help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Marcus, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marcus, C. L.
American Journal of Respiratory and Critical Care Medicine Vol 169. pp. 140-141, (2004)
© 2004 American Thoracic Society


Editorial

Evaluating the Upper Airway during Wakefulness

What Can It Tell Us about Sleep?

Carole L. Marcus, M.B.B.Ch.

University of Pennsylvania Philadelphia, Pennsylvania

The medical profession has known about the childhood obstructive sleep apnea syndrome since at least the 19th century (1). It is only in the past two decades, however, that this disease has been systematically studied. In the last few years, aided by funding from the National Institutes of Health, there has been a marked increase in the number of studies of this disease. We now know that childhood sleep apnea is common, occurring in approximately 2% of young children (2). Studies have shown that childhood sleep apnea results in serious sequelae, including growth failure, right and left ventricular dysfunction, systemic hypertension, behavioral changes, and poor academic performance. Nevertheless, we still know little about the pathophysiology of this disease and, in particular, its long-term prognosis.

In this issue of the Journal (pp. 163–167), Gozal and Burnside (3) describe the evaluation of upper airway collapsibility in awake children with sleep apnea as compared with controls. Upper airway collapsibility was determined by measuring the change in upper airway size, using acoustic pharyngometry, following the application of topical anesthetic. Previous studies have used magnetic resonance imaging during sedation (4), and acoustic pharyngometry during wakefulness (5), to show that children with sleep apnea have narrower upper airways than normal controls. This was confirmed in the current study. The finding of a narrow upper airway is similar to findings in adults with obstructive sleep apnea, the difference being the etiology. In children, the narrowing is due to adenotonsillar hypertrophy (4), whereas in adults it is due to thickness of the lateral pharyngeal muscular walls (6).

Previous studies of upper airway pressure–flow relationships have shown that children with obstructive sleep apnea have more collapsible airways during sleep than normal controls (7). In the current study, the investigators show changes in upper airway collapsibility in children with sleep apnea even during wakefulness. Surprisingly, few other studies have evaluated upper airway collapsibility during wakefulness, although one study in adults with obstructive sleep apnea did demonstrate increased collapsibility in response to the application of subatmospheric pressure even during wakefulness (8).

The current findings are not very surprising in view of our knowledge regarding the role of upper airway muscles in maintaining airway patency during wakefulness in sleep apnea. In a series of studies, White and colleagues have shown that adults with obstructive sleep apnea compensate for their narrower upper airway by increasing upper airway muscle tone; this compensatory mechanism is lost during sleep (9, 10); Katz recently extended this observation to children (11). Topical anesthesia is known to worsen sleep-disordered breathing (12, 13), presumably because of a decrease in the afferent loop of the upper airway reflex response to subatmospheric pressure. The resultant worsening of apnea appears to be due at least in part to changes in muscle tone (14), but also to blunting of the arousal response (12, 15).

The most interesting finding of the current study was the results of testing following treatment. Patients underwent adenotonsillectomy, the standard treatment for childhood sleep apnea. Following surgery, obstructive sleep apnea improved in all subjects. Upper airway collapsibility, however, remained in the elevated range in one-third of patients. This supports previous studies showing that some children with obstructive sleep apnea have residual abnormalities of upper airway function following adenotonsillectomy (7).

The natural course and long-term prognosis of childhood sleep apnea are unknown. Specifically, it is not known whether childhood sleep apnea is a precursor of the adult disorder, or whether these are two distinct diseases affecting discrete populations. There are very few longitudinal studies of childhood sleep apnea. Guilleminault and colleagues reevaluated adolescents who had been successfully treated with adenotonsillectomy during childhood (16). Of those who returned for reevaluation, 13% had recurrence of sleep apnea; all patients with recurrence were male. The studies by Gozal and others (3, 7) suggest that some children with sleep apnea have persistent abnormalities of upper airway neuromotor tone following adenotonsillectomy, even though they are asymptomatic. It is possible that these children have subtle abnormalities of central ventilatory control or upper airway neuromotor tone, or predisposing anatomic factors other than adenotonsillar hypertrophy. These abnormalities may be clinically inapparent until the adenotonsillar hypertrophy results in an increased mechanical load on a marginal upper airway, thus precipitating obstructive apneas. Following surgical treatment, patients may again become asymptomatic. It is possible, however, that these high-risk children will develop a recurrence of OSAS during adulthood if they acquire additional risk factors, such as weight gain, or androgen secretion at puberty. Long-term, epidemiologic studies are sorely needed to determine the natural history of this disease.

On a practical level, can the technique used in this study (acoustic reflectance measurements during wakefulness before and after topical anesthesia) be used for screening children for obstructive sleep apnea? There is a great appeal for this concept because children can be evaluated quickly, cheaply, and during daylight hours. Unfortunately, the answer is not that simple. In the current study, the investigators found acoustic pharyngometry to be successful in 94% of subjects, and it was reproducible. In contrast, Monahan and coworkers (5) obtained high-quality data in only 54% of subjects, despite studying an older age group. The reason for the difference is unclear. Presumably, however, the yield will be even lower in a clinical setting than in a tightly controlled research setting. Acoustic pharyngometry cannot be used in children too young or developmentally delayed to cooperate with testing, which will comprise a fair amount of the pediatric sleep apnea population. There is also a small but definite risk of aspiration following the application of pharyngeal anesthesia. Furthermore, while screening for the presence or absence of sleep apnea would be beneficial, it is also necessary to determine the severity of the apneas, if for no other reason than to assess operative risk (Should surgery be performed as an inpatient or an outpatient?) (17). Thus, further large-scale studies are needed to determine the practicality of this technique in the "real world."

In summary, this study has shed light on the pathophysiology of childhood obstructive sleep apnea syndrome, and, like all good studies, leads to further questions.

FOOTNOTES

Conflict of Interest Statement: C.L.M. has no declared conflict of interest.

REFERENCES

  1. Osler W. Chronic tonsillitis. In: Osler W, editor. The principles and practice of medicine. New York: Appleton and Co., 1892: 335–339.
  2. Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med 1999;159:1527–1532.[Abstract/Free Full Text]
  3. Gozal D, Burnside MM. Increased upper airway collapsibility in children with obstructive sleep apnea during wakefulness. Am J Respir Crit Care Med 2004;169:163–167.[Abstract/Free Full Text]
  4. Arens R, McDonough JM, Costarino AT, Mahboubi S, Tayag-Kier CE, Maislin G, Schwab RJ, Pack AI. Magnetic resonance imaging of the upper airway structure of children with obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2001;164:698–703.[Abstract/Free Full Text]
  5. Monahan KJ, Larkin EK, Rosen CL, Graham G, Redline S. Utility of noninvasive pharyngometry in epidemiologic studies of childhood sleep-disordered breathing. Am J Respir Crit Care Med 2002;165:1499–1503.[Abstract/Free Full Text]
  6. Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing: significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673–1689.[Abstract]
  7. Marcus CL, McColley SA, Carroll JL, Loughlin GM, Smith PL, Schwartz AR. Upper airway collapsibility in children with obstructive sleep apnea syndrome. J Appl Physiol 1994;77:918–924.[Abstract/Free Full Text]
  8. Suratt PM, Wilhoit SC, Cooper K. Induction of airway collapse with subatmospheric pressure in awake patients with sleep apnea. J Appl Physiol 1984;57:140–146.[Abstract/Free Full Text]
  9. Mezzanotte WS, Tangel DJ, White DP. Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). J Clin Invest 1992;89:1571–1579.
  10. Mezzanotte WS, Tangel DJ, White DP. Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls. Am J Respir Crit Care Med 1996;153:1880–1887.[Abstract]
  11. Katz ES, White DP. Genioglossus activity in children with obstructive sleep apnea during wakefulness and sleep onset. Am J Respir Crit Care Med 2003;168:664–670.[Abstract/Free Full Text]
  12. Berry RB, Kouchi KG, Bower JL, Light RW. Effect of upper airway anesthesia on obstructive sleep apnea. Am J Respir Crit Care Med 1995;151:1857–1861.[Abstract]
  13. Chadwick GA, Crowley P, Fitzgerald MX, O'Regan R, McNicholas WT. Obstructive sleep apnea following topical oropharyngeal anesthesia in loud snorers. Am Rev Respir Dis 1991;143:810–813.[Medline]
  14. Berry RB, McNellis MI, Kouchi K, Light RW. Upper airway anesthesia reduces phasic genioglossus activity during sleep apnea. Am J Respir Crit Care Med 1997;156:127–132.[Abstract/Free Full Text]
  15. Basner RC, Ringler J, Garpestad E, Schwartzstein RM, Sparrow D, Weinberger SE, Lilly J, Weiss JW. Upper airway anesthesia delays arousal from airway occlusion induced during human NREM sleep. J Appl Physiol 1992;73:642–648.[Abstract/Free Full Text]
  16. Guilleminault C, Partinen M, Praud JP, Quera-Salva MA, Powell N, Riley R. Morphometric facial changes and obstructive sleep apnea in adolescents. J Pediatr 1989;114:997–999.[CrossRef][Medline]
  17. American Academy of Pediatrics. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109:704–712.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Marcus, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marcus, C. L.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2004 American Thoracic Society