Much Ado about Sleep: Current Concepts on Mechanisms and Predisposition to Pediatric Obstructive Sleep Apnea

Abstract

Obstructive Sleep Apnea (OSA) is a form of sleep-disordered breathing characterized by upper airway collapse during sleep resulting in recurring arousals and desaturations. However, many aspects of this syndrome in children remain unclear. Understanding underlying pathogenic mechanisms of OSA is critical for the development of therapeutic strategies. In this article, we review current concepts surrounding the mechanism, pathogenesis, and predisposing factors of pediatric OSA. Specifically, we discuss the biomechanical properties of the upper airway that contribute to its primary role in OSA pathogenesis and examine the anatomical and neuromuscular factors that predispose to upper airway narrowing and collapsibility.

Keywords: adenotonsillar hypertrophy; craniofacial; critical pressure; inflammatory cytokines; mechanisms; neuromuscular control; pediatric obstructive sleep apnea; starling resistor model; upper airway.

Figure 1

Intrinsic and Extrinsic Determinants of Upper Airway Collapsibility that affect the fine balance of airway patency during sleep.

Figure 2

The Starling Resistor Model is a diagram that assists with the explanation of upper airway dynamics and the management of obstructive sleep apnea. The oropharynx is presented as a collapsible tube. Increased nasal airway resistance increases the probability that pharyngeal pressure will decrease below the CRITICAL pressure (Pcrit) and close the pharynx, which is a large proponent of obstructive events [2].

Figure 3

This child has “adenoid facies”, a term commonly used to describe facial characteristics of a mouth-breathing child with anterior face, retrusive mandible, sunken eyes, naroow pinched nostrils, and open mouth with crowded teeth [1].

Figure 4

Changes in maxillary-mandibular growth contributes to formation of the (a) retrognathic mandible, which may result in decreased space between the cervical column and mandible, leading to the (b) posteriorly postured tongue and soft palate, resulting in airway obstruction [41].

Figure 5

Tonsil Grading System. (a) Size 0, absence of tonsillar tissue. (b) Size 1, tonsils within the pillars. (c) Size 2, tonsils extended to the pillars. (d) Size 3, tonsils extended past the pillars. (e) Size 4, tonsils extended to the midline. Adapted from Friedman [48].