Pathophysiology of Pediatric Obstructive Sleep Apnea

Abstract

Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

The use of magnetic resonance imaging in the evaluation of upper airway structures in paediatric obstructive sleep apnoea syndrome: a systematic review and meta-analysis

“…These parameters can also indirectly affect the genesis of the syndrome as they alter normal muscle insertion sites. [7][8][9][10] The gold standard for the diagnosis of OSAS is polysomnography (PSG).…”

Obstructive Sleep Apnea in Children

“…These findings suggest that OSA represents the end point of the interactions between multiple factors contributing to upper airway collapsibility during sleep, which also include neuromotor responses as well as other important anatomic factors such as retrognathia and upper airway length. 17,18 The prevalence and severity of overweight and obesity in children and adolescents has witnessed dramatic increases in the last few decades worldwide. 19,20 For example, the prevalence of childhood overweight doubled among children 6 to 11 years of age and tripled among children 12 to 17 years of age in the United States between 1980 and 2000.…”

Estimation of Newborn Risk for Child or Adolescent Obesity: Lessons from Longitudinal Birth Cohorts

“…Similar to nonobese children, airway obstruction by adenotonsillar hypertrophy is a fairly common cause of OSA among obese children [31][32][33] affecting approximately 45% of all obese children with OSA [34]. However, alarmingly, following adenotonsillectomy, OSA persists in about 50% of obese children [35] which is significantly higher than the observed persistence rate of 10-20% amongst nonobese children [36,37].…”