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Symptoms of OSA in kids with apnea predominance may not resolve after adenotonsillectomy: JAMA
Obstructive sleep apnea (OSA) is characterized by upper airway obstruction and can be associated with oxygen desaturation and sleep fragmentation. Approximately 4% of healthy school-aged children receive a diagnosis of OSA, with a much higher prevalence of this disease found in children with certain comorbidities including obesity. OSA can have substantial sequelae in children, including poor focus, behavioral problems, and daytime sleepiness.
The current criterion standard for diagnosing pediatric OSA is full-night polysomnogram (PSG).The PSG measures upper airway airflow during sleep; respiratory sensors are used to detect apneas and hypopneas. Apneas represent the most severe form of obstruction, featuring a 90% decrease in air movement, whereas hypopneas represent a partial (30%) cessation in airflow associated with arousal or desaturation. Researchers have hypothesized that OSA characterized by mostly hypopneas may be a less-severe form of disease compared with OSA in which apneic events predominate.
The current pediatric OSA classification system is based on the apnea-hypopnea index (AHI) and does not include this parameter when accounting for disease severity. In addition to the objective sleep parameters provided by PSG, other pediatric OSA outcomes include quality of life (QOL) and symptom burden assessment. Interestingly, OSA severity as determined by AHI fails to correlate with QOL scores in children. There is a lack of data on the relationship between QOL and apnea and hypopnea predominance.
Adenotonsillar hypertrophy is a common cause of obstruction in children with OSA. Thus, adenotonsillectomy (AT) is the primary treatment for pediatric OSA. Although AT results in improvement in both PSG parameters and QOL in children with OSA, 25% to 70% of children can have persistent disease, including ongoing evidence of obstruction on PSG, following surgery. Certain demographic and clinical factors, including Black race and craniofacial anomalies, predispose children to persistent disease. Polysomnography can also estimate residual OSA, as children with severe OSA at baseline (typically AHI >10) are also at risk for residual disease after AT. However, research is lacking as to whether children with apnea-predominant baseline OSA are at increased risk for persistent obstruction following AT.
Authors Saadhana Kukkala et al hypothesized that children with apnea-predominant OSA at baseline would be at higher risk for persistent obstruction following AT or watchful waiting with supportive care (WWSC). The objective of this case-control study was to assess the association of baseline apnea predominance vs hypopnea predominance with pediatric OSA treatment outcomes.
This case-control study was a secondary analysis of a randomized clinical trial, the Childhood Adenotonsillectomy Trial, which was conducted at multiple tertiary children's hospitals from October 2007 to June 2012. Children aged 5.0 to 9.9 years with OSA were randomized to WWSC or AT and underwent polysomnography and completed validated QOL and symptom assessments at baseline and 7 months. The current data analysis was performed from October 2020 to February 2022.
Apnea-predominant OSA was defined as an apnea hypopnea index (AHI) greater than 2 with more than 50% of the obstructive events being apneas. Patients were considered to have hypopnea-predominant OSA if they had an AHI greater than 2 and more than 50% of the obstructive events were hypopneas.
A total of 386 children were analyzed. The mean (SD) obstructive AHI for patients was 6.98 (5.62), with 198 patients (51%) having mild disease. Thirty-seven children (10%) had apnea-predominant OSA at baseline. Black children were at increased risk for apnea-predominant OSA vs White children. Children with apnea predominance were more likely to have severe OSA (AHI >10) compared with children with hypopnea predominance; baseline Pediatric Sleep Questionnaire and OSA-18 QOL scores were similar between the 2 groups. Among children undergoing AT, those with baseline apnea predominance were more likely to have a Pediatric Sleep Questionnaire score greater than 0.33 at follow-up. Rates of OSA resolution and improvements in QOL scores following AT or WWSC were similar between the apnea-predominant and hypopnea-predominant groups.
Study findings did show improvements in both PSG and QOL outcomes after AT, regardless of apnea or hypopnea predominance. In this study, baseline apnea predominance was not associated with PSG outcomes in terms of disease resolution; rates of resolution were similar between AT groups with baseline apnea predominance vs baseline hypopnea predominance. This finding is surprising as apneas have been considered to be a more severe form of obstruction. Certainly, the low number of children with apnea predominance may have affected this finding. If future research that includes children with more severe disease confirms that apnea predominance is not associated with OSA treatment outcomes in children, the utility of distinguishing apnea vs hypopnea when scoring PSGs may need to be revisited.
This study adds to the literature information regarding the association of baseline apnea predominance with outcomes in children with OSA who are being managed with WWSC. There was not an association with disease progression as assessed by AHI on PSG in those children with apnea predominant disease who were managed with WWSC. Thus, in children with OSA, having more apneas at baseline is not associated with short-term prognosis.
In this case-control study, among patients with OSA, only a small portion of otherwise healthy children had apnea predominant disease. Severe OSA was associated with baseline apnea predominance. Apnea predominance may affect symptom resolution in children undergoing AT for OSA but was not associated with postintervention PSG outcomes. Further research is needed to assess whether apnea predominance affects treatment response in children with more severe disease.
Source: Saadhana Kukkala, MS; Turaj Vazifedan, DHSc; Cristina M. Baldassari, MD; JAMA Otolaryngology–Head & Neck Surgery
doi:10.1001/jamaoto.2022.3031