnea in children
G Aljadeff1, D Gozal, S L Bailey-Wahl
1Division of Neonatology and Pediatric Pulmonology, Childrens Hospital Los Angeles, University of Southern California School of Medicine 90027, USA.
Insights
Supplemental oxygen therapy for children with obstructive sleep apnea syndrome (OSAS) improved oxygen levels without worsening ventilation. This suggests supplemental O2 may be a safe, temporary treatment for pediatric OSAS.
Area of Science:
- Pediatric Pulmonology
- Sleep Medicine
- Respiratory Physiology
Background:
- Obstructive sleep apnea syndrome (OSAS) in children can cause hypoxemia.
- Supplemental oxygen (O2) is a potential palliative treatment but may impair ventilation.
- The safety of O2 in pediatric OSAS requires further investigation.
Purpose of the Study:
- To evaluate the safety and efficacy of supplemental O2 in children with OSAS.
- To assess the impact of O2 on oxygenation and ventilation during sleep.
- To determine changes in respiratory events and sleep architecture with O2 therapy.
Main Methods:
- 16 children (ages 2-8) with OSAS underwent two overnight polysomnograms.
- One study was on room air (RA), the other with supplemental O2 titrated to SpO2 > 95%.
- Measurements included oxygen saturation, PETCO2, respiratory event indices, and sleep stages.
Main Results:
- Supplemental O2 significantly improved oxygenation (SpO2 89.5% on RA vs. 97.7% on O2).
- Alveolar ventilation (PETCO2) remained unchanged, indicating no worsening of ventilation.
- O2 reduced hypopnea density, obstructive apnea index, and paradoxical breathing, while increasing REM sleep and decreasing microarousals.
Conclusions:
- Supplemental oxygen appears to be a safe and beneficial temporary treatment for children with OSAS.
- It effectively improves oxygenation and sleep quality without compromising ventilation.
- Further research may support its role in managing pediatric OSAS.
Abstract:
Supplemental oxygen during sleep may be useful as a temporary palliative treatment in children with obstructive sleep apnea syndrome (OSAS) associated with significant hypoxemia. However, supplemental O2 may also blunt hypoxic ventilatory drive and worsen ventilation. To assess the safety of the use of supplemental O2 in children with OSAS, we studied 16 children ages 2-8 (mean: 4.28 +/- 2.88 yr) with OSAS secondary to adenotonsillar hypertrophy. Patients underwent two overnight polysomnograms within 1 mo, one on room air (RA) and one while receiving supplemental O2 via nasal cannula titrated by 1/4 lpm increments to achieve SpO2 > 95% during the first hour of sleep. Oxygenation measurements were significantly improved during supplemental O2 nights (average SpO2 increased from 89.5 +/- 4.8% on RA to 97.7 +/- 1.8% on supplemental O2 [p < 0.00001]) while alveolar ventilation remained unchanged (PETCO2 > 50 mm Hg: 3.6 +/- 8.9% total sleep time on RA and 3.3 +/- 6.3% total sleep time on supplemental O2 [p = NS]). Supplemental O2 significantly reduced hypopnea density, obstructive apnea index, and paradoxical breathing. The density and average duration of central apneas remained unchanged. In addition, supplemental O2 increased the percentage of REM sleep time and decreased the number of microarousals. We conclude that supplemental O2 might be a safe and beneficial temporary treatment in children with OSAS.