Ontogeny of Obstructive Sleep Apnea

Abstract

Obstructive sleep apnea (OSA) affects 2–4% of children and has been linked to metabolic, cardiovascular, and neurocognitive morbidity. Pediatric OSA has a distinctive pathophysiology, natural history, and treatment compared to adult OSA. All cases of OSA are associated with increased upper airway resistance during sleep, resulting in intermittent partial or complete airway closure. The increased upper airway resistance results in increased respiratory effort, sleep fragmentation, and/or gas exchange abnormalities. Thus, OSA induces a sequence of hormonal disturbances, oxidative stress, inflammation, autonomic activation, and/or disruption of sleep architecture. Causes of airway narrowing include soft tissue hypertrophy such as adenotonsillar hypertrophy, craniofacial abnormalities including micrognathia and mid-facial hypoplasia, and/or neuromuscular deficits. In addition to anatomical abnormalities, the maintenance of upper airway patency is dependent upon neuromuscular activation of pharyngeal dilators, ventilatory control, and the arousal threshold. During sleep, most children with OSA are capable of reaching stable breathing patterns for long periods of time, indicating successful neuromuscular compensation. Airway muscle activity declines at sleep onset but is offset by recruitment of pharyngeal dilator muscles. Oscillations in the levels of carbon dioxide (CO 2 ) produce nadirs in which there is a reduction in airway muscle activity, thus promoting obstruction during nonrapid eye movement sleep. Sudden airway opening and arousal from sleep results in a ventilatory overshoot that may worsen obstructive cycling. Diagnosing OSA in children requires knowledge of normative data related to gestation and postconceptual age for apnea, arousal, and oxygenation. Both genetic and environmental factors may influence the expression of OSA consequences, and therefore strict polysomnographic guidelines for the diagnosis and treatment of OSA are not possible. Common surgical treatment options for pediatric OSA include adenotonsillectomy for enlarged soft tissues, supraglottoplasty for laryngomalacia, maxillary expansion for a constricted mandible, and mandibular distraction for micrognathia. Continuous positive airway pressure is generally reserved for children without a routine surgical therapy. Snoring alone, without scorable obstructive events or gas exchange abnormalities, may also be associated with adverse neurobehavioral outcomes. The clinical history for symptoms of sleep-disordered breathing has a poor positive predictive value for the diagnosis of OSA and therefore diagnostic polysomnographic testing as well direct airway visualization is frequently indicated.