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A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Hypoxic Burden in Children With Sleep-Disordered Breathing: Determinants and Correlates
Plamen Bokov1, Benjamin Dudoignon1, Christophe Delclaux1
1Université de Paris-Cité, AP-HP, Hôpital Robert Debré, Service de Physiologie Pédiatrique-Centre du Sommeil, INSERM NeuroDiderot, Paris, France.
Insights
Hypoxic burden (HB) quantifies intermittent hypoxia in children with sleep apnea, showing higher levels in severe cases. Increased HB is linked to sleepiness and obesity, suggesting it as a key marker for sleep-disordered breathing severity.
Area of Science:
- Pediatric Pulmonology
- Sleep Medicine
- Biomedical Engineering
Background:
- Intermittent hypoxia from sleep apnea is a concern in children.
- Hypoxic burden (HB) is a novel metric for quantifying intermittent hypoxia.
- Traditional metrics like the apnea-hypopnea index (AHI) may not fully capture the impact of hypoxia.
Purpose of the Study:
- To evaluate the distribution and clinical significance of non-respiratory event-specific HB in children and adolescents with habitual snoring.
- To explore the relationship between HB and sleepiness, obesity, tonsillar hypertrophy, and other clinical parameters.
- To determine if HB is an independent marker of sleep-disordered breathing (SDB) severity in pediatric populations.
Main Methods:
- Retrospective analysis of polysomnography data from 380 children with suspected SDB.
- Calculation of HB based on oxygen saturation (SpO2) desaturation events (≥3%).
- Statistical analysis to correlate HB with AHI, oxygen desaturation index (ODI), minimum SpO2, obesity, tonsillar hypertrophy, and sleepiness scores.
Main Results:
- Median HB was 1.7% min/h, with significantly higher values in moderate-to-severe OSAS (7.5% min/h) compared to mild OSAS (2.7% min/h) or primary snoring (1.1% min/h).
- HB correlated strongly with AHI (ρ=0.61), ODI (ρ=0.73), and inversely with minimum SpO2 (ρ=-0.70).
- Increased HB was associated with obesity and tonsillar hypertrophy, and independently linked to parent-reported sleepiness in primary snoring cases (OR=1.39 per SD increase in HB).
Conclusions:
- Hypoxic burden is a significant and independent marker of SDB severity in children and adolescents.
- HB reflects the impact of hypoxia, particularly desaturation depth, in SDB.
- This metric holds potential for understanding SDB-related cognitive deficits in pediatric populations.
Abstract:
Hypoxic burden (HB) is an emerging metric for quantifying intermittent hypoxia associated with sleep apnea, offering potential advantages over traditional measures such as the apnea-hypopnea index (AHI). This study evaluated the distribution and clinical significance of non-respiratory event-specific HB in children and adolescents with habitual snoring, exploring its relationship with sleepiness and other clinical parameters. The data were gathered from 512 children referred for suspected sleep-disordered breathing (SDB), focusing on 380 subjects with available HB data. HB was calculated as the total area under oxygen saturation (SpO2) curves for events with ≥ 3% oxygen desaturation, with a median value of 1.7% min/h [IQR: 0.6% min/h-4.6% min/h]. Children with moderate-to-severe obstructive sleep apnea syndrome (OSAS) exhibited significantly higher HB than those with mild OSAS or primary snoring (7.5% min/h, 2.7% min/h, and 1.1% min/h, respectively). HB was notably linked to the AHI (rhos = 0.61), the oxygen desaturation index (rhos = 0.73), and minimum SpO2 (rhos = -0.70). Furthermore, increased HB was observed in obese children and those with tonsillar hypertrophy, underscoring their synergistic impact. These effects were reflected in desaturation depth rather than their duration. In children with primary snoring, HB showed a significant association with parent-reported sleepiness. Specifically, there was a 39% increase in the odds ratio for a modified Epworth sleepiness scale score exceeding 10 for each standard deviation increase in HB (p = 0.040). These findings suggest HB as an independent marker of SDB severity, with potential implications for understanding cognitive deficits linked to SDB in children.
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