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6. Verkest V, Verhulst S, Van Hoorenbeeck K, Vanderveken O, Saldien V, Boudewyns
A.Prevalence of obstructive sleep apnea in children with laryngomalacia and value of polysomnography in treatment decisions. Int J Pediatr Otorhinolaryngol. 2020;137:110255. https://
doi.org/10.1016/j.ijporl.2020.110255.
7. Rutter MJ.Evaluation and management of upper airway disorders in children. Semin Pediatr
Surg. 2006;15(2):116–23. https://doi.org/10.1053/j.sempedsurg.2006.02.009.
8. Thompson DM.Abnormal sensorimotor integrative function of the larynx in congenital laryngomalacia: a new theory of etiology. Laryngoscope. 2007;117(6 Pt 2 Suppl 114):1–33. https://
doi.org/10.1097/MLG.0b013e31804a5750.
9. Giannoni C, Sulek M, Friedman EM, Duncan NO 3rd. Gastroesophageal reux association
with laryngomalacia: a prospective study. Int J Pediatr Otorhinolaryngol. 1998;43(1):11–20.
https://doi.org/10.1016/s0165- 5876(97)00151- 1.
10. Amin MR, Isaacson G. State-dependent laryngomalacia. Ann Otol Rhinol Laryngol.
1997;106(11):887–90. https://doi.org/10.1177/000348949710601101.
11. Chan DK, Truong MT, Koltai PJ.Supraglottoplasty for occult laryngomalacia to improve
obstructive sleep apnea syndrome. Arch Otolaryngol Head Neck Surg. 2012;138(1):50–4.
https://doi.org/10.1001/archoto.2011.233.
12. Boudewyns A, Verhulst S, Maris M, Saldien V, Van de Heyning P. Drug-induced sedation
endoscopy in pediatric obstructive sleep apnea syndrome. Sleep Med. 2014;15(12):1526–31.
https://doi.org/10.1016/j.sleep.2014.06.016.
13. Thevasagayam M, Rodger K, Cave D, Witmans M, El-Hakim H.Prevalence of laryngomalacia
in children presenting with sleep-disordered breathing. Laryngoscope. 2010;120(8):1662–6.
https://doi.org/10.1002/lary.21025.
14. Wilcox LJ, Bergeron M, Reghunathan S, Ishman SL.An updated review of pediatric druginduced sleep endoscopy. Laryngoscope Investig Otolaryngol. 2017;2(6):423–31. https://doi.
org/10.1002/lio2.118.
15. Sessler CN, Grap MJ, Ramsay MA.Evaluating and monitoring analgesia and sedation in the
intensive care unit. Crit Care. 2008;12(Suppl 3):S2. https://doi.org/10.1186/cc6148.
16. Mahmoud M, Radhakrishman R, Gunter J, Sadhasivam S, Schapiro A, McAuliffe J, etal.
Effect of increasing depth of dexmedetomidine anesthesia on upper airway morphology in
children. Paediatr Anaesth. 2010;20(6):506–15. https://doi.org/10.1111/j.1460- 9592.2010.
03311.x.
17. Hartl TT, Chadha NK.A systematic review of laryngomalacia and acid reux. Otolaryngol
Head Neck Surg. 2012;147(4):619–26. https://doi.org/10.1177/0194599812452833.
18. Brockbank J, Astudillo CL, Che D, Tanphaichitr A, Huang G, Tomko J, etal. Supplemental
oxygen for treatment of infants with obstructive sleep apnea. J Clin Sleep Med.
2019;15(8):1115–23. https://doi.org/10.5664/jcsm.7802.
19. Hawkins SM, Jensen EL, Simon SL, Friedman NR.Correlates of pediatric CPAP adherence. J
Clin Sleep Med. 2016;12(6):879–84. https://doi.org/10.5664/jcsm.5892.
20. Denoyelle F, Mondain M, Gresillon N, Roger G, Chaudre F, Garabedian EN. Failures
and complications of supraglottoplasty in children. Arch Otolaryngol Head Neck Surg.
2003;129(10):1077–80.; ; discussion 80. https://doi.org/10.1001/archotol.129.10.1077.
21. Tunkel DE, Hotchkiss KS, Ishman S, Brown D.Supraglottoplasty in infants using sinus instruments. Medscape J Med. 2008;10(11):269.
22. Camacho M, Dunn B, Torre C, Sasaki J, Gonzales R, Liu SY, etal. Supraglottoplasty for laryngomalacia with obstructive sleep apnea: a systematic review and meta-analysis. Laryngoscope.
2016;126(5):1246–55. https://doi.org/10.1002/lary.25827.
23. Lee CF, Hsu WC, Lee CH, Lin MT, Kang KT. Treatment outcomes of supraglottoplasty
for pediatric obstructive sleep apnea: a meta-analysis. Int J Pediatr Otorhinolaryngol.
2016;87:18–27. https://doi.org/10.1016/j.ijporl.2016.05.015.
24. Zalzal HG, Davis K, Carr MM, Coutras S.Epiglottopexy with or without aryepiglottic fold
division: comparing outcomes in the treatment of pediatric obstructive sleep apnea. Am J
Otolaryngol. 2020;41(4):102478. https://doi.org/10.1016/j.amjoto.2020.102478.
A. L. Soaper et al.
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25. Oomen KP, Modi VK.Epiglottopexy with and without lingual tonsillectomy. Laryngoscope.
2014;124(4):1019–22. https://doi.org/10.1002/lary.24279.
26. Baljosevic I, Minic P, Trajkovic G, Markovic-Sovtic G, Radojicic B, Sovtic A.Surgical treatment of severe laryngomalacia: six month follow-up. Pediatr Int. 2015;57(6):1159–63. https://
doi.org/10.1111/ped.12706.
27. Fajdiga I, Beden AB, Krivec U, Iglic C.Epiglottic suture for treatment of laryngomalacia. Int
J Pediatr Otorhinolaryngol. 2008;72(9):1345–51. https://doi.org/10.1016/j.ijporl.2008.05.009.
28. Reddy DK, Matt BH.Unilateral vs. bilateral supraglottoplasty for severe laryngomalacia in
children. Arch Otolaryngol Head Neck Surg. 2001;127(6):694–9. https://doi.org/10.1001/
archotol.127.6.694.
29. Kanotra SP, Givens VB, Keith B.Swallowing outcomes after pediatric epiglottopexy. Eur Arch
Otorhinolaryngol. 2020;277(1):285–91. https://doi.org/10.1007/s00405- 019- 05664- 6.
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The Role ofObesity inEpiglottis
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Collapse
ChristelA.L.de Raaff
12.1 Obesity
Obesity represents a certain amount of excessive adipose tissue, negatively affecting
health status, life expectancy, and medical outcomes. The exact denition is formulated with the body mass index (BMI), a ratio of weight in relation to length. It can
be calculated by dividing someone’s weight in kilograms by his or her height in
meters squared (kg/m2) and enables us to categorize a person as underweight, normal weight, overweight, obese, morbidly obese, or super obese (Table12.1). Obesity
is dened as a BMI≥30kg/m2. The basis of the BMI was formulated by Adolphe
Quetelet between 1830 and 1850 when interest in an index measuring weight came
with increasing obesity [1]. Due to its simplicity, the BMI has become a universally
used metric for weight.
The overall global population is progressively affected by obesity. Between 1975
and 2016, the prevalence nearly tripled. Worldwide, more than 1.9 billion and over
650 million adults were overweight and obese, respectively. This represents a prevalence of 39% and 13% of the worldwide population [2].
By the year 2030, the number of obese US adults is expected to rise to 40–50%
[2]. Knowing that obesity causes multi-organ diseases and decreased life expectancy, this is a threatening perspective for global health.
12
C. A. L. de Raaff (*)
Department of Albert Schweitzer Hospital, Dordrecht, The Netherlands
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
M. Delakorda, N. de Vries (eds.), The Role of Epiglottis in Obstructive Sleep
Apnea, https://doi.org/10.1007/978-3-031-34992-8_12
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C. A. L. Raa
Table 12.1 Body Mass
Index and weight categories
Body Mass Index (kg/m2) Weight category
< 18 Underweight
18–24.9 Normal weight
25–29.9 Overweight
30–34.9 Obesity
35–49.9 Morbid obesity
≥ 50
Super obesity
12.2 Obesity andObstructive Sleep Apnea (OSA)
Excessive adipose tissue negatively affects the function of organ systems.
Anatomical, cardiovascular, metabolic, neuromuscular, and hormonal changes all
occur due to obesity. Many of these changes are associated with the presence of
obstructive sleep apnea (OSA), being the most prevalent sleep disordered breathing
problem and affecting more obese individuals than type II diabetes, hypertension,
and dyslipidemia [3].
The pathogenesis of OSA is multifactorial and complex. Local anatomy, obesity,
gender, age, sleep position, and sedative drugs are examples of risk factors for OSA
and its severity. The prevalence of OSA increases with BMI and age and is more
common in men than women. Around 2% and 4% of middle aged women and men,
respectively, suffer from OSA in the general population [4]. In morbidly obese individuals, the prevalence increases up to 70% [5]. One of the hypothesis explaining
obesity as an important risk factor for OSA is that fat deposition results in diminished pharyngeal airway size, thereby increasing the risk of apneas.
12.3 Fat Tissue inthePharyngeal Airway
The pharyngeal airway is the upper part of the airway located anteriorly of the cervical spine and between the maxillary and mandibular plane. Besides these bony
structures, it is also surrounded by soft tissues including the soft palate, tongue,
tonsils, and pharyngeal fat pads. Excessive adipose tissue may be deposited in all
parts of these soft tissues, resulting in an increased volume and hence reduced pharyngeal airway or even airway collapse.
Few studies investigating this matter using magnetic resonance imaging (MRI)
found a greater amount of fat at several levels surrounding the collapsible segment
of the pharynx in patients with OSA.
In 1989, Horner etal. performed MRI in six obese patients with OSA and ve
weight-matched controls without OSA.Fat deposits were found at all levels of the
airway, but were signicantly greater posterolateral at the level of the soft palate in
OSA patients [6]. In another MRI study of 30 patients with a range of OSA severity
and obesity, a signicant correlation was found between the AHI as measured with
12 The Role ofObesity inEpiglottis Collapse
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polysomnography and the size of the region enclosed by the mandible [7]. Schwab
etal. compared MRI data of 48 OSA patients with data from 48 controls who were
matched for gender, age, and ethnicity. Enlargement of the soft tissues at all upper
airway levels was observed in OSA patients, yet multivariable analysis identied
pharyngeal wall volume and tongue volume as independent risk factors for OSA
[8]. A Chinese study group also found a greater thickness of the lateral and posterior
pharyngeal wall in the epiglottal region in 18 OSA patients when compared with 19
age-matched controls [9].
The role of obesity and tongue volume was demonstrated by Nashi etal. who
assessed fat depositions within the tongue musculature using autopsy specimens
from the general population. The amount of fat tissue in the posterior part of the
tongue was greater than the anterior part (30% vs. 10%) and was positively correlated with BMI [10].
Although the role of BMI in the development in OSA is well known, excessive
fat tissue in the upper airway causing OSA may also be present in normal weight
subjects. Mortimore and colleagues compared excess fat deposition between
nine obese OSA patients, nine non-obese OSA patients, and nine non-obese nonOSA patients. MRI data showed a 10% and 28% greater neck tissue volume in
non-obese OSA and obese-OSA patients, respectively, when compared to control
subjects. This excess fat was localized in the anterolateral part of the upper airway [11].
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12.4 Role ofBMI inEpiglottis Shape
The posterior surface of the epiglottis is slightly concave. It is hypothesized that
deformity occurs due to pressure of the excessive fat deposits in the soft tissues surrounding the pharyngeal airway. One study demonstrated the effect of BMI in epiglottis shape changes [12]. Gazayerli and colleagues performed
esophagogastroduodenoscopy in more than 50 patients with a varying BMI between
21 and 61kg/m2 and noticed a positive correlation between BMI and the extent of
epiglottis concavity. Total closure of the epiglottis was observed in extreme cases.
The authors evaluated the degree of concavity by drawing lines from the edge points
of the epiglottis and measuring the angle between these lines. This angle was 100°
in a patient with a BMI of 28kg/m2, and 360° in a patient with a BMI of 62kg/m2
(Fig.12.1). This deformity appears to improve after weight loss as a change in epiglottis change was observed in patients who achieved weight loss after laparoscopic
gastric banding [12].
However, conclusions on epiglottis convexity should be taken with precautions.
This study published an observation rather than a scientic study on the omega
shape and the cause of its changes. No scientic background has been published on
this matter.
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Fig. 12.1 Comparison between the epiglottis of a patient with a BMI of 28 (a) and that of a
patient with a BMI of 62 (b). (Source: Gazayerli etal. Obesity Surgery 2006)
12.5 BMI andEpiglottis Collapse
The gold standard for diagnosing OSA is polysomnography (PSG). Levels of
obstruction can be evaluated by MRI, computed tomography (CT), or drug-induced
sleep endoscopy (DISE) (Chap. 9). Nowadays, DISE is frequently used in guiding
the surgical management of upper airway obstruction and its ndings are often
graded using VOTE (Velum, Oropharynx, Tongue base and Epiglottis).
Several studies have investigated the role of BMI in epiglottis obstruction. One of
the rst studies was published by Kuo etal., who performed drug-induced sleep CT
in 35 patients with a median AHI of 55.4/h and a median BMI of 26.9 kg/m2.
Epiglottis collapse (EC) was seen in twelve patients (34%). BMI was not different
between patients with and without EC [13]. Two studies performed DISE in patients
diagnosed with OSA by PSG and evaluated the prevalence and type of EC [14, 15].
Ravesloot and de Vries included 100 consecutive patients with a mean BMI of
27.4kg/m2 (SD 4.1). EC was found in 38% of patients; 12% partial anteroposterior
(A-P), 16% complete A-P, 2% partial lateral, and 8% complete lateral [14]. In the
study of Lan etal. (N=64, mean BMI 27,6kg/m2 SD 4.7), EC occurred in 42.2% of
patients; 12.5% partial A-P, 26.6% complete A-P, 0% partial lateral, and 3.1% complete lateral [15]. No difference in BMI was found in patients with epiglottis obstruction in both studies. Similar results were published recently in two retrospective
studies using DISE after PSG.The rst divided patients in to three groups: normalor underweight (N=24), overweight (N=56), or obese (N=31). Overweight and
obese patients showed increasing grades of obstruction at the velum and oropharynx,
whereas decreasing grades were noticed at the tongue base and epiglottis [16]. In a
large retrospective study of 627 patients, patients were classied in four BMI groups:
BMI<20.75kg/m2 (group 1, n=45), BMI 20.75–23kg/m2 (group 2, n=79), BMI
23–25kg/m2 (group 3, n=151), and BMI >25kg/m2 (group 4, n=352). EC occurred
in 127 patients (20%). Again, no difference was found between BMI groups [17].
C. A. L. Raa
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179
A study that reports other ndings was the study by Vroegop etal. who performed DISE after PSG in 1249 patients. Hypopharyngeal collapse including the
epiglottis occurred in 38.7% and was more prevalent in the obese population
(BMI≥ 30 kg/m2). BMI was positively correlated with the occurrence of partial
lateral, complete concentric, and complete lateral hypopharyngeal collapse.
However, the exact role of the epiglottis in these hypopharyngeal collapses was not
described [18].
In contrast, Sung etal. retrospectively reviewed 590 patients with complete PSG
and DISE data and found a negative correlation of the epiglottis with the BMI
(p< 0.01), also after adjusting for AHI [19]. This was also shown in the study of
Kim and colleagues (n=224), showing a lower BMI in the epiglottic collapse [20].
With these results, it can be concluded that increasing BMI is no risk factor for
epiglottis obstruction. Most studies found no role; two found a negative correlation
of BMI and EC.As sleep surgery has shown not to be successful in morbidly obese
patients, these studies performing DISE prior to sleep surgery included patients
with lower BMIs. In order to provide a full overview of the role of obesity in EC, it
would be interesting to evaluate the occurrence of EC in the morbidly obese population (BMI>35kg/m2) with OSA.
References
1. Quetelet, Adolphe. Most widely held works by Adolphe Quetelet. 1796–1874. http://www.
worldcat.org/identities/lccn- n50050539/.
2. Obesity and overweight. Key facts. Quetelet, Adolphe 1796–1874. Most widely held works by
Adolphe Quetelet. http://www.worldcat.org/identities/lccn- n50050539/.
3. White DP.The pathogenesis of obstructive sleep apnea: advances in the past 100 years. Am J
Respir Cell Mol Biol. 2006;34(1):1–6.
4. Malhotra A, White DP.Obstructive sleep apnoea. Lancet. 2002;360(9328):237–45.
5. De Raaff CAL, Pierik AS, Coblijn UK, De Vries N, Bonjer HJ, Van Wagensveld BA.Value of
routine polysomnography in bariatric surgery. Surg Endosc. 2017;31(1):245–8.
6. Horner RL, Mohiaddin RH, Lowell DG, etal. Sites and sizes of fat deposits around the pharynx in obese patients with obstructive sleep apnea and weight matched controls. Eur Respir
J. 1989;2:613–22.
7. Shelton KE, Gay SB, Hollowell DE, etal. Mandible enclosure of upper airway and weight in
obstructive sleep apnea. Am Rev Respir Dis. 1993;148:195–200.
8. Schwab RJ, Pasirtstein M, Pierson R, etal. Identicatin of upper airway anatomic risk factors
for obstructive sleep apnea with volumetric mangetic resonance imaging. Am J Respir Crit
Care Med. 2003;18:522–30.
9. Lin Z, Zhang H, Wang T, Li C, Bai Z.The upper airway MRI of obstructive sleep apnea
patients. Zhonghua Er Bi Yan Hou Ke Za Zhi. 2000;35(1):51–4.
10. Nashi N, Kang S, Barkdull GC, etal. Lingual fat at autopsy. Laryngoscopy. 2007;117:1467–73.
11. Mortimore IL, Marshall I, Wraith PK, etal. Neck and total body fat deposition in nonobese
and obese patients with sleep apnea compared with that in control subjects. Am J Respir Crit
Car Med. 1998;157:280–3.
12. Gazayerli M, Bliebel W, Elhorr A, Elakkary E.The shape of the epiglottis reects improvement in upper airway obstruction after weight loss. Obes Surg. 2006;16(7):945–7.
13. Kuo I, Hsin L, Lee L, etal. Prediction of epiglottic collapse in obstructive sleep apnea patients:
epiglottic length. Nat Sci Sleep. 2021;13:1985–92.
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14. Ravesloot MJ, de Vries N.One hundred consecutive patients undergoing drug-induced sleep
endoscopy: results and evaluation. Laryngoscope. 2011;121(12):2710–6.
15. Lan MC, Lui SYC, Lan MY, Modi R, Capasso R.Lateral pharyngeal wall collapse associated
with hypoxemia in obstructive sleep apnea. Laryngoscope. 2015;125(10):2408–12.
16. Wong SJ, Luitje ME, Karelsky S.Patterns of obstruction on DISE in adults with obstructive
sleep apnea change with BMI.Laryngoscope. 2021;131(1):224–9.
17. Woo HJ, Lim JH, Ahn JC, etal. Characteristics of obstructive sleep apnea patients with a low
body mass index: emphasis on the obstruction site determined by drug-induced sleep endoscopy. Clin Exp Otorhinolaryngol. 2020;13(4):415–21.
18. Vroegop AV, Vanderveken OM, Boudewyns AN, etal. Drug-induced sleep endoscopy in sleepdisordered breathing: report on 1,249 cases. Laryngoscope. 2014;124:797–802.
19. Sung CM, Tan SH, Shin MH, etal. The site of airway collapse in sleep apnea, its associations
with disease severity and obesity, and implications for mechanical interventions. Am J Respir
Crit Care Med. 2021;204(1):103–6.
20. Kim HY, Sung CM, Jan HB, Kim HC, Lim SC, Yang HC.Patients with epiglottic collapse
showed less severe obstructive sleep apnea and good response to treatment other than continuous positive airway pressure: a case-control study of 224 patients. J Clin Sleep Med.
2021;17(3):413–9.
C. A. L. Raa
The Role oftheNose inPharyngeal
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Obstructions
ThomasVerse
13.1 Introduction
Neither the generation of snoring sounds nor airway obstruction occur in the nose.
Nevertheless, the nose is rarely lacking on the agendas of conferences and textbooks
about sleep medicine. Already the often-cited Hippokrates (460–370BC) described
a causal connection between nasal polyps and non-restorative sleep. As early as
1581, Levinus Lemnious rst mentioned non-restorative sleep caused by oral
breathing in supine position [1]. First modern scientic reports date back to the end
of the nineteenth century (Table13.1). In 1898, Wells [2] reported an improvement
of vigilance in 8 out of 10 patients following nasal septoplasty.
Looking on modern scientic reports, Stadling etal. [3] investigated 1002 middle aged men, 17% snored. Risk factors for snoring were increased neck circumference, smoking and nasal congestion. Deegan etal. [4] looked for the prevalence of
nasal septal deviation in snorers and non-snoring control. Prevalence was found to
be 15% in snorers and 13% in non-snorers. Young and colleagues [5] described a
three-fold increase of snoring and daytime sleepiness in patients with self-reported
nasal congestion. Magliulo etal. [6] examined 50 patients with obstructive sleep
apnoea (OSA), only 20% showed no nasal pathology. Nasal obstruction was found
in 70% of the patients, allergic and non-allergic rhinitis in 18% and 26%, respectively.
All these data implicate a causal connection of impaired nasal breathing, snoring, daytime fatigue and obstructive sleep apnoea, and thus pharyngeal and maybe
laryngeal obstruction.
13
T. Verse (*)
Department for Otorhinolaryngology, Head and Neck Surgery, Asklepios Klinikum Hamburg,
Asklepios Campus, Hamburg, Germany
Semmelweis University, Budapest, Hungary
e-mail: t.verse@asklepios.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
M. Delakorda, N. de Vries (eds.), The Role of Epiglottis in Obstructive Sleep
Apnea, https://doi.org/10.1007/978-3-031-34992-8_13
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Table 13.1 First reports about the inuence of nasal breathing on sleep and well-being
Author Major Result
Hippocrates 460–370BC Nasal polyps are associated with restless sleep
Levinus 1581 Oral breathing in supine position causes unquiet sleep
Catlin 1861 First book: “The breath of life”
Catlin 1890 New edition: “Shut your mouth and save your life”
Guye 1889 Book “Shut your mouth and save your brain”
Cline 1892 Case report: Increase of daytime alertness after
septoplasty
Wells 1898 First case series: Alertness increases after septoplasty
(N=8/10)
T. Ve rse
Both, during the awake state and during sleep, the nasal breathing is the physiological route of breathing [7, 8]. Under normal circumstances, less than 10% of
human beings breath through their mouths. This makes the nose our major portal for
inspired air and hence makes nasal pathology a signicant cause for disturbance of
the inspirational air ow [9, 10]. With this in mind, many people and physicians
likewise assume that nasal pathology also plays a signicant role in the pathophysiology of sleep-related breathing disorders (SDB).
In addition, many patients suffering from acute or chronic impairment of nasal
breathing report a subjective detoriation of their individual sleep quality with consecutive daytime symptoms like fatigue, sleepiness, lack of concentration, etc. This
in turn is leading to many rhinologists having to face expectations of their patients,
that improvement of nasal obstruction not only solves daytime symptoms but also
reduces the severity of SDB in their daily practice.
This chapter focuses on the relationship between nasal obstruction and sleep
quality, as well as on the relationship between nasal obstruction and severity of
SDB.As this book deals with the role of the epiglottis in sleep disordered breathing,
this chapter tries to nd information concerning the inuence of nasal breathing on
the epiglottis and vice versa.
13.2 Pathophysiology
13.2.1 Nasal Breathing During theAwake State
In the awake state, about 50–60% of the resistance of the complete upper airway is
allotted to the nose [11]. This means the biggest part of the entire upper airway
resistance is located in the nose. As stated above, the nose can be regarded as the
physiological breathing path. In healthy, awake and upright sitting subjects, as much
as 92% of the entire airway resistance was found in the nose and only 8% in the oral
section of the upper airway [12].
The body position has a considerable inuence on nasal resistance. Nasal resistance
(Rn) increases if the body position changes from sitting to supine. A shift as little as 10°
leads to a signicant alteration of Rn. These changes were even more clearly seen in
patients with allergic or acute rhinitis as compared to a control group [13].
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