Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4458_Библиотеки_им_академика_М_И_Перельмана
.pdf
Sleep Disorders andtheNose:
https://t.me/medicina_free
What Is theEvidence Base?
ThomasVerse andStefanMüller
10
Summary
This chapter considers the evidence base between
the nasal airway and sleep. This important relationship will be considered for both obstructive
sleep apnoea and simple snoring.
The pathophysiology is explained and will
cover the various theories of airway dynamics
and airway collapse during sleep. This includes a
short resumé of nitric oxide and its physiological
effects.
The evidence base for effects of medication
and alar splints is presented. The effect of nasal
surgery on obstructive sleep apnoea in the application of positive airway pressure and simple
snoring is then considered.
Introduction
Neither airway obstruction nor the generation of
snoring sounds occur in the nose. Nevertheless,
the topic ‘Nose’ always features prominently on
the agenda of conferences about sleep medicine.
Even the often-cited Hippocrates (460–370 BC)
described a causal connection between nasal polyps and non-restorative sleep. As early as 1581,
T. Verse (*) · S. Müller
Department for Otorhinolaryngology, Head and Neck
Surgery, Asklepios Klinikum Harburg, Asklepios
Campus Hamburg, Semmelweis University Budapest,
Hamburg, Germany
e-mail: t.verse@asklepios.com
Levinus Lemnious rst mentioned non- restorative
sleep caused by oral breathing in supine position
[1]. The rst modern scientic reports date back to
the end of the nineteenth century. In 1898, Wells
[2] reported an improvement of vigilance in eight
out of ten patients following nasal septoplasty.
Both, during the awake state and during sleep,
nasal breathing is the natural physiological route
for breathing [3, 4]. Under normal circumstances,
less than 10% of humans breathe through their
mouth. The nose is our major portal for inspired
air, and nasal pathology is responsible for causing signicant disturbance of inspirational air
ow [5, 6]. 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 deterioration of their individual sleep quality with consecutive daytime symptoms such as fatigue, sleepiness and lack of
concentration. This in turn leads to many rhinologists having to face expectations from their
patients that improvement of nasal obstruction
not only solves their daytime nasal symptoms but
also reduces the severity of SDB and the effects
on their daily routines.
This chapter focusses on the relationship
between nasal obstruction and sleep quality, as
well as on the relationship between nasal obstruction and severity of SDB.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
A. C. Swift et al. (eds.), Contemporary Rhinology: Science and Practice,
https://doi.org/10.1007/978-3-031-28690-2_10
117
118
https://t.me/medicina_free
T. Verse and S. Müller
Pathophysiology
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 [7]. This means the largest component 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 [8].
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 [9].
Nasal Breathing During Sleep
In comparison to being awake, nasal resistance
(Rn) does not change if the subject falls asleep
[10], but the entire upper airway resistance
increases distinctively. This implies an increased
airway resistance within the pharyngeal sections
of the upper airway. In fact, during sleep, the
largest contributor to total upper airway resistance is located in the pharynx. In other words,
the most signicant change of the entire upper
airway resistance, whilst falling asleep, occurs in
the pharynx and not the nose.
How Can Nasal Obstruction Promote
Upper Airway Collapse?
This important question has several hypotheses
and is still open to debate. Currently, there are
four possible theories.
Starling Resistor
An increase in nasal resistance (Rn) increases the
total resistance of the upper airway (RUA).
However, during sleep, Rn only represents a
small component of R
in Rn result in relatively slight changes in R
This infers that changes
UA.
UA.
In contrast to the nose, the pharynx lacks bony
or cartilaginous structures to resist the negative
pressure of inspiration. Hence, we can assume
that the pharynx reacts like a Starling resistor. A
higher preload, in terms of an increased Rn,
should create a greater negative pressure that
induces collapse during inspiration, causing
obstruction in the weakest segment of the chain,
namely the pharynx.
Investigations with unilateral nasal dressings
were able to provoke some obstructive apnoeas in
non-OSA patients, but the effects were not
enough to induce clinically signicant obstructive sleep apnoea [11–13].
The effects of temporary nasal obstruction
were investigated in subjects with seasonal allergic rhinitis as a more natural, physiological
model. Polysomnographic data showed signicantly more obstructive breathing events during
the allergic season as compared to the period outside of the allergic season [14]. However, whilst
the effect was statistically signicant, the change
in absolute values was not strong enough to
induce clinically signicant OSA (apnoea index:
0.7/h versus 1.7/h).
In conclusion, if we consider the background
of reported published data, we can assume that
partial nasal obstruction may worsen pre-existing
OSA or annoying snoring. However, based on
current evidence, partial nasal obstruction is most
unlikely to represent a major factor in the pathogenesis of OSA.
Increase inOral Breathing
When the nose is completely blocked there is an
automatic switch to oral breathing. It has been
demonstrated that, in healthy subjects, the critical
collapse pressure (Pcrit) during sleep is signicantly reduced by blocking both nares with a
dressing [15]. A decreased Pcrit in turn increases
the likeliness of airway obstruction. In other
words, increased oral breathing destabilizes the
upper airway.
A similar study showed the upper airway
resistance to increase signicantly for oral compared with nasal breathing [16]. Two out of ten
10 Sleep Disorders andtheNose: What Is theEvidence Base?
https://t.me/medicina_free
119
healthy subjects developed clinically signicant
OSA whilst their noses were completely
occluded, but the other eight subjects showed
little or no change in their polysomnographic
data [17]. The evidence suggests that the change
from nasal to oral breathing results in clinically
notable consequences a subgroup of patients
(20% in the before mentioned study), whilst the
majority of patients do not show any signicant
clinical effects. It may be surmised that this particular subgroup already had pre-existing subclinical SDB, even with an open nasal airway.
Loss ofNasal Reexes
Trigeminally mediated nasal reexes are crucial
to maintaining nasal patency. Several studies
show that the application of local anaesthesia to
the nasal mucosa induces a combination of central and obstructive apnoeas [18, 19]. White etal.
described transient, severe OSA after local anaesthesia in the nose in three out of ten healthy subjects, whilst seven patients did not show any
change in their sleep parameters. When the local
anaesthetic was replaced by a placebo, none of
the subjects developed transient OSA.
In addition to this, there seems to be a subgroup of patients in whom nasal reexes play an
important role in maintaining airway patency.
Nitric Oxide (Nitrogen Monoxide: NO)
Nitric oxide (NO) is produced in a signicant
quantity within the nose and the paranasal
sinuses. Nitric oxide reaches the lower parts of
the airway with the nasal inspirational airow
[20]. NO is a bronchial dilator, thereby increasing oxygen saturation of arterial blood [21].
In addition to enhancing oxygenation, NO has
several other signicant effects that include
maintaining muscle tone, the neuromuscular control of the pharynx, the respiratory drive and the
regulation of sleep.
To our knowledge, a thorough, comprehensive
analysis of the role of NO in the pathogenesis of
sleep-disordered breathing does not exist.
In summary: Nasal obstruction seems to be
associated with snoring and apnoeas. However, a
direct correlation between nasal obstruction and
the severity of SDB has not been demonstrated
[22]. Currently, this implies that the nose adds
very little to the severity of obstructive sleep
apnoea (OSA).
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 apnea in
adults’ [23] and the German S3 Guideline ‘The
diagnosis and treatment of snoring in adults’
[24]. These guidelines only include studies investigating nasal interventional treatments, and
excludes interventions that do not include the
nose. Whilst the chapter does not include all of
the references within the guidelines, the list
includes more recent, additional references.
Eects ofConservative Treatment
Medication
In a recent meta-analysis, that included 58 RCTs,
medication had no signicant effect on the severity of OSA in adults [25]. Altogether, a respectable 44 drugs and drug-combinations were
investigated. The medications could be classied
into seven pathomechanism groups, but none of
these focused on nasal obstruction.
The above-mentioned German guidelines
include two case–control series with only 22
patients. These two series focused on the effect of
nasal decongestion (with xylometazoline) on
sleep in patients with OSA.Neither study show
any effect on the severity of sleep apnoea, but one
report described a subjective improvement in
sleep quality.
Anti-allergic Treatments
Topical nasal corticosteroids improve both subjective and objective quality of sleep in adults
with allergic rhinitis. The degree of improvement
signicantly correlates with the width of the
nasal airway. Two randomized controlled trials
(RCTs) demonstrated a statistically signicant
reduction of the apnoea–hypopnea index (AHI)
after treatment topical steroids for several weeks
but use of a placebo showed no effect. However,
120
https://t.me/medicina_free
T. Verse and S. Müller
the effect was limited to a decrease of 10–20% of
the pre-treatment baseline AHI.
In a recent Cochrane review of children with
OSA [26], ve RCTs were identied (three using
topical steroids and two based on Montelukast).
All studies could show the superiority of verum
versus placebo with regard to objective polysomnographic parameters including AHI, oxygen
desaturation index (ODI), respiratory arousal
index and nadir oxygen saturation. Again, whilst
these effects are highly signicant, in most cases
they are not sufcient to achieve cure of the
underlying OSA. Another meta-analysis [27],
including ve RCTs (Montelukast with or without additional topical steroids), describes the
same effects in a total of 166 children.
It is therefore clear from the present data that
anti-allergic treatments can decrease the severity
of OSA.However, one question that is left unanswered in our knowledge is the duration of these
effects once the anti-allergic treatment is stopped.
Nasal Dilators
These can be divided into external (plasters) and
internal nasal dilators (Fig.10.1). The question as
to whether nasal dilators affect the severity of
OSA has been considered by probing two metaanalyses. The German guideline [23] included
data of 194 patients (11 studies) under this category. The more recent meta- analysis [28]
included 147 patients (9 studies). Both metaanalyses were unable to demonstrate any signicant effects of nasal dilators on OSA severity.
However, two individual studies within the considered papers provided additional information
on subjective outcome: both studies demonstrated signicant benet from the nasal dilation
in reducing daytime sleepiness, although the
objective AHI remained unchanged.
The effect of nasal dilators on simple snoring
has also been considered. Several clinical trials
reported nasal dilators having a positive effect on
simple snoring [24]. The German guideline recommend a trial with a nasal dilator for the treatment of simple snoring. Trial data has shown that
a positive effect from using nasal dilators during
sleep can predict the likely effect from nasal surgery. In our unit, we use nasal dilators in this
manner in our daily practice, with relatively good
results.
Results ofSurgical Intervention
Nasal Surgery forOSA
The meta-analysis 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
post-operative polysomnographic data. A further
four articles on this topic have since been identied [29–32]. With the exception of ve studies,
27 papers were case series with a low grade of
evidence (Table 10.1 summarizes the data). On
collating the data, the average AHI was reduced
from 30.5 to 27.9 breathing events per hour of
sleep. Only 7 out of 32 studies described a statistically signicant decrease of the AHI. These
ndings are consistent with data that shows that
additional nasal surgery does not improve the
success rates of multi-level surgery concepts for
treating OSA [33]. It is therefore clearly apparent
that it is not possible to successfully treat OSA in
the vast majority of patients by only performing
nasal surgery. Further reviews come to the same
conclusion [6, 34, 35].
In contrast, focusing on subjective outcome
parameters for nasal surgery, it has a huge impact
on the patient’s well-being. Altogether, data from
16 studies (446 patients) concerning daytime
sleepiness, as assessed by the Epworth Sleepiness Fig. 10.1 Internal nasal dilator
10 Sleep Disorders andtheNose: What Is theEvidence Base?
https://t.me/medicina_free
121
Author N Follow-up AHI pre AHI post P value ESS pre ESS post P value EBM
Rubin AH etal. (1983) 9 1–6 37.8 26.7 <0.05 No data No data 4
Dayal VS and Phillipson EA (1985) 6 4–44 46.8 28.2 n.s. No data No data 4
Caldarelli DD etal. (1985) 23 No data 44.2 41.5 n.s. No data No data 4
Aubert-Tulkens G etal. (1989) 2 2–3 47.5 48.5 - No data No data 4
Sériès F etal. (1992) 20 2–3 39.8 36.8 n.s. No data No data 4
Table 10.1 Effect of isolated nasal surgery on severity of obstructive sleep apnea
Sériès F etal. (1993) 14 2–3 17.8 16 n.s. No data No data 4
Utley DS etal. (1997) 4 No data 11.9 27 - 7.8 6.8 n.s. 4
Verse T etal. (1998) 2 3–4 14 57.7 - 6 12 n.s. 4
Friedman M etal. (2000) 22 >1.5 31.6 39.5 n.s. No data No data 4
Kalam I. (2002) 21 No data 14 11 <0.05 No data No data 4
Verse T etal. (2002) 26 3–50 31.6 28.9 n.s. 11.9 7.7 <0.001 4
Kim ST etal. (2004) 21 1 39 29 <0.0001 No data No data 4
Balcerzak J etal. (2004) 22 2 48.1 48.8 n.s. No data No data 4
Nakata S etal. (2005) 12 No data 55.9 47.8 n.s. 11.7 3.3 <0.045 4
Virkkula P etal. (2006) 40 2–6 13.6 14.9 n.s. No data No data 4
Koutsourelakis I etal. (2008) 27 3–4 31.5 31.5 n.s. 13.4 11.7 <0.01 2b
Li HY etal. (2008) 51 3 37.4 38.1 n.s. 10.0 8.0 <0.001 4
Nakata S etal. (2008) 49 No data 49.6 42.5 n.s. 10.6 4.5 4
Morinaga M etal. (2009) 35 No data 43.5 38.6 n.s. No data No data 4
Tosun F etal. (2009) 27 3 6.7 5.6 n.s. 9.4 4.1 <0.01 4
Li HY etal. (2009) 44 3 36.4 37.5 n.s. 10.6 7.6 <0.05 3b
Bican A etal. (2010) 20 3 43.1 24.6 <0.05 17.1 11.1 <0.01 4
Choi JH etal. (2011) 22 3 28.9 26.1 n.s. 8.8 6.3 <0.001 4
Suoglu M etal. (2012) 28 3 32.5 32.4 n.s. 9.3 5.9 <0.001 4
Victores AJ and Takashima M (2012) 24 3 23.6 20.4 n.s. 12.3 6.6 <0.05 4
Hu B etal. (2013) 79 6 27.7 26.3 n.s. No data No data 3b
Poirier J etal. (2014) 11 6 33.2 29.4 n.s. No data No data 4
Yalamanchali S etal. (2014) 56 1.5 33.5 29.4 n.s. No data No data 4
Moxness MH etal. (2014) 59 3 18.2 16.6 n.s. 10.7 8.9 <0.001 3b
Park CY etal. (2014) 25 2 23.9 12.2 <0.05 9.7 5.8 <0.05 4
Shuaib SW etal. (2015) 26 4 24.7 16.0 <0.05 11.5 7.5 0.003 4
Xiao Y etal. (2016) 30 3 49.7 43.1 <0.05 No data No data 3b
Total 857 1–44 30.52 27.89 11.06 6.79 B
AHI apnea hypopnea index, ESS Epworth Sleepiness scale
122
https://t.me/medicina_free
T. Verse and S. Müller
Scale (ESS; Table 10.1), shows that the mean
ESS values decreased from 11.0 to 7.0. Similar
results are shown by a meta-analysis from Li and
colleagues [34].
Several other studies demonstrate signicant
improvements to other parameters and dimensions of quality of life. The Patient Related
Outcome Measure (PROMS) tools used include
the ‘Snore Outcome Survey’ [36], the ‘SF-36’
[37], the NOSE-questionnaire [38], the Pittsburgh
Sleep Quality Index [32] amongst various other
outcome measure tools.
In summary, isolated nasal surgery rarely completely eliminates OSA, but more recent studies
show at least a limited effect on OSA severity.
However, nasal surgery has various positive
effects on the sleep quality. As patients with OSA
often suffer from non-restorative sleep, many
patients will benet from nasal surgery. Our personal belief is that this fact is too often neglected.
Nasal Surgery andPAP
Nasal surgery has been shown to improve or even
enable necessary PAP-treatment in patients with
various nasal pathologies [39, 40]. Current data
shows that the effective level of positive airway
pressure can be successfully reduced by about
2cmH2O following nasal surgery (Table10.2).
However, the data sets are from non-controlled
case series and should therefore be regarded as
preliminary. Future scientic results may well
change this assessment.
Nasal Surgery andSimple Snoring
The work on the German guideline on snoring in
adults [24] identied a number of case–control
series, whereby the follow-up period was generally 6 months. A retrospective study compared
septoplasty and turbinoplasty with other surgical
procedures for simple snoring, and found the former to be effective in signicantly improving
subjective snoring intensity. Prospective case–
control series have also demonstrated the positive
effect of septoplasty as the only procedure 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 data, the German
guideline suggests that nasal surgery should be
offered to patients with objective nasal pathology
combined with a subjective nasal breathing
impairment. Due to a lack of evidence, a statement cannot be 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?
Table 10.2 Effect of isolated nasal surgery on effective PAP (positive airway pressure)
Autor N
Mayer-Brix J etal.
(1989)
Friedman M etal.
(2000)
Dorn M etal. (2001) 5 11.8 8.6 <0.05 4
Masdon JL etal.
(2004)
Nakata S etal.
(2005)
Zonato AI etal.
(2006)
Sooglu M etal.
(2012)
Poirier J etal. (2014) 18 11.9 9.2 n.s. 4
Total 117 11.2 9.4 C
3 9.7 6 No data 4
6 9.3 6.7 <0.05 4
35 9.7 8.9 n.s. 4
5 16.8 12 <0.05 4
17 12.4 10.2 <0.001 4
28 11.2 10.4 n.s. 4
CPAP pre
(cmH2O)
CPAP post
(cmH2O) p-Wert EBM
10 Sleep Disorders andtheNose: What Is theEvidence Base?
https://t.me/medicina_free
Conclusion
In the healthy awake subject, the nose contributes
up to 60% of the normal airow and plays a signicant role in the total resistance of the upper
airway. However, during sleep, the pharyngeal
sections of the upper airway become the predominant factor. This is why the nose does not signicantly change its resistance during transition
from awake to sleep, whilst the resistance of the
pharynx considerably increases, thus increasing
the overall total airway resistance.
From the evidence base, it is not surprising
that the relief of nasal obstruction hardly affects
the severity of OSA. Simple snoring, however,
does improve to some extent. Patients suffering
from allergic or acute rhinitis should benet from
anti-allergic treatment.
In contrast to the relatively discrete objective
changes in respiratory parameters, the benet of
nasal surgery regarding the quality of sleep and
daytime symptoms, and hence quality of life, is
impressive. These subjective improvements
apply to patients with sleep disordered breathing
disorders as well for sleep-healthy subjects.
In this respect, we should consider including
sleep disorders caused by impaired nasal breathing into the international classication of sleep
disorders. At present, this clinical scenario is not
included nor mentioned.
In conclusion, treatment of nasal obstruction
should be considered for patients suffering from
subjectively impaired nasal breathing or those
with signicant daytime fatigue that cannot be
successfully treated otherwise.
Working Examples of Clinical Scenarios
Case 1: Presentation and Management
A 54-year-old man with: BMI 32.5kgm−2; ESS
12; PSQI 6; AHI 28.9; supine: AHI 38.0; nonsupine: AHI 20.5.
Signicant nasal obstruction due to septal deviation and enlarged conchae.
Tonsillar hypertrophy (Brodsky Grade 3), long
uvula, webbing 8mm (Fig.10.2).
Small lingual tonsils (Friedman 1). Regular epiglottis (Fig.10.3).
Non-compliant to PAP treatment.
Fig. 10.2 Case 1. Enlarged uvula and tonsillar hypertrophy (Brodsky Grade 3)
Fig. 10.3 Case 1. Small lingual tonsils (Friedman 1).
Regular epiglottis
• The nasal obstruction can be resolved by nasal
• The pharyngeal obstruction can be resolved
• We usually avoid performing nasal and pha-
123
Factors to consider:
The options
septoplasty and reduction of inferior turbinates.
by uvulopalatopharyngoplasty in combination
with tonsillectomy. We usually perform radiofrequency treatment of the base of tongue in
addition, as this combination does not increase
post-operative morbidity and is likely to have
an additional positive effect on the clinical
outcome of OSA.
The management plans
ryngeal surgery at the same time. Combining
124
https://t.me/medicina_free
T. Verse and S. Müller
both operations would incur much greater
post-operative risk and morbidity.
• We would recommend performing the nasal
surgery rst.
• Following nasal surgery, we offer a new trial
with PAP.Effective and successful nasal sur-
gery is likely to improve both the effectiveness
and tolerance of PAP.
• Should PAP still be problematic for the patient
or something that they would prefer not to use,
we would then recommend pharyngeal sur-
gery as described above.
• Nasal surgery can substantially improve sleep
quality and daytime symptoms. This may lead
to difculty in convincing some patients that
they still have sleep apnoea that requires inter-
ventional treatment. We therefore recommend
further sleep studies in such patients.
Case 2: Presentation and Management
A 48-year-old woman: BMI 35.5kgm−2; ESS 7;
PSQI 4.
She had severe septal deviation and chronic rhinosinusitis with large nasal polyps.
She was successfully treated with PAP.
Sinonasal surgery was therefore not
recommended.
Factors to consider:
• The combination of OSA, general anaesthesia
and nasal surgery is associated with increased
perioperative risk and is only recommended
when necessary.
• Sinonasal surgery in patients with moderate to
severe OSA is always preformed as an
inpatient.
• The anaesthesiologist should be experienced
and informed about the presence of OSA prior
to surgery.
• We try to manage these patients without nasal
dressings wherever possible.
Post-operative care
• Postoperatively, patients with moderate to
severe OSA (AHI >20) are monitored for 4h
in the recovery room. Complications will typi-
cally occur within the very rst few hours fol-
lowing extubation.
• Patients with complications are monitored
overnight in an intermediate care unit.
• Patients are otherwise managed overnight on a
regular ward.
Key Learning Points
• Nasal obstruction seems to be associated with
snoring and apnoeas.
• Evidence suggests that the nose adds very little to the severity of obstructive sleep apnoea
(OSA).
• Medication has no identiable effect on the
severity of sleep apnoea, but subjective
improvement in sleep quality may occur.
• Anti-allergic treatments can decrease the
severity of OSA.
• Meta-analyses are unable to demonstrate any
signicant effect from nasal dilators on OSA
severity.
• Nasal dilators have a positive effect on simple
snoring.
• OSA cannot be successfully treated in the vast
majority of patients by only performing nasal
surgery.
• Nasal surgery has various positive effects on
the sleep quality.
• Nasal surgery has been shown to improve or
even enable necessary PAP treatment in
patients with various nasal pathologies.
• Septoplasty as the only procedure is effective on
subjective, but not objective, snoring intensity.
Conict of Interest T.Verse and S.Müller do not have
any conicts of interest.
References
1. Levinus Lemnious. The touchstone of complexions.
London; 1581
2. Wells WA.Some nervous and mental manifestations
occurring in connection with nasal disease. Am J Med
Sci. 1898;116:677–92.
3. Ogura JH. Presidential address. Fundamental
understanding of nasal obstruction. Laryngoscope.
1977;87:1225–32.
4. Niinimaa V, Cole P, Mintz S, Shephard RJ.Oronasal
distribution of respiratory airow. Respir Physiol.
1981;43:69–75.
10 Sleep Disorders andtheNose: What Is theEvidence Base?
https://t.me/medicina_free
125
5. Olsen KD, Kern EB, Westbrook PR. Sleep and
breathing disturbance secondary to nasal obstruction.
Otolaryngol Head Neck Surg. 1981;89:804–10.
6. Georgalas C. The role of the nose in snoring and
obstructive sleep apnoea: an update. Eur Arch
Otorhinolaryngol. 2011;268:1365–73.
7. Ferris BG Jr, Mead J, Opie LH. Partitioning of
respiratory ow resistance in man. J Appl Physiol.
1964;19:653–8.
8. Fitzpatrick MF, Driver HS, Chatha N, Voduc N, Girard
AM. Partitioning of inhaled ventilation between the
nasal and oral routes during sleep in normal subjects.
J Appl Physiol. 2003;94:883–90.
9. Rundcrantz H. Postural variations of nasal patency.
Acta Otolaryngol. 1969;68:435–43.
10. Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich
CW.Respiration during sleep in normal man. Thorax.
1982;37:840–4.
11. Lavie P, Fischel N, Zomer J, Eliaschar I.The effects
of partial and complete mechanical occlusion of the
nasal passages on sleep structure and breathing in
sleep. Acta Otolaryngol. 1983;95:161–6.
12. Suratt PM, Turner BL, Wilhoit SC. Effect of intranasal obstruction on breathing during sleep. Chest.
1986;90:324–9.
13. Miljeteig H, Hoffstein V, Cole P.The effect of unilateral and bilateral nasal obstruction on snoring and
sleep apnea. Laryngoscope. 1992;102:1150–2.
14. McNicholas WT, Tarlo S, Cole P, Zamel N, Rutherford
R, Grifn D, Phillipson EA.Obstructive apneas during sleep in patients with seasonal allergic rhinitis.
Am Rev Respir Dis. 1982;126:625–8.
15. Meurice JC, Marc I, Carrier G, Sériès F. Effects of
mouth opening on upper airway collapsibility in normal sleeping subjects. Am J Respir Crit Care Med.
1996;153:255–9.
16. Fitzpatrick MF, McLean H, Urton AM, Tan A,
O'Donnell D, Driver HS. Effect of nasal or oral
breathing route on upper airway resistance during
sleep. Eur Respir J. 2003;22:827–32.
17. Zwillich CW, Pickett C, Hanson FN, Weil
JV. Disturbed sleep and prolonged apnea during
nasal obstruction in normal men. Am Rev Respir Dis.
1981;124:158–60.
18. White DP, Cadieux RJ, Lombard RM, Bixler EO,
Kales A, Zwillich CW.The effects of nasal anesthesia on breathing during sleep. Am Rev Respir Dis.
1985;132:972–5.
19. McNicholas WT, Coffey M, McDonnell T, O’Regan
R, Fitzgerald MX. Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. Am Rev Respir Dis.
1987;135:1316–9.
20. Djupesland PG, Chatkin JM, Qian W, Cole P, Zamel
N, McClean P, Furlott H, Haight JS. Aerodynamic
inuences on nasal nitric oxide output measurements.
Acta Otolaryngol. 1999;119:479–85.
21. Blitzer ML, Lee SD, Creager MA. Endotheliumderived nitric oxide mediates hypoxic vasodilation of resistance vessels in humans. Am J Physiol.
1996;271:H1182–5.
22. Leitzen KP, Brietzke SE, Lindsay RW. Correlation
between nasal anatomy and objective obstructive
sleep apnea severity. Otolaryngol Head Neck Surg.
2014;150:325–31.
23. Verse T, Dreher A, Heiser C, Herzog M, Maurer JT,
Pirsig W, Rohde K, Rothmeier N, Sauter A, Steffen
A, Wenzel S, Stuck BA.S2e-guideline: ENT-specic
therapy of obstructive sleep apnea in adults. Sleep
Breath. 2016;20:1301–11.
24. Stuck BA, Hofauer B.The diagnosis and treatment of
snoring in adults. Dtsch Arztebl Int. 2019;116:817–24.
25. Gaisl T, Haile SR, Thiel S, Osswald M, Kohler
M. Efcacy of pharmacotherapy for OSA in adults:
a systematic review and network meta-analysis. Sleep
Med Rev. 2019;46:74–86.
26. Kuhle S, Urschitz MS. Anti-inammatory medications for obstructive sleep apnea in children. Cochrane
Database Syst Rev. 2011;19:CD007074.
27. Liming BJ, Ryan M, Mack D, Ahmad I, Camacho
M. Montelukast and nasal corticosteroids to treat
pediatric obstructive sleep apnea: a systematic review
and meta-analysis. Otolaryngol Head Neck Surg.
2019;160:594–602.
28. Camacho M, Malu OO, Kram YA, Nigam G, Riaz M,
Song SA, Tolisano AM, Kushida CA.Nasal dilators
(breathe right strips and NoZovent) for snoring and
OSA: a systematic review and meta-analysis. Pulm
Med. 2016;2016:4841310.
29. Moxness MH, Nordgard S.An observational cohort
study of the effects of septoplasty with or without
inferior turbinate reduction in patients with obstructive sleep apnea. BMC Ear Nose Throat Disord.
2014;14:11.
30. Park CY, Hong JH, Lee JH, Lee KE, Cho HS, Lim
SJ, Kwak JW, Kim KS, Kim HJ. Clinical effect of
surgical correction for nasal pathology on the treatment of obstructive sleep apnea syndrome. PLoS One.
2014;9:e98765.
31. Shuaib SW, Undavia S, Lin J, Johnson CM, Stupak
HD. Can functional septorhinoplasty independently
treat obstructive sleep apnea? Plastic Reconstr Surg.
2015;135:1554–65.
32. Xiao Y, Han D, Zang H, Wang D.The effectiveness of
nasal surgery on psychological symptoms in patients
with obstructive sleep apnea and nasal obstruction.
Acta Oto-Laryngol. 2016;136:626–32.
33. Verse T, Baisch A, Maurer JT, Stuck BA, Hörmann
K. Multilevel surgery for obstructive sleep apnea:
short-term results. Otolaryngol Head Neck Surg.
2006;134:571–7.
34. Li HY, Wang PC, Chen YP, Lee LA, Fang TJ, Lin
HC.Critical appraisal and meta-analysis of nasal surgery for obstructive sleep apnea. Am J Rhinol Allergy.
2011;25:45–9.
35. Rombaux P, Liistro G, Hamoir M, Bertrand B,
Aubert G, Verse T, Rodenstein D.Nasal obstruction
and its impact on sleep-related breathing disorders.
Rhinology. 2005;43:242–50.
36. Li HY, Lee LA, Wang PC, Chen NH, Lin Y, Fang
TJ.Nasal surgery for snoring in patients with obstructive sleep apnea. Laryngoscope. 2008;118:354–9.
126
https://t.me/medicina_free
T. Verse and S. Müller
37. Li HY, Lin Y, Chen NH, Lee LA, Fang TJ, Wang
PC.Improvement in quality of life after nasal surgery
alone for patients with obstructive sleep apnoea and
nasal obstruction. Arch Otolaryngol Head Neck Surg.
2008;134:429–33.
38. Stapelton AL, Chang YF, Soose RJ, Gillman GS.The
impact of nasal surgery on sleep quality: a prospective outcome study. Otolarynghol Head Neck Surg.
2014;151:868–73.
39. Verse T, Hörmann K.The surgical treatment of sleeprelated upper airway obstruction. Dtsch Arztebl Int.
2011;108:216–21.
40. Randerrath WJ, Verbraecken J, Andreas S, Bettega G,
Boudewyns A, Hamans E, Jalbert F, Paoli JR, Sanner
B, Smith I, Stuck BA, Lacassagne L, Marklund M,
Maurer JT, Pepin JL, Valipour A, Verse T, Fietze
I. Non-CPAP therapies in obstructive sleep apnoea.
Eur Respir J. 2011;37:1000–28.
Соседние файлы в папке Библиотека им академика М.И. Перельмана