Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

Abstract

Normal children have a smaller upper airway than adults, but, nevertheless, snore less and have less apnea. We have previously shown that normal children have an upper airway that is resistant to collapse during sleep. We hypothesized that this resistance to collapse is due to preservation of upper airway neuromotor responses during sleep. Furthermore, we hypothesized that upper airway responses would be diminished in children with the obstructive sleep apnea syndrome (OSAS). We therefore compared the upper airway pressure-flow relationship during sleep between children with OSAS and controls. Measurements were made by correlating maximal inspiratory airflow with the level of nasal pressure applied via a mask. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We found that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatment of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalization of upper airway responses. We conclude that upper airway dynamic responses are decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a compensatory response for a relatively narrow upper airway. Further, we speculate that this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to mechanical damage to the upper airway. In children, OSAS is related to adenotonsillar hypertrophy. Most children with OSAS have large tonsils and adenoids, and improve after T&A (1). Nevertheless, studies suggest that childhood OSAS is not due to anatomic abnormalities alone. Most obvious is the fact that patients with OSAS do not obstruct during wakefulness, when upper airway muscle tone is high. Although the upper airway may be narrower in children with OSAS than in those without, there is overlap between the groups (2). A small percentage of children with adenotonsillar hypertrophy but no other known risk factors for OSAS are not cured by T&A (1). Furthermore, a small percentage of children who were cured of their OSAS by T&A have been reported to develop a recurrence during adolescence (3,4). Thus, it appears that childhood OSAS is a dynamic process resulting from a combination of structural and neuromotor abnormalities, rather than from structural abnormalities alone. The upper airway above the level of the cartilaginous airway is a collapsible muscular tube that usually remains patent but has the potential to collapse to facilitate such functions as speech and swallowing. It comprises more than 30 pairs of muscles (5). Thus, neuromotor control of this area is important to maintain airway patency. Upper airway collapsibility during sleep is modulated by the central ventilatory drive (6). The upper airway dilatory muscles are respiratory musc...

High-Flow, Heated, Humidified Air Via Nasal Cannula Treats CPAP-Intolerant Children With Obstructive Sleep Apnea

“…[30][31][32][33][34][35][36] Children with OSA are unable to activate airway tone to maintain airway patency. [37][38][39] The lack of sensation of nasal airflow, as by adenotonsillar hypertrophy or nasal obstruction common in the pediatric population, is associated with increased nasopharyngeal resistance and contributes to OSA, [40][41][42][43][44][45] suggesting that sensation of nasal airflow reduces airway resistance and elicits compensatory increase in pharyngeal tone. 36,46 Therefore, the delivery of heated and humidified air to the nasopharynx at higher than usual flow rates may activate, or reactivate, the protective airway reflex via nasopharyngeal mechanoreceptor or thermoreceptor stimulation, as well as reduce irritation, swelling, and congestion associated with dryness.…”

Understanding the Anatomic Basis for Obstructive Sleep Apnea Syndrome in Adolescents

“…In one study, researchers reported the prevalence of OSAS in adolescents to be 2% (1), but the prevalence is probably higher in the United States because of the adolescent obesity epidemic (2). OSAS in children is thought to be secondary to a combination of enlargement of the lymphoid tissue (tonsils and adenoid) (3) and, sometimes, obesity, as well as to reductions in neuromuscular tone (4). In adults, there are known anatomic risk factors for OSAS, including enlargement of the tongue, soft palate, parapharyngeal fat pads, and lateral pharyngeal walls (5) in conjunction with craniofacial restriction (retrognathia) (6).…”

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

“…In most children, OSAS is related to adenotonsillar hypertrophy or obesity. However, these structural factors cannot fully explain the degree of upper airway collapsibility (1,2). Studies have shown that upper airway neuromotor tone and reflexes during sleep play an important role in maintaining airway patency during sleep in the pediatric population (3,4).…”