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Diagnosis and Treatment of Obstructive Sleep Apnea of the Larynx

Diagnosis and Treatment of Obstructive Sleep Apnea of the Larynx Abstract To determine the mechanism for obstructive sleep apnea in two patients with clinical abnormalities of laryngeal function, airflow dynamics during sleep were analyzed. The site of airway obstruction was assessed by examining pressure gradients across specific airway segments. The relation between maximal inspiratory airflow and nasal pressure was analyzed to determine (1) the critical pressure, a measure of the collapsibility of the laryngeal airway, and (2) the effect of nasal continuous positive airway pressure on airflow during sleep. Large inspiratory pressure gradients developed during sleep between the supraglottic and pleural spaces, indicating that collapse had occurred in the larynx. Elevated critical pressures of —6.4 and +1.2 cm H2O, respectively, occurred in the two patients. When the nasal pressure was raised to 10 cm H2O, normal levels of tidal airflow occurred, and obstructive apneas were eliminated. These findings indicate that sleep apnea was caused by laryngeal airflow obstruction that resulted from elevations in the collapsibility of the larynx. The response to nasal continuous positive airway pressure suggested that laryngeal sleep apnea was similar to pharyngeal sleep apnea in pathophysiologic characteristic and response to treatment. (Arch Otolaryngol Head Neck Surg. 1995;121:335-339) References 1. Gastaut H, Tassinari CA, Duron B. Étude polygraphique des manifestations épisodiques (hypniques et respiratoires), diures et nocturnes, du syndrome de Pickwick . Rev Neurol Paris . 1965;112:568-579. 2. Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep . J Appl Physiol . 1978;44:931-938. 3. Lehrman KL, Guilleminault C, Schroeder JS, Tilkian A, Forno LN. Sleep apnea syndrome in a patient with Shy-Drager syndrome . Arch Intern Med . 1978;138:206-209.Crossref 4. Ruff ME, Oakes WJ, Fisher SR, Spock A. Sleep apnea and vocal cord paralysis secondary to type l Chiari malformation . Pediatrics . 1987;80:231-234. 5. Anonsen C. Laryngeal obstruction and obstructive sleep apnea syndrome . Laryngoscope . 1990; 100:775-778.Crossref 6. Gleadhill IC, Schwartz AR, Wise RA, Permutt S, Smith PL. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea . Am Rev Respir Dis . 1991;143:1300-1303.Crossref 7. Schwartz AR, Smith PL, Wise RA, Permutt S. Effect of nasal pressure on upper airway pressure flow relationships . J Appl Physiol . 1989; 66:1626-1634. 8. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S. Upper airway pressure-flow relationships in obstructive sleep apnea . J Appl Physiol . 1988;64( (2) ):789-795. 9. Sullivan CE, Berthon-Jones M, Issa FG, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares . Lancet . 1981;1:862-865.Crossref 10. Smith PL, Haponik EF, Allen RP, Bleecker ER. The effects of protriptyline in sleep disordered breathing . Am Rev Respir Dis . 1983;127:8-13. 11. Hudgel DW. Variable site of airway narrowing among obstructive sleep apnea patients . J Appl Physiol . 1986;61:1403-1409. 12. Smaldone GC, Smith PL. Location of flowlimiting segments via airway catheters near residual volume in humans . J Appl Physiol . 1985; 59:502-508. 13. Smaldone GC, Bergofsky EH. Delineation of flowlimiting segment and predicted airway resistance by movable catheter . J Appl Physiol . 1976; 40:943-952. 14. Schwartz AR, Thut D, Brower RG, et al. Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2 . J Appl Physiol . 1993;74:1597-1605.Crossref 15. Chaban R, Cole P, Hoffstein V. Site of upper airway obstruction in patients with idiopathic obstructive sleep apnea . Laryngoscope . 1988;98: 641-647.Crossref 16. Schwartz AR, Smith PL, Gold AR, Wise RA, Permutt S. Induction of upper airway occlusion in sleeping normal humans . J Appl Physiol . 1988; 64:535-542. 17. Shepard JW Jr, Thawley SE. Localization of upper airway collapse during sleep in patients with obstructive sleep apnea . Am Rev Respir Dis . 1990; 141:1350-1355.Crossref 18. Brouillette RT, Thach BT. A neuromuscular mechanism maintaining extrathoracic airway patency . J Appl Physiol . 1979;46:772-779. 19. Orem J, Lydic R. Upper airway function during sleep and wakefulness: experimental studies on normal and anesthetized cats . Sleep . 1978;1:49-68. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Otolaryngology - Head & Neck Surgery American Medical Association

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References (21)

Publisher
American Medical Association
Copyright
Copyright © 1995 American Medical Association. All Rights Reserved.
ISSN
0886-4470
eISSN
1538-361X
DOI
10.1001/archotol.1995.01890030063010
Publisher site
See Article on Publisher Site

Abstract

Abstract To determine the mechanism for obstructive sleep apnea in two patients with clinical abnormalities of laryngeal function, airflow dynamics during sleep were analyzed. The site of airway obstruction was assessed by examining pressure gradients across specific airway segments. The relation between maximal inspiratory airflow and nasal pressure was analyzed to determine (1) the critical pressure, a measure of the collapsibility of the laryngeal airway, and (2) the effect of nasal continuous positive airway pressure on airflow during sleep. Large inspiratory pressure gradients developed during sleep between the supraglottic and pleural spaces, indicating that collapse had occurred in the larynx. Elevated critical pressures of —6.4 and +1.2 cm H2O, respectively, occurred in the two patients. When the nasal pressure was raised to 10 cm H2O, normal levels of tidal airflow occurred, and obstructive apneas were eliminated. These findings indicate that sleep apnea was caused by laryngeal airflow obstruction that resulted from elevations in the collapsibility of the larynx. The response to nasal continuous positive airway pressure suggested that laryngeal sleep apnea was similar to pharyngeal sleep apnea in pathophysiologic characteristic and response to treatment. (Arch Otolaryngol Head Neck Surg. 1995;121:335-339) References 1. Gastaut H, Tassinari CA, Duron B. Étude polygraphique des manifestations épisodiques (hypniques et respiratoires), diures et nocturnes, du syndrome de Pickwick . Rev Neurol Paris . 1965;112:568-579. 2. Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep . J Appl Physiol . 1978;44:931-938. 3. Lehrman KL, Guilleminault C, Schroeder JS, Tilkian A, Forno LN. Sleep apnea syndrome in a patient with Shy-Drager syndrome . Arch Intern Med . 1978;138:206-209.Crossref 4. Ruff ME, Oakes WJ, Fisher SR, Spock A. Sleep apnea and vocal cord paralysis secondary to type l Chiari malformation . Pediatrics . 1987;80:231-234. 5. Anonsen C. Laryngeal obstruction and obstructive sleep apnea syndrome . Laryngoscope . 1990; 100:775-778.Crossref 6. Gleadhill IC, Schwartz AR, Wise RA, Permutt S, Smith PL. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea . Am Rev Respir Dis . 1991;143:1300-1303.Crossref 7. Schwartz AR, Smith PL, Wise RA, Permutt S. Effect of nasal pressure on upper airway pressure flow relationships . J Appl Physiol . 1989; 66:1626-1634. 8. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S. Upper airway pressure-flow relationships in obstructive sleep apnea . J Appl Physiol . 1988;64( (2) ):789-795. 9. Sullivan CE, Berthon-Jones M, Issa FG, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares . Lancet . 1981;1:862-865.Crossref 10. Smith PL, Haponik EF, Allen RP, Bleecker ER. The effects of protriptyline in sleep disordered breathing . Am Rev Respir Dis . 1983;127:8-13. 11. Hudgel DW. Variable site of airway narrowing among obstructive sleep apnea patients . J Appl Physiol . 1986;61:1403-1409. 12. Smaldone GC, Smith PL. Location of flowlimiting segments via airway catheters near residual volume in humans . J Appl Physiol . 1985; 59:502-508. 13. Smaldone GC, Bergofsky EH. Delineation of flowlimiting segment and predicted airway resistance by movable catheter . J Appl Physiol . 1976; 40:943-952. 14. Schwartz AR, Thut D, Brower RG, et al. Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2 . J Appl Physiol . 1993;74:1597-1605.Crossref 15. Chaban R, Cole P, Hoffstein V. Site of upper airway obstruction in patients with idiopathic obstructive sleep apnea . Laryngoscope . 1988;98: 641-647.Crossref 16. Schwartz AR, Smith PL, Gold AR, Wise RA, Permutt S. Induction of upper airway occlusion in sleeping normal humans . J Appl Physiol . 1988; 64:535-542. 17. Shepard JW Jr, Thawley SE. Localization of upper airway collapse during sleep in patients with obstructive sleep apnea . Am Rev Respir Dis . 1990; 141:1350-1355.Crossref 18. Brouillette RT, Thach BT. A neuromuscular mechanism maintaining extrathoracic airway patency . J Appl Physiol . 1979;46:772-779. 19. Orem J, Lydic R. Upper airway function during sleep and wakefulness: experimental studies on normal and anesthetized cats . Sleep . 1978;1:49-68.

Journal

Archives of Otolaryngology - Head & Neck SurgeryAmerican Medical Association

Published: Mar 1, 1995

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