What is the role of anatomic narrowing in the pathophysiology of childhood obstructive sleep apnea (OSA)?

Updated: Feb 13, 2019
  • Author: Mary E Cataletto, MD; Chief Editor: Denise Serebrisky, MD  more...
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Answer

At any point in life, a smaller cross-sectional area of the upper airway is associated with decreased ability to maintain upper airway patency. In adults, the upper airway behaves as predicted by the Starling resistor model. According to this model, under conditions of flow limitation, maximal inspiratory flow is determined by the pressure changes upstream (nasal) to a collapsible site of the upper airway, and flow is independent of downstream (tracheal) pressure generated by the diaphragm. Pressures at which the airway collapses have been termed critical closing pressures, or Pcrit. In other words, in the presence of a collapsible segment of the upper airway, such as the pharyngeal introitus, the overall resistance to airflow proximal to that segment is the major factor responsible for occlusion of the collapsible segment. This model explains why, for example, snoring and obstructive apnea worsen during a common cold (increased nasal-upstream resistance).

The validity of this model was also confirmed in children, and interestingly, the collapsibility of the upper airway in children was reduced when compared with that of adults. As predicted by the Starling resistor model, the collapsible segment of the upper airway in children displayed less negative (higher and, therefore, more collapsible) pressures in children with obstructive sleep apnea. Components that affect the upstream segment pressures or increase Pcrit are of major consequence to the ability to maintain airway patency. For example, a viral cold or allergic rhinitis that induces increased secretion in the nasal passages and mucosal swelling is associated with increased nasal resistance to airflow. Not surprisingly, the magnitude of snoring and the severity of obstructive apnea are increased during periods in which the upstream segment pressure has been adversely affected.

The contribution of the various anatomical nasopharyngeal structures to Pcrit and the interactions between these structures that lead to upper airway patency or obstruction during sleep are of obvious importance in increasing the understanding of the pathophysiology of obstructive sleep apnea in children. For most children, enlargement of the tonsils and/or adenoid is the proximate cause for the development of obstructive sleep apnea.

The static pressure and/or area relationships of the passive pharynx were endoscopically measured in 14 children with obstructive sleep apnea and in 13 healthy children under general anesthesia with complete paralysis, [2] and it was determined that children with obstructive sleep apnea closed their airways at the level of enlarged adenoids and tonsils at low positive pressures, whereas healthy children required subatmospheric pressures to induce upper airway closure. The cross-sectional area of the narrowest segment was significantly smaller in children with obstructive sleep apnea and particularly involved the retropalatal and retroglossal segments. Thus, both congenital and acquired anatomic factors clearly play a significant role in the pathogenesis of pediatric obstructive sleep apnea.


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