Brooks DM, Brooks LJ. Reevaluating norms for childhood obstructive sleep apnea. J Clin Sleep Med. 2019;15(11):1557–1558.
Obstructive sleep apnea (OSA) has long been recognized as a significant cause of morbidity in adults and is increasingly recognized as a problem in children as well. The prevalence of OSA among children ranges from 1% to 4%1 and short- and long-term consequences include excessive daytime sleepiness, attention problems, hyperactivity, and mood issues.2 There has been some thought that OSA in children can be divided into categories, one that is unique in childhood and caused by adenotonsillar hypertrophy that usually responds to surgery, and the more adult type associated with obesity wherein continuous positive airway pressure is the primary treatment.2 While the jury is still out on whether this is true, in this issue of the Journal of Clinical Sleep Medicine, Au and colleagues designed and executed a prospective case-control study of 229 Chinese children ages 6–18 years with OSA and 412 first-degree relatives to examine the hereditary nature of OSA and whether one potential subtype may have more heritability and familial aggregation than the other.3
The goal of this study by Au et al was to ascertain if pediatric OSA is associated with OSA in parents and siblings and if so, is familial aggregation and hereditability present in both obese and normal weight children. Children were recruited from both the sleep clinic and the community. All children had full in-laboratory polysomnography (PSG), while adult relatives underwent 16 channel home PSG. For this study, OSA was defined as an apnea-hypopnea index (AHI) ≥ 1 event/h in children, and ≥ 5 events/h in adults. Moderate-to-severe OSA was defined as AHI ≥ 5 events/h in children and ≥ 15 events/h in adults. This study developed some important information into how OSA is viewed in children, including some inferences about the relative contributions of genetic and environmental influences and implications about the validity of current PSG norms in children.
The results of this study showed that overall, relatives of the probands did not have a significantly higher AHI than relatives of control children. However, when looking specifically at children with AHI > 5 events/h, relatives of these probands did have a higher AHI than relatives of the other children. Familial aggregation was also only seen in families of children with AHI > 5 events/h. Heritability, on the other hand, was only significant in overweight probands.
Overall, there were no differences in the AHI of parents of probands v. parents of control children. When broken down by family member, fathers of overweight children with AHI > 5 events/h had a higher AHI than the fathers of overweight children who had an AHI < 5 events/h; there was no difference between fathers of normal weight children with or without OSA. Mothers of children with AHI > 5 events/h also had a higher AHI than mothers of children with AHI < 5 events/h. In terms of siblings, the main effect of probands’ severity of OSA on siblings’ AHI was not significant; there was also no difference between siblings of normal weight probands regardless of OSA status. Siblings of children with AHI > 5 events/h had a higher AHI than siblings of children with an AHI < 5 events/h. These data showed that being overweight significantly modified the results.
Heritability, a main focus of this paper, was mainly associated with obesity. This reinforces the idea that OSA is heritable but does not identify which factor or factors are heritable. These may include airway size and airway compliance, which may be affected by craniofacial characteristics, muscle responsiveness, airway length, and/or lymphatic tissue. The data in this study support the relationship between children with OSA and parents with OSA, but more so in the obese. This finding does not necessarily mean that there are two distinct types of OSA but it could mean that obesity is a risk factor for OSA in children as it is in adults.
In this study, relationships were seen only in children with an AHI > 5 events/h. This is similar to other studies that have shown no difference in sequelae between a child that has an AHI < 1 event/h and one who has an AHI between 1 and 5 events/h.4 Other studies have found that there was no difference in systolic or diastolic blood pressure between children with primary snoring (AHI around 1 event/h) and children with AHI of 5 events/h.5,6 This raises the question of the validity of the common classification of pediatric OSA into “normal” (AHI < 1 event/h), “mild” (AHI 1–5 events/h), and “moderate to severe” (AHI > 5 events/h).7 In fact, there are very little data to support this classification.8 The seminal study of pediatric norms was limited by a small sample size, lack of electroencephalography confirmation of sleep, and no consideration of hypopneas or central events. They suggested an obstructive apnea index of 1 event/h as a cutoff for normal, and noted “the clinical significance of short apneas in children has not yet been ascertained.”9 The author of the current study previously reported that “normative standards for PSG determination have been chosen on the basis of statistical distribution of data, and it has not been established that those standards have any validity as predictors of long-term outcome.”10 Perhaps it is time for a reevaluation of the classification of pediatric OSA with more attention paid to physiology and outcomes.
All authors have seen and approved the manuscript. The authors report no financial support or conflicts of interest.