What are the adverse effects of the increased work of breathing due to childhood obstructive sleep apnea (OSA)?

Updated: Feb 13, 2019
  • Author: Mary E Cataletto, MD; Chief Editor: Denise Serebrisky, MD  more...
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A major cardiovascular consequence of obstructive sleep apnea in adults is arterial hypertension. Although the pathophysiological mechanisms of elevation in arterial tension are still under debate, intermittent arousal, hypoxemia, and increases in cardiac afterload during the obstructive apneic event apparently lead to enhanced sympathoadrenal discharge and heightened sympathetic tone, even during waking hours. Significant alterations in autonomic nervous system tone have been documented in children with obstructive sleep apnea, and modest diurnal elevations in arterial blood pressure have also been reported.

Sleep-disordered breathing is associated with higher systolic blood pressures in children aged 5-12 years and supports the use of an apnea hypopnea index (AHI) threshold of 5 for initiating treatment. [12] The long-term effects of this process in childhood and the effect on adult health are unknown.

A prominent clinical manifestation of increased work of breathing in children with obstructive sleep apnea is failure to thrive (FTT). Indeed, reports from the early 1980s found more than a 50% prevalence of FTT in patients with pediatric obstructive sleep apnea, and significant catch-up growth patterns have been reported after tonsillectomy and adenoidectomy, even in children with obesity and obstructive sleep apnea. The causes of poor growth include anorexia and dysphagia due to tonsillar and adenoid hypertrophy, diminished or altered patterns of nocturnal growth hormone secretion, hypoxemia, acidosis, and increased work of breathing during sleep.

In one study, a substantial reduction in resting energy expenditure was reported after adenotonsillectomy in children with obstructive sleep apnea and FTT with concomitant gains in body weight. [13] Another study demonstrated significant recovery in the insulin growth factor 1 axis. [14] These findings suggest that an important factor that mediates FTT in pediatric obstructive sleep apnea involves the combination of increased energy expenditure caused by increased respiratory effort and disruption of the pathways of the growth hormone somatomedin.

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