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13.2.2 Nasal Breathing During Sleep
Compared to being awake, Rn does not change if probants fall asleep [14], but the
entire upper airway resistance increases distinctively. This implies an increased airway resistance within the pharyngeal and maybe laryngeal sections of the upper
airway. In fact, during sleep the biggest part of the entire upper airway resistance is
located in the pharyngeal sections. There is no information available that deals with
the role of the epiglottis. In other words, relevant changes regarding the entire upper
airway resistance while falling asleep occur in the pharynx (and maybe larynx) and
not in the nose.
13.2.3 How Can Nasal Obstruction Nonetheless Promote Upper
Airway Collapse?
This important question is still open to debate and currently, there are 4 theories
being discussed:
13.2.3.1 Starling Resistor
First of all, an increased Rn contributes to the entire resistance of the upper airway
(RUA). However, during sleep, Rn only represents a smaller part of R
that changes in Rn result in relatively slight changes in R
UA.
This means
UA.
In contrast to the nose, the pharynx lacks bony or cartilageous structures to resist
the negative pressure on inspiration. Hence, the pharynx is assumed to react like a
Starling resistor. A higher preload in terms of an increased Rn is supposed to
increase the negative pressure and therefore collapse during inspiration, resulting in
an obstruction in the weakest segment of the chain, namely the pharynx.
Investigations with unilateral nasal dressings were able to provoke some obstructive
apnoea’s in non-OSA patients, although the effects were not strong enough to
induce a clinically signicant obstructive sleep apnoea [15–17]. Another, very interesting study on that matter chose seasonal allergic rhinitis (AR) as a more physiological model for temporary nasal obstruction. Here, polysomnography showed
signicantly more obstructive breathing events during the season as compared to
off-season [18]. Despite the reported result being statistically signicant, looking at
the absolute values (apnoea index: 0.7/h vs. 1.7/h) shows that this effect is not strong
enough to induce clinically signicant OSA.
Against the background of the reported data, it can be assumed that a partial
nasal obstruction may worsen a preexisting OSA or annoying snoring, but based on
the current evidence, it most unlikely represents a major factor in the pathogenesis of OSA.
Increase inOral Breathing
In case the nose is completely blocked, a switch to oral breathing occurs. By blocking both nares in healthy subjects with a dressing, it could be shown that the critical
collapse pressure (Pcrit) during sleep is signicantly reduced [19]. A decreased
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T. Ve rse
Pcrit in turn increases the likeliness of airway obstruction. In other words, increased
oral breathing destabilises the upper airway. A similar study showed signicantly
increased upper airway resistance for oral compared with nasal breathing [20]. Two
out of 10 healthy subjects developed a clinically signicant OSA while their noses
were completely occluded, while the other 8 subjects showed little or no changes
[21] in their polysomnographies. Apparently, there is a subgroup of patients (20%
in the before mentioned study) in which the change from nasal to oral breathing
results in clinically notable consequences, while the majority of patients do not
show considerable clinical changes. It could be discussed whether the relevant
group of patients had either an already existing subclinical SDB or another underlying pathology, even with an open nasal airway.
Loss ofNasal Reflexes
Trigeminally mediated nasal reexes are crucial to maintaining nasal patency.
Several studies could show that local anaesthesia in the nose is able to induce both,
central and obstructive, apnoeas [22, 23]. In the rst-mentioned study, 3 out of 10
healthy subjects developed transient severe OSA after local anaesthesia in the nose.
The other 7 patients did not show any change in their sleep parameters. Using placebo instead of local anaesthesia, no patient developed transient OSA.Additionally,
there seems to be a subgroup of patients in which nasal reexes play an important
role in maintaining airway patency.
Nitrogen Monoxide (NO)
Nitric oxide (NO) is produced in signicant quantity within the nose and the paranasal sinuses. With the nasal inspiratory airow, it reaches the lower parts of the
airway [24]. NO plays an important role as a bronchial dilator, thereby increasing
arterial oxygen saturation [25]. In addition to this important mechanism, NO plays
a role in maintaining muscle tone, the neuromuscular control of the pharynx, the
respiratory drive, and the regulation of sleep. To our knowledge, a thorough and
comprehensive assessment of the role of NO in the pathogenesis of sleep disordered
breathing does not exist. To sum it up, nasal obstruction seems to be associated with
snoring and apnoeas caused by pharyngeal obstructions. However, a direct correlation between nasal obstruction and the severity of SDB has not been found so far
[26]. Currently, this leads to the conclusion that the nose only adds little to the
severity of OSA in most patients.
Potential Causal Connection ofNasal Breathing andEpiglottic
Obstruction inOSA
The question is, how can impaired nasal breathing lead to a laryngeal airway
obstruction caused by the epiglottis? Unfortunately, to date there is almost no data
in the literature to answer this question. We know that the epiglottis while asleep
may fall back during inspiration causing a complete airway obstruction. We published our rst case in a 71-year-old Caucasian male as early as 1999 [27]. This
patient had an enlarged and lax epiglottis. This epiglottis appeared unstable in the
video endoscopy, was sucked back the posterior wall of the hypopharynx during
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inspiration and nally obstructed the hypopharynx completely (Fig. 13.1). As a
result, the patient was no longer able to accept his CPAP, as with increasing continuous positive airway pressure, the epiglottis was more and more pressed downwards
and backwards to the larynx. In other words, the patient developed a secondary
CPAP failure with increased AHI-values under PAP-treatment, although he was
treated successfully with PAP for a couple of years. So, what changed? Beside the
pinna of the ear, the epiglottis is the only organ of the head and neck exclusively
consisting of elastic cartilage. Pellnitz 1961 [28] has shown a signicant increase in
the length, breadth and weight of the epiglottis in males with increasing age, while
females show reductions of the same parameters. A histological study of 500 epiglottis specimens obtained at autopsy showed that size increase in male epiglottis is
due to the secondary intercellular deposits of by-products of metabolism. This probably reduces the stiffness of the epiglottis in the ageing male, which may increase
the risk of airway obstruction during sleep at this level.
Can this context hypothesise a causal connection between impaired nasal breathing and epiglottic obstruction, at least in elder male patients or patients with for
other reasons lax epiglottis?
As stated above, impaired nasal breathing implies a higher preload in terms of an
increased Rn, and thus is supposed to increase the negative pressure during inspiration within the hypopharynx. The increased negative pressure may result in an epiglottic collapse in patients with a lax epiglottis.
Secondly, mouth breathing narrows the hypopharyngeal section of the upper airway as the tongue moves backwards if the mouth is opened. This means that the
upper margin of the epiglottis approximates the posterior pharyngeal wall. This fact
again may facilitate epiglottic obstruction.
Thirdly, our case report shows that increasing ventilation pressure may worsen
the epiglottic airway collapse. Nasal surgery can help to reduce effective PAP (see
below), and might therefore help to avoid airway obstruction caused by the epiglottis.
Fig. 13.1 Epiglottic collapse in a 71-year-old male patient. Left side: endoscopic view. Right
side: X-ray showing enlarged epiglottis (arrow)
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All these theories are speculative. Surprisingly, there is little information about
the nose and epiglottis in the literature. Future research seems mandatory.
T. Ve rse
13.3 Clinical Results
The following data is based on two meta-analyses (published in German and
English), which form the basis of the German S2E guideline “ENT-specic therapy
of obstructive sleep apnoea in adults” [29] and the German S3 Guideline “The diagnosis and treatment of snoring in adults” [30]. These guidelines only include studies
investigating nasal treatments. No other treatments without the nose had been done.
Not all references can be mentioned in this book chapter. Please refer to the guidelines. More recent and additional references are given in the reference list below.
13.4 Results ofConservative Treatments
13.4.1 Medication
In a recent metanalysis [31] including 58 RCT, no signicant effect of drugs on the
severity of OSA in adults could be found. Altogether, a respectable 44 drugs and
drug-combinations were investigated. These drugs can be classied into 7
pathomechanism groups. None of these focused on nasal obstruction.
The above-mentioned German guidelines include 2 case-control-series with
only 22 patients. These 2 series focused on the effect of nasal decongestion
(with xylometazoline) on sleep in patients with OSA.Both did not show any
effect on sleep apnoea severity. However, one could report an improvement of
sleep quality.
13.4.1.1 Anti-Allergic Treatments
Topical steroids improve both, subjective and objective, quality of sleep in adults
with an underlying AR.The amount of improvement signicantly correlates with
the width of the nasal airway. Two RCT’s could show a signicant reduction of
apnoea-hypopnea-index (AHI) after treatment with several weeks of topical steroids, whilst patients treated with placebo did not show this effect. The effect however was limited to a decrease of 10–20% of the baseline AHI.
In children, a recent Cochrane review [32] detected 5 RCT’s (3 using topical
steroids and 2 based on Montelucast). All studies could show the superiority of
verum versus placebo with regards to objective polysomnographic parameters like
AHI, oxygen desaturation index (ODI), respiratory arousal index and nadir oxygen
saturation. Again, these effects are highly signicant, but in most cases not sufcient to achieve cure of the underlying OSA.Another metanalysis [33], including 5
RCT (Montelucast with or without additional topical steroids), describes the same
effects in altogether 166 kids.
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Present data prove that anti-allergic treatments may decrease the severity of
OSA.One question left unanswered in our knowledge is the duration of these effects
after ceasing the anti-allergic treatment.
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13.4.2 Nasal Dilators
These can be divided into external (plasters) and internal nasal dilators. The German
guideline [29] included data of 194 patients (11 studies) under this category. A
recent metanalysis [34] included 147 patients (9 studies). Both metanalysis were
not able to nd any signicant effects of nasal dilators on OSA severity. Two
included studies provide additional information on subjective outcome. In both
studies, patients signicantly beneted from the nasal dilation in terms of reduction
of daytime sleepiness although their objective AHI did not change.
Focussing on simple snoring, a number of clinical trials indicate nasal dilators
having an effect on snoring [30]. A most recent study [35] including 70 simple snorers did not show any effect of an external nasal dilator on objective snoring parameters. However, as side effects are limited, the German guideline recommends a trial
with a nasal dilator for the treatment of simple snoring. There is some trial data
indicating that a positive effect of nasal dilators can predict the effect of nasal surgery. In our daily practice, we use nasal dilators in this indication with relatively
good results.
13.5 Results ofSurgical Treatments
13.5.1 Nasal Surgery forOSA
The metanalysis conducted for the German guideline identied 28 studies including
717 patients having isolated nasal surgery for the treatment of OSA.All studies
provided pre- and postoperative polysomnographic data. Since then, a further 4
articles on that topic could be identied [36–39]. All but 5 studies are case-series
with a low grade of evidence. An additional most recently published study [40] adds
data of 35 patients with and without AR.Table13.2 summarises the data. Putting all
data together, on average the AHI was reduced from 30.4 to 27.5 breathing events
per hour of sleep. Only 8 out of 32 studies described a statistically signicant
decrease of the AHI.This result is in accordance with data that additional nasal
surgery does not improve the success rates of multi-level surgery concepts for treating OSA [41]. However, many of the cited studies include individuals that substantially beneted from isolated nasal surgery in terms of their apnoea-hypopnea-index
(AHI). The most recent study [40] included 8 patients with and 27 patients without
AR.The subgroup of AR-patients proted much more from nasal septoplasty. The
surgical success rate was given as 50% (4/8) in patients with AR and only 3.7%
(1/27) in patients without AR.
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T. Ve rse
Table 13.2
Author
Rubin AH etal.
1983
Dayal VS,
Phillipson EA
1985
Caldarelli DD
etal. 1985
Aubert-Tulkens
G etal. 1989
Sériès F etal.
1992
Sériès F etal.
1993
Utley DS etal.
1997
Verse T etal.
1998
Friedman M
etal. 2000
Kalam I 2002 21 No data 14 11 < 0.05 No
Verse T etal.
2002
Kim ST etal.
2004
Balcerzak J etal.
2004
Nakata S etal.
2005
Virkkula P etal.
2006
Koutsourelakis I
etal. 2008
Li HY etal.
2008
Nakata S etal.
2008
Morinaga M
etal. 2009
Tosun F etal.
2009
Li HY etal.
2009
Bican A etal.
2010
Choi JH etal.
2011
Effect of isolated nasal surgery on AHI and ESS
AHI
N Follow-up
9 1–6 37.8 26.7 < 0.05 No
6 4–44 46.8 28.2 n.s. No
23 No data 44.2 41.5 n.s. No
2 2–3 47.5 48.5 – No
20 2–3 39.8 36.8 n.s. No
14 2–3 17.8 16 n.s. No
4 No data 11.9 27 – 7.8 6.8 n.s. 4
2 3–4 14 57.7 – 6 12 n.s. 4
22 > 1.5 31.6 39.5 n.s. No
26 3–50 31.6 28.9 n.s. 11.9 7.7 <
21 1 39 29 <0.0001 No
22 2 48.1 48.8 n.s. No
12 No data 55.9 47.8 n.s. 11.7 3.3 <
40 2–6 13.6 14.9 n.s. No
27 3–4 31.5 31.5 n.s. 13.4 11.7 <
51 3 37.4 38.1 n.s. 10.0 8.0 <
49 No data 49.6 42.5 n.s. 10.6 4.5 4
35 No data 43.5 38.6 n.s. No
27 3 6.7 5.6 n.s. 9.4 4.1 <
44 3 36.4 37.5 n.s. 10.6 7.6 <
20 3 43.1
22 3 28.9 26.1 n.s. 8.8 6.3 <
AHI
pre
post P value
24.6 <0.05 17.1 11.1 <
ESS
pre
data
data
data
data
data
data
data
data
data
data
data
data
ESS
postP value
No
data
No
data
No
data
No
data
No
data
No
data
No
data
No
data
0.001
No
data
No
data
0.045
No
data
0.01
0.001
No
data
0.01
0.05
0.01
0.001
EBM
4
4
4
4
4
4
4
4
4
4
4
4
4
2b
4
4
4
3b
4
4
(continued)
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Table 13.2 (continued)
AHI
Author
Suoglu M etal.
2012
Victores
AJ+Takashima
M 2012
Hu B etal. 2013 79 6 27.7 26.3 n.s. No
Poirier J etal.
2014
Yalamanchali S
etal. 2014
Moxness MH
etal. 2014
Park CY etal.
2014
Shuaib SW etal.
2015
Xiao Y etal.
2016
Kim SD etal.
2021
All 892 1–44 30.44 27.52 10.82 6.71 B
N Follow-up
28 3 32.5 32.4 n.s. 9.3 5.9 <
24 3 23.6 20.4 n.s. 12.3 6.6 <
11 6 33.2 29.4 n.s. No
56 1.5 33.5 29.4 n.s. No
59 3 18.2 16.6 n.s. 10.7 8.9 <
25 2 23.9 12.2 < 0.05 9.7 5.8 <
26 4 24.7 16.0 < 0.05 11.5 7.5 =
30 3 49.7 43.1 < 0.05 No
35 6 28.5 18.5 < 0.001 7.9 5.3 <
pre
AHI
post P value
ESS
pre
data
data
data
data
ESS
postP value
0.001
0.05
No
data
No
data
No
data
0.001
0.05
0.003
No
data
0.001
189
EBM
4
4
3b
4
4
3b
4
4
3b
3b
Obviously, it is not possible to successfully treat OSA in the vast majority of
cases by only performing nasal surgery. Further reviews come to the same conclusion [10, 42, 43].
In contrast, focusing on subjective outcome parameters, nasal surgery has a huge
impact on the patient’s well-being. Altogether, 17 studies (481 patients) provide
data concerning daytime sleepiness as measured with the Epworth Sleepiness Scale,
ESS (Table13.2). Mean ESS values decreased from 10.2 to 6.7. Similar results are
shown by a metanalysis from Li and colleagues [42].
Other studies prove signicant improvements to other parameters and dimensions of quality of life. Instruments that were used are the “Snore Outcome Survey”
[44], the “SF-36” [45], the NOSE-questionnaire [46] and the Pittsburgh Sleep
Quality Index [39] amongst other test instruments.
In summary, isolated nasal surgery rarely eliminates OSA completely. More
recent studies show at least a limited effect on OSA severity. Maybe patients with
AR benet more. However, nasal surgery has various positive effects on the sleep
quality. As patients with OSA often suffer from not-restorative sleep, many patients
will benet from nasal surgery. Another indication for nasal surgery is persisting
daytime symptoms after objective relief of OSA (i.e. normalisation of the apneahypopnea-index and other polysomnographic parameters). To my personal belief,
this fact is too often neglected in our daily practice.
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Table 13.3 Effect of isolated nasal surgery on effective PAP (positive airway pressure)
CPAP post
Author
Mayer-Brix J etal. 1989 3 9.7 6 No data 4
Friedman M etal. 2000 6 9.3 6.7 < 0.05 4
Dorn M etal. 2001 5 11.8 8.6 < 0.05 4
Masdon JL etal. 2004 35 9.7 8.9 n.s. 4
Nakata S etal. 2005 5 16.8 12 < 0.05 4
Zonato AI etal. 2006 17 12.4 10.2 < 0.001 4
Sooglu M etal. 2012 28 11.2 10.4 n.s. 4
Poirier J etal. 2014 18 11.9 9.2 n.s. 4
All 117 11.2 9.4 C
N CPAP pre (cm H2O)
(cm H2O) p-Wert
T. Ve rse
EBM
13.5.2 Nasal Surgery andPAP
Nasal surgery proved to facilitate or even enable required PAP-treatments in patients
with nasal pathologies [47, 48]. Current data show that the effective positive airway
pressure can successfully be reduced by about 2cm H2O following nasal surgery
(Table13.3). As results in Table13.3 show, these data are from non-controlled case
series, hence the data need to be regarded as preliminary. Further scientic results
may change this assessment.
A recent published series [49] of 14 patients with OSA showed that CPAP can
safely be used in the very rst night after nasal surgery. Adherence to PAP was
reduced in the rst week after surgery, but increased to preoperative values in the
second week.
13.5.3 Nasal Surgery andSimple Snoring
The work on the German guideline on snoring in adults [30] detected a number of
case control series, whereby the follow-up period was generally 6months. A retrospective study compared the effectiveness of septoplasty and turbinoplasty with
other surgical procedures for snoring, and a signicant improvement in subjective
snoring intensity was seen. Prospective case control series also demonstrated the
effect of septoplasty alone on subjective, but not objective, snoring intensity. The
results of the above-mentioned studies suggest that a surgical improvement in nasal
airow leads to a subjective reduction in snoring. Not surprisingly, possible side
effects and complications of the procedure do not differ from nasal surgery for a
primary rhinological indication.
Against the background of these data, the German guideline suggests to offer
nasal surgery to patients with objective nasal pathology and a resulting subjective
nasal breathing impairment. Due to a lack of evidence, no statement was made on
the effectiveness of nasal surgery in snorers with no subjective nasal breathing
impairment but objective nasal pathologies. Maybe nasal surgery can help in these
cases, too.
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13.6 Conclusion
While being awake, the nose contributes up to 60% and therefore plays a great role
in the entire resistance of the upper airway; during sleep, the predominant part is
contributed by the pharyngeal sections of the upper airway. This is why the nose
does not change its resistance during transition from awake to sleep, while the resistance of the pharynx considerably increases. Surprisingly there is little in literature
about the nose and epiglottis. Future research is requested.
Against this background it is not surprising that the solvation of nasal obstruction
does not signicantly affect the severity of OSA in most cases. However, there are
exceptions to this rule. Snoring does improve by a certain extent. Patients suffering
from allergic or acute rhinitis benet from anti-allergic treatment.
In contrast to the relatively discrete objective changes in respiratory parameters,
the benet of nasal surgery with regard to the quality of sleep and daytime symptoms and hence quality of life are impressive. This applies to patients with sleep
disordered breathing disorders as well for sleep-healthy subjects. In this respect, it
should be considered to include sleep disorders caused by impaired nasal breathing
into the International Classication of Sleep Disorders (ICSD), where they are not
mentioned so far.
In any case, a treatment of nasal obstruction should be considered if a patient is
either suffering from subjectively impaired nasal breathing or if his/her relevant
daytime fatigue cannot be successfully treated otherwise.
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