Abstract
The present study aimed at reporting the incidence of Salpingopharyngeal Fold (SPF) hypertrophy on Drug Induced Sleep Endoscopy (DISE) in patients with Obstructive Sleep Apnoea (OSA, validate a grading system and analyse the impact of various grades on the clinical presentation while ascertaining its relation with Apnoea-Hypopnoea Index (AHI). A retrospective analysis of 169 patients with polysomnographic confirmation of obstructive sleep apnoea has been done in the study. The DISE video data of 169 patients was evaluated by two ENT surgeons individually and they graded the hypertrophy of the fold as Grade 0 being normal anatomy, Grade 1 being hypertrophy causing partial obstruction and Grade 2 being hypertrophy causing complete obstruction of lateral pharyngeal wall. It was found that the presence of SPF hypertrophy independently adds considerably to the severity of the obstruction, attributing to lateral collapse at the upper retropalatal level and also significantly increases AHI. It is thus advised to consider the grade of SPF hypertrophy while surgically planning the management of patients with OSA.
Keywords: Obstructive sleep apnoea, SPF hypertrophy, Agrawal’s grading
Introduction
Obstructive Sleep Apnoea (OSA) is by far the most common cause of sleep disordered breathing [1], leading to a spectrum of potentially serious physiological, social and neurocognitive consequences. Though widely prevalent, it is often unrecognized and underdiagnosed [1]. Epidemiological studies report a prevalence of 2–9% for women and 4–24% for men; with an increased prevalence of 40% for obese [2, 3].
OSA significantly impairs health-related quality of life [4], reduces efficiency of those affected and also increases home and motor vehicle accidents by 2–3 folds [5]. A number of studies and meta analyses have indicated the association of OSA with increased risk of hypertension, diabetes mellitus, coronary artery disease, stroke and all-cause mortality [6–10]. Non-surgical or surgical, management of OSA is thus, rendered vital to alleviate the physiological complications and improve the patient’s quality of life.
Patients who exhibit symptoms of snoring and sleep apnoea are evaluated with overnight polysomnography followed by Drug Induced Sleep Endoscopy (DISE) which has the advantage of simulating the upper airway collapse that occurs during physiological sleep [11] and also provides an opportunity to observe directly and define the pathophysiology. Currently, DISE is the most reliable standard method to determine the level, number and severity of site of obstruction in sleep apnoea patients [12] and is shown to be safe, diagnostic and influential in surgical decision making [13].
Non-surgical treatment mainly includes the use of Continuous Positive Airway Pressure (CPAP). CPAP therapy, though is impactful in improving clinical symptoms, quality of life and potential consequences associated with OSA, the effectiveness of same is strongly related to patient compliance [14, 15]. Recent studies have reported CPAP compliance of only 35.3% over a period 12 months of usage [16]. Since the first description of uvulopalatopharyngoplasty (UPPP) by Fujita et al. [17], surgical options and techniques for obstructive sleep apnoea are constantly upgrading. Available surgical treatment options include, surgery of nose, palate, base of tongue, epiglottis, maxilla and mandible. In spite of the range of armamentarium available, dissatisfactory results have been reported [18, 19].
Special mention regarding our observation about the presence and need for management of SPF hypertrophy is proposed thus to aid as an adjunctive procedure to reduce failure rates. A previous study by Agrawal, 2015 [20] has reported better surgical outcome. Thus, the present study aims at reporting the incidence of SPF hypertrophy on DISE in patients with OSA, validate a grading system and analyse the impact of various grades on the clinical presentation while ascertaining its relation with AHI.
Materials and Method
A retrospective analysis of patients with polysomnographic confirmation of obstructive sleep apnoea has been done in the study. ApneaLink™ Air was used, which is a tool validated for the purpose [21]. These patients underwent Drug Induced Sleep Endoscopy (DISE) using KARL STORZ flexible video rhino-laryngoscope under BIS™ monitoring which is a valid bispectral index monitor for measuring the depth of sedation [22]. Dexmedetomidine and midazolam was used in titrating doses to maintain BIS™ score in the range of 60–80. The DISE video data of 169 patients was evaluated by two ENT surgeons individually. Each of them were instructed to grade the hypertrophy of the fold as Grade 0 being normal anatomy, Grade 1 being hypertrophy causing partial obstruction and Grade 2 being hypertrophy causing complete obstruction of lateral pharyngeal wall. Data of 154 patients of the 169 had 100% agreement between the two experts while grading the hypertrophy. Thus 154 patients’ data was included in the study for further analyses. Figure 1 shows the representative image of SPF hypertrophy as different grades.
Fig. 1.
A representative picture of SPF hypertrophy as different grades. Grade 0 of the grading system—normal anatomy causing < 25% obstruction of lateral pharyngeal wall. Grade 1 of the grading system—hypertrophy causing partial (25–75%) obstruction of lateral pharyngeal wall. Grade 2 of the grading system—hypertrophy causing complete (> 75%) obstruction of lateral pharyngeal wall
The patient’s data was further classified into two groups. Group 1 included 107 patients who had isolated palatal level obstruction whereas group 2 constituted 47 patients suffering with sleep apnoea due to obstruction at multiple levels BMI of the patient was calculated. There was no significant difference between the two groups for age (p > 0.05), AHI (p > 0.05) and BMI (p > 0.05) Shapiro Wilks test of Normality was administered to check for the distribution of the data, however as most of the parameters showed non-normal distribution the data was subjected to non-parametric analyses.
Results
Overall
Incidence
It was observed that 76/154 patients had hypertrophy of the SPF, as reported by the experts, amounting to 49%. Out of the 76 patients, 35% of the patients had grade 1 hypertrophy of the salpingopharyngeal fold while 14% had grade 2. Figure 2 shows the representation of patients whose SPF hyperetrophy was graded as 0, 1 and 2 respectively.
Fig. 2.
The relation between SPF hypertrophy and AHI
SPF Hypertrophy and AHI
Mann Whiteny U test showed that there was no significant difference between the two groups for AHI for grade 0 hypertrophy (Z = 1.6, p = 0.11), for grade 1 hypertrophy (Z = 1.38, p = 0.17) and grade 2 hypertrophy (Z = 0.81, p = 0.47), thus the data of the two groups were combined to find the effect of hypertrophy on AHI. Table 1 shows the AHI values of the patients with SPF hypertrophy across groups.
Table 1.
AHI score of patients with SPF hypertrophy (Agrawals grading) across groups
| Grade 0 | Grade 1 | Grade 2 | ||||||
|---|---|---|---|---|---|---|---|---|
| X | M | SD | X | M | SD | X | M | SD |
| Group 1 (107) | ||||||||
| 37.61 | 38 (N = 58) | 25.15 | 49.32 | 50 (N = 32) | 26.7 | 55.4 | 60.2 (N = 16) | 25.08 |
| Group 2 (47) | ||||||||
| 34.52 | 37.5 (N = 19) | 24.21 | 46.4 | 49 (N = 23) | 25.8 | 55.1 | 56.58 (N = 5) | 28.1 |
0, normal anatomy; 1, moderate hypertrophy; 2, severe hypertrophy; X, mean; M, median; SD, standard deviation
Kruskals Wallis H test showed that there occurred significant increase in the AHI scores as the hypertrophy increased (χ2 = 12.22, p = 0.002). Mann whitney U test showed that patient with no hypertrophy (grade 0) had significantly lesser AHI values as compared to patients with grade 1 (Z = 3.001 p = 0.003) and grade 2 hypertrophy (Z = 2.653 p = 0.008). Figure 2 shows the relation between SPF hypertrophy and AHI.
BMI and AHI
Out of 154 patients, 64 patients had BMI > 30 and 90 of them had BMI < 30. Mann whitney U test showed that patients with high BMI values had higher AHI as compared to those having low BMI (Z = 3.50, p = 0.00). Spearman’s correlation showed that there was significant increase in the AHI with increase in BMI (rs = 0.297 p = 0.000). Figure 3 shows the scatter plot of AHI versus BMI.
Fig. 3.
Shows that there occurs significant positive correlation between BMI an AHI
SPF and BMI
Kruskal Wallis H test showed that there was no significant difference for the BMI across patients having different grade of SPF hypertrophy [χ2(2) = 2.75, p = 0.45]. There was no significant relation between BMI and SPF (rs = 0.019, p > 0.05).
Group 1 (Isolated Palatal Obstruction)
This group included 107 patients with palate as the sole cause for obstruction. On comparison of two groups it was observed that among the patients included in this group, 30% of them had grade 1, while 15% had grade 2 hypertrophy.
SPF and AHI
We can see from Table 1 that as the hypertrophy of SPF increased, there was an increase in the AHI scores. Kruskal Wallis H test also showed that patients having higher grade of SPF hypertrophy had higher AHI scores [χ2(2) = 27.93, p = 0.00]. Mann Whitney U test showed that patients with grade 2 hypertrophy had significantly higher AHI score compared to grade 1 (Z = 2.1, p = 0.04), grade 1 had significantly higher AHI compared to grade 0 (Z = 3.63 p = 0.000) and grade 2 had significantly higher AHI compared to grade 0 (Z = 4.16, p = 0.00).
BMI and AHI
Out of 107 patients, 47 had BMI > 30 and 60 had BMI < 30, It was observed that patients with high BMI had significantly higher AHI compared to patients having low BMI (Z = 2.44 p = 0.01) on administration of Mann Whitney U test. Spearmans test of correlation showed that the BMI scores had significantly positive correlation with AHI (rs = 0.401 p = 0.000) i.e as BMI increased AHI also increased.
SPF and BMI
Kruskal Wallis H test showed that there was no significant difference for the BMI across patients having different grade of SPF hypertrophy [χ2(2) = 1.99, p = 0.78]. There was no significant relation between BMI and SPF (rs = 0.026, p > 0.05).
Group 2 (Multiple Level Obstruction)
This group included 47 patients with multiple level obstruction. Of these, 49% had grade 1 hypertrophy while 11% had grade 2.
SPF and AHI
We can see from Table 1 that as the hypertrophy of SPF increased, there was an increase in the AHI scores. Kruskal Wallis H test also showed that patients having higher grade of SPF hypertrophy had higher AHI scores [χ2(2) = 16.61, p = 0.01]. Mann Whitney U test showed that patients with grade 1 hypertrophy had significantly higher AHI compared to grade 0 (Z = 2.5 p = 0.01) and grade 2 had significantly higher AHI compared to grade 0 (Z = 3.91 p = 0.00). Though the difference was seen for AHI score between grade 1 and grade 2 hypertrophy it was not statistically significant (Z = 1.76 p = 0.08).
BMI and AHI
Out of 47 participants, 17 had BMI > 30 and 30 had BMI < 30. It was seen that patients with high BMI had significantly higher AHI compared to patients having low BMI (Z = 2.27 p = 0.02) on administration of Mann Whitney U test. Spearmans test of correlation showed that there was no significant correlation between BMI and AHI (rs = 0.24 p = 0.087).
SPF and BMI
Kruskal Wallis H test showed that there was no significant difference for the BMI across patients having different grade of SPF hypertrophy [χ2(2) = 2.12, p = 0.88]. There was no significant relation between BMI and SPF (rs = 0.038, p > 0.05).
To summarize,
Incidence of SPF hypertrophy amounts to approximately half (49%) of the patients evaluated with DISE for OSA. It was observed that 35% of the positive cases had grade 1, while 14% had grade 2.
Group 1 (patients with isolated palatal level obstruction)—of the patients included in this group, 30% of had grade 1, while 15% had grade 2 hypertrophy with AHI increasing with increasing grades and no significant correlation with variations in BMI and SPF hypertrophy.
Group 2 (patients with multiple level obstruction)—of these patients, 49% had grade 1 while 11% had grade 2 hypertrophy with AHI increasing with increasing grades and no significant correlation with variations in BMI and SPF hypertrophy.
Between the two grades, grade 2 hypertrophy is observed to have higher contribution in increasing AHI as compared to grade 1 in patients with isolated palatal level block.
In patients with multilevel obstruction, presence of SPF hypertrophy either grade 1 or grade 2 is observed to cause an increase in AHI, warranting management of even grade 1 hypertrophy.
BMI has no particular correlation with SPF hypertrophy.
Discussion
The salpingopharyngeal muscle is a slender muscle which arises from the medial and inferior borders of the tubal cartilage through slips of muscular and tendinous fibres. The muscle then courses posteroinferiorly to blend as a fan-shaped insertion into the palatopharyngeus muscle at the junction of the velum and lateral pharyngeal wall [23]. A raised ridge of mucous membrane extending from the lower end of the tubal elevation along the wall of the pharynx overlying the salpingopharyngeus muscle forms the salpingopharyngeal fold [23]. Through the available literature, function assigned to the muscle, is limited to closing the Eustachian tube [24], opening of the Eustachian tube [25], elevating the lateral wall of the oropharynx [26] and elevating the velum [27] rendering it vestigial, poorly developed and probably nonfunctional [28, 29].
Since decades studies have reported SPF with limited function. However, the present study has contention of further functionality. Plethora of professionals are often perplexed when it comes to treating OSA, owing to its complexity in presentation and various surgical options available [19].
Retropalatal obstruction is reported as the most common site of obstruction in patients with OSA [19, 30]. It can present as an anteroposterior collapse owing to the soft patate, lateral collapse by the lateral pharyngeal wall and circular as a combined entity. A missing entity here could be the SPF which is prevalent but unrecognised. SPF plays a significant role in being additive to the obstruction due to the lateral wall collapse in patients with OSA.
A number of procedures designed for the treatment, aim at the managing the palate and not the retropalatal region [19]. As can be appreciated, dealing with isolated palatal obstruction with omission of retropalatal SPF hypertrophy is partial treatment and leads to failure or incomplete surgery with patient still having apnoea and hypopneas as reported by a number of studies [31].
We therefore propose, Agrawal’s grading system for SPF hypertrophy.
By definition,
| Grade | Description |
|---|---|
| 0 | Normal anatomy causing < 25% obstruction of lateral pharyngeal wall |
| 1 | Hypertrophy causing partial (25–75%) obstruction of lateral pharyngeal wall |
| 2 | Hypertrophy causing complete (> 75%) obstruction of lateral pharyngeal wall |
The AHI showed significant increase with increase in hypertrophy as well. This provides a testimony to the possible role of SPF hypertrophy in patients with OSA. The increased AHI and hypertrophy was seen in patients with having multiple level obstruction as well. It has been found that BMI has no correlation with the presence of hypertrophy, indicating its value as an independent contributor to increase in AHI and the severity. Thus, the role of SPF hypertrophy needs more attention than it is usually given. To the best of knowledge there has been no study which have reported structural changes of SPF in OSA however in a study presented by the author [20], it was propagated that channeling of the SPF in grade 1 and 2 with coblation plasma wand provided significantly better post-operative outcome. Thus the management of these patients must consider role fo SPF in causing OSA and its subsequent channeling if required must be done.
Limitation
The study is novel and to the best of our knowledge nothing in this aspect has been reported previously, thus more research and better acknowledgement in this aspects is warranted.
Conclusion
Thus with the study, we conclude that though vestigial / non functional, hypertrophy of SPF significantly increases AHI in patients with OSA. The presence of SPF hypertrophy adds considerably to the severity of the obstruction, attributing to lateral collapse at the upper retropalatal level and also significantly increases AHI. It is thus wise to consider management of the SPF hypertrophy while surgically dealing with OSA.
Acknowledgements
We would like to thank the participants of the study.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Compliance with Ethical Standards
Ethical Standards
The study followed the ethical guidelines given by Helinski declaration of Medical research involving human subjects.
Contributor Information
Vikas K. Agrawal, Phone: +9820407543, Email: doctor@enthospital.com
Swati Kodur, Phone: +9741878730, Email: drswatikodur@gmail.com.
Raghav Hira Jha, Phone: +9987602545, Email: raghav.jha415@gmail.com.
References
- 1.Foldvary-Schaefer NR, Waters TE. Sleep-disordered breathing. CONTINUUM Lifelong Learn Neurol. 2017;23(4, Sleep Neurology):1093–1116. doi: 10.1212/01.CON.0000522245.13784.f6. [DOI] [PubMed] [Google Scholar]
- 2.Heinzer R, Vat S, Marques-Vidal P, et al. Prevalence of sleep-disordered breathing in the general population: the HypnoLaus study. Lancet Respir Med. 2015;3:310–318. doi: 10.1016/S2213-2600(15)00043-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230–1235. doi: 10.1056/NEJM199304293281704. [DOI] [PubMed] [Google Scholar]
- 4.Baldwin CM, Griffith KA, Nieto FJ, O’Connor GT, Walsleben JA, Redline S. The association of sleep-disordered breathing and sleep symptoms with quality of life in the Sleep Heart Health Study. Sleep. 2001;24(1):96–105. doi: 10.1093/sleep/24.1.96. [DOI] [PubMed] [Google Scholar]
- 5.Ward KL, Hillman DR, James A, Bremner AP, Simpson L, Cooper MN, Palmer LJ, Fedson AC, Mukherjee S. Excessive daytime sleepiness increases the risk of motor vehicle crash in obstructive sleep apnea. J Clin Sleep Med. 2013;9(10):1013–1021. doi: 10.5664/jcsm.3072. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Loke YK, Brown JW, Kwok CS, et al. Association of obstructive sleep apnea with risk of serious cardiovascular events: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2012;5:720–728. doi: 10.1161/CIRCOUTCOMES.111.964783. [DOI] [PubMed] [Google Scholar]
- 7.Dong JY, Zhang YH, Qin LQ. Obstructive sleep apnea and cardiovascular risk: meta-analysis of prospective cohort studies. Atherosclerosis. 2013;229:489–495. doi: 10.1016/j.atherosclerosis.2013.04.026. [DOI] [PubMed] [Google Scholar]
- 8.Ge X, Han F, Huang Y, et al. Is obstructive sleep apnea associated with cardiovascular and all-cause mortality? PLoS ONE. 2013;8:e69432. doi: 10.1371/journal.pone.0069432. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Wang X, Ouyang Y, Wang Z, et al. Obstructive sleep apnea and risk of cardiovascular disease and all-cause mortality: a meta-analysis of prospective cohort studies. Int J Cardiol. 2013;169:207–214. doi: 10.1016/j.ijcard.2013.08.088. [DOI] [PubMed] [Google Scholar]
- 10.Al-Delaimy WK, Manson JE, Willett WC, et al. Snoring as a risk factor for type II diabetes mellitus: a prospective study. Am J Epidemiol. 2002;155:387–393. doi: 10.1093/aje/155.5.387. [DOI] [PubMed] [Google Scholar]
- 11.Rodriguez-Bruno K, Goldberg AN, McCulloch CE, Kezirian EJ. Test–retest reliability of drug-induced sleep endoscopy. Otolaryngol Head Neck Surg. 2009;140(5):646–651. doi: 10.1016/j.otohns.2009.01.012. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.De Corso E, Fiorita A, Rizzotto G, Mennuni GF, Meucci D, Giuliani M, Marchese MR, Levantesi L, Della Marca G, Paludetti G, Scarano E. The role of drug-induced sleep endoscopy in the diagnosis and management of obstructive sleep apnoea syndrome: our personal experience. Acta Otorhinolaryngol Ital. 2013;33(6):405. [PMC free article] [PubMed] [Google Scholar]
- 13.Charakorn N, Kezirian EJ. Drug-induced sleep endoscopy. Otolaryngol Clin N Am. 2016;49(6):1359–1372. doi: 10.1016/j.otc.2016.06.002. [DOI] [PubMed] [Google Scholar]
- 14.Bratton DJ, Stradling JR, Barbé F, et al. Effect of CPAP on blood pressure in patients with minimally symptomatic obstructive sleep apnoea: a meta-analysis using individual patient data from four randomised controlled trials. Thorax. 2014;69:1128–1135. doi: 10.1136/thoraxjnl-2013-204993. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Martínez-García MA, Campos-Rodríguez F, Catalán-Serra P, et al. Cardiovascular mortality in obstructive sleep apnea in the elderly: role of long-term continuous positive airway pressure treatment: a prospective observational study. Am J Respir Crit Care Med. 2012;186:909–916. doi: 10.1164/rccm.201203-0448OC. [DOI] [PubMed] [Google Scholar]
- 16.Florés M, Martinez-Alonso M, Sánchezde-la-Torre A, Aldomà A, Galera E, Barbé F, Sánchezde-la-Torre M, Dalmases M. Predictors of long-term adherence to continuous positive airway pressure in patients with obstructive sleep apnoea and acute coronary syndrome. J Thorac Dis. 2018;10(Suppl 1):S124. doi: 10.21037/jtd.2017.12.128. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg. 1981;89:923–934. doi: 10.1177/019459988108900609. [DOI] [PubMed] [Google Scholar]
- 18.Khan A, Ramar K, et al. Uvulopalatopharyngoplasty in the management of obstructive sleep apnea: the mayo clinic experience. Mayo Clin Proc. 2009;84(9):795–800. doi: 10.4065/84.9.795. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Caples SM, Rowley JA, Prinsell JR, Pallanch JF, Elamin MB, Katz SG, Harwick JD. Surgical modifications of the upper airway for obstructive sleep apnea in adults: a systematic review and meta-analysis. Sleep. 2010;33(10):1396–1407. doi: 10.1093/sleep/33.10.1396. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Agrawal V. Role of salpingopharyngeal fold in lateral pharyngeal wall collapse causing obstructive sleep apnea. Sleep Med. 2015;16(Supplement 1):S7. [Google Scholar]
- 21.Aparicio HJ, Sturzoiu T, Lau H, Clark J, Grimes J, Masoud H, Nguyen T, Auerbach S, Pyatkevich Y. Stroke unit evaluation of sleep apnea: validity of screening tools and use of a portable sleep study. Neurology. 2016;86(16 Supplement):I8-008. [Google Scholar]
- 22.Sadhasivam S, Ganesh A, Robison A, Kaye R, Watcha MF. Validation of the bispectral index monitor for measuring the depth of sedation in children. Anesth Analg. 2006;102(2):383–388. doi: 10.1213/01.ANE.0000184115.57837.30. [DOI] [PubMed] [Google Scholar]
- 23.Graves GO, Edwards LE. The Eustachian tube. A review of its descriptive, microscopic, topographic and clinical anatomy. Arch Otolaryngol. 1944;39(1944):359–397. [Google Scholar]
- 24.Simkins CS. Functional anatomy of the eustachian tube. Arch Otolaryngol. 1943;38:476. [Google Scholar]
- 25.Fara M, Dvorak J. Abnormal anatomy of the muscles of palatopharyngeal closure in cleft palates. Plast Reconstr Surg. 1970;46:488. [PubMed] [Google Scholar]
- 26.Bosma JF. A correlated study of the anatomy and motor activity of the upper pharynx by cadaver dissection and by cinematic study of patients after maxillofacial surgery. Ann Otol. 1953;62:51. doi: 10.1177/000348945306200106. [DOI] [PubMed] [Google Scholar]
- 27.Harrington R. A study of the mechanism of velopharyngeal closure. J Speech Hear Dis. 1944;9:325. [Google Scholar]
- 28.Dickson DR. Anatomy of the normal velopharyngeal mechanism. Clin Plast Surg. 1975;2:235. [PubMed] [Google Scholar]
- 29.Rosen LM (1970) The morphology of the salpingopharyngeus muscle, 2nd edn. Thesis, University of Pittsburgh, Pittsburgh
- 30.Kavcic P, Koren A, Koritnik B, Fajdiga I, Groselj LD. Sleep magnetic resonance imaging with electroencephalogram in obstructive sleep apnea syndrome. Laryngoscope. 2015;125(6):1485–1490. doi: 10.1002/lary.25085. [DOI] [PubMed] [Google Scholar]
- 31.Metes A, Hoffstein V, Mateika S, Cole P, Haight JS. Site of airway obstruction in patients with obstructive sleep apnea before and after uvulopalatopharyngoplasty. Laryngoscope. 1991;101(10):1102–1108. doi: 10.1288/00005537-199110000-00013. [DOI] [PubMed] [Google Scholar]