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O. Friedman and K. Wang
nitis medicamentosa is established by history,
and weaning of the medication is the rst-line
therapy.
22.4.2.6 Allergic Rhinitis
Allergic rhinitis is present in 10% to 30% of
adults and up to 45% of children. Nearly 50% of
patients with allergic rhinitis experience symptoms for >4months of the year as a result of seasonal changes, which introduce allergens that
cause increased mucus secretion and blood vessel
dilation within the nasal cavity [27]. Other symptoms include nasal itching, rhinorrhea, sneezing,
ocular itching, redness, and tearing.
Symptoms of allergic rhinitis are primarily
due to a combination of the early and late phase
allergic inammatory response. Repeat exposure
to a particular allergen sensitize the host. When
the allergen comes in contact with the nasal
mucosa of a sensitized host, immunoglobulin E
(IgE) receptors on mast cells cross-link, resulting
in the degranulation of these cells and the release
of histamine and proteases. A wide array of proinammatory molecules is also released. It is the
release of these proinammatory molecules that
causes swelling and mucus secretion seen in
allergic rhinitis [28].
22.4.2.7 Nasal Polyposis
Nasal polyps are semitranslucent, pale gray,
benign inammatory lesions of asymmetric size
found in the paranasal sinuses or nasal cavity. It
is estimated that they may affect as much as 4%
of the population. Nasal polyps can reach
3–4 cm in length and may cause symptoms,
such as nasal obstruction, nasal discharge, and
impairment of olfaction. Although the cause of
nasal polyposis is not clear, it is hypothesized to
be a result of chronic inammation due to
chronic infection, aspirin intolerance, alteration
in aerodynamics with trapping of pollutants,
epithelial disruptions, epithelial cell defects, or
inhalant and food allergies [29]. Histologically,
they are characterized by the inltration of
inammatory cells, mainly eosinophils. As a
result, total IgE concentration is signicantly
higher in nasal polyp tissue compared with
healthy nasal tissue [30].
22.4.2.8 Epistaxis
Also known as a nosebleed, epistaxis occurs
when a vessel within the nasal cavity is ruptured.
To facilitate proper humidifying and air conditioning of inspired air, the nasal mucosa contains
a rich vascular network that can rupture either
spontaneously or due to trauma. In the pediatric
population, epistaxis occurs most commonly due
to digital trauma. Another common cause of epistaxis is the improper use of topical nose sprays
causing trauma to the epithelium of the septal
mucosa. Epistaxis occurs more frequently in the
winter months due to the decrease in humidity
and temperature, which can cause a drying effect
on the nasal mucosa, increasing the opportunity
for mucosal disruption. A patient can be predisposed to epistaxis if they have anatomical deformities, such as septal deections, bony spurs, or
fractures. Additionally, any nasal obstruction that
disrupts airow can have a drying effect on the
nasal mucosa, also causing epistaxis.
Systemic epistaxis is commonly due to cardiovascular or hematological disorders, such as
hypertension, aberrations in clotting ability, or
inherited bleeding disorders. While there is an
undeniable association between hypertension
and epistaxis, the exact mechanism still remains
unclear. The ability to form blood clots is essential to both the prevention and control of epistaxis
[31, 32].
22.5 Treatment
In the last 10–15 years, there has been an
increased awareness of the nasal valve as a key
contributor of nasal airway obstruction, resulting
in a urry of scientic publications on the matter,
innovations in therapeutic options, and increasing applications of a multitude of both surgical
and nonsurgical treatments to correct the nasal
valve contribution to nasal obstruction.
Evaluation of the patient begins with a thorough
history, eliciting signs that may hint at nasal
obstruction and nasal valve collapse. Does the
patient mouth breathe, snore, awaken tired? Has
the patient used breathing dilator devices in the
past or had prior nasal surgery? The answers to
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these questions will help guide the patient and
surgeon in deciding whether there is a nasal valve
component to the nasal obstruction and whether
nasal surgery might be of benet.
In the past, surgical techniques described for
nasal valve repair have focused on secondary
nasal surgery following nasal valve damage as a
result of rhinoplasty [32–36]. With a better understanding of nasal valve physiology in the last
couple of decades, coupled with renements in
surgical techniques and thorough preoperative
examination, valve disorders can be better identied in previously unoperated individuals complaining of nasal obstruction. These patients can
initially be treated by the use of external nasal
dilator devices or other breathing devices to help
them experience the quality of life improvement
associated with corrective nasal valve surgery,
helping them make a more informed decision
before going through with surgery. Additionally,
the application of such breathing devices helps in
dening the site of obstruction more precisely in
order to optimize surgical outcomes [37]. Primary
and secondary functional nasal surgery with correction of the dysfunctional nasal valve has been
previously shown to signicantly improve quality of life in patients complaining of nasal
obstruction who have preoperative ndings of
nasal valve collapse [38–40].
22.5.1 Surgical Techniques
There have been many surgical techniques identied addressing the dysfunctional nasal valve in
the past few decades [21]. Although there is no
“gold standard” or “one size t all” technique
that can treat all causes and types of nasal valve
collapse, there are many useful techniques that
can be integrated into a surgical plan depending
on the needs of the patient. Nasal valve collapse
is the result of a narrow nasal valve or weak nasal
structures—thus, the overall goal of nasal valve
surgery is to widen the existing nasal valve area
and to strengthen the structural support elements
that maintain a patent valve area at rest, and minimize dynamic collapse of the nose that results
from the negative inspiratory forces of nasal
breathing. This section highlights a number of
techniques that have been found useful and are
used routinely as part of a comprehensive surgical correction of nasal valve dysfunction. There
are many others that may be found in the surgical
literature.
Both endonasal and external approaches may
be utilized for various nasal valve procedures
depending on the needs of the patient and surgeon preferences. Nasal valve surgery can be performed with either general anesthesia or local
anesthesia with sedation. In order to preserve
nasal anatomy, it is important to use as little anesthetic as necessary. These procedures are typically performed on an outpatient basis. It is also
essential to allow adequate time for the anesthetic
to take effect in order to minimize the bleeding
and maximize visualization. As with all surgeries, the general principle is to minimize the
aggressiveness of the surgical intervention in
order to minimize the potential risks of the procedure, but at the same time, to maximize the benet to the patient by selecting the proper group of
techniques for the proper situation.
22.5.2 Spreader Grafts
Spreader grafts can be used to treat both static
and dynamic internal nasal valve collapse. This
technique widens the narrowed valve angle,
thereby enlarging the nasal valve area, and is
advantageous in its ability to avoid affecting the
nasal septum, turbinate, and nasal mucosa. In
cases of static collapse, the widening of the middle third of the nose also results in a smoothening of the brow-tip aesthetic line. Ideally,
spreader grafts are made of septal cartilage, but
in cases of previous surgery in which inadequate
septal cartilage remains, conchal cartilage or rib
cartilage may be utilized. In patients with a
prominent dorsum undergoing dorsal reduction,
the upper lateral cartilage excess may be folded
on itself to lie between the septum and upper lateral cartilage to serve as an “auto-spreader graft”
or a “spreader ap.” Standard left hemitransxion incision is made to access the septal cartilage. Mucoperichondrial aps are elevated on
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one or both sides of the septum depending on the
septal pathology. Septoplasty is performed in
standard fashion, and septal cartilage is harvested for use as a spreader graft. The upper lateral cartilages are separated from the dorsal
septum to create space for the spreader grafts.
The spreader grafts should be long enough to
extend from under the nasal bones to the caudal
edge of the upper lateral cartilage. They measure
approximately 3–5 mm in height, and are the
thickness of the septal cartilage. Occasionally,
wider grafts may be required in which case a layering of multiple pieces of septal cartilage may
be stacked together to provide adequate thickness. Auto-spreader grafts or spreader aps
involve the turning of upper lateral cartilages to
lie between the septum and lateral upper lateral
cartilage in order to take advantage of the local
tissue excess. Spreader grafts have been shown
to be an effective treatment for internal nasal
valve collapse [41].
22.5.3 Alar Batten Grafts
Alar batten grafts are versatile grafts that may
also be used for both internal and external nasal
valve collapse depending on where they are positioned. These grafts are typically limited to use in
patients with idiopathic or congenital causes of
valve collapse. The rst step in an alar batten
graft is identication of the region of collapse [5].
If collapse is noted in the external nasal valve,
along the alar rim, the graft may be placed along
the rim of the nose to provide greater strength and
an outward curvature to the nasal rim. A marginal
incision is made along the inferior margin of the
lower lateral cartilage with a 15 blade scalpel,
while a double prong skin hook is utilized for
countertraction. A sharp scissor is used to dissect
a precise pocket along the nasal rim to the alarfacial groove. A cartilage graft measuring
3–10mm in width by approximately 7–10mm in
length is harvested from either the septum or the
conchal bowl and applied to the pocket. The graft
should extend from the alar-facial groove to
either the dome or to the area just lateral to the
soft tissue triangle in order to avoid a sharp edge
being seen through the skin of the soft tissue triangle. It may overlap the lateral crus superiorly.
If less support is needed, a smaller graft may be
used and has been referred to as an alar rim graft.
The marginal incision is closed with simple interrupted 5-0 chromic suture.
If collapse is noted in the middle third of the
nose, the alar batten graft is placed in the middle
third of the nose. An intercartilaginous incision is
made with the 15 blade scalpel and a precise
pocket is created supercial to the upper lateral
cartilage down to the pyriform aperture. The graft
is applied to the pocket, directly on the upper lateral cartilage. As the skin thins, these grafts may
become visible over time. An alternative technique involves the placement of the graft deep to
the upper lateral cartilage, most often at the scroll
region (the junction of the upper and lower lateral
cartilage) which is commonly the region of greatest collapse. The grafts are then sutured to the
overlying cartilage with 2 or 3 throws of 5-0
chromic or PDS suture to avoid movement of the
graft. These underlay grafts (similar to lateral
crural strut grafts) often hide better than the alar
batten grafts. The intercartilaginous incision is
then closed with interrupted 5-0 chromic suture.
22.5.4 Buttery Graft
The “buttery graft” is a highly effective procedure to correct nasal valve obstruction. It relies
on the elastic nature of conchal cartilage to spring
open the internal nasal valve. This graft provides
an outward force that widens the nasal airway,
leading to an increased internal valve angle [5].
Conchal cartilage is harvested through an
anterior helical rim incision or postauricularly. A
skin incision is made, followed by blunt and
sharp dissection to free the conchal cartilage. A
1-centimeter-wide by 2-cm-long cartilage graft
is harvested. Cautery to ensure hemostasis of the
ear harvest site is performed. Running 6-0 fast
absorbing gut suture was used to close the skin
incision and a compressive dressing was placed
on the donor site to prevent hematoma formation. The ear dressing is removed on postoperative day one.
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Intercartilaginous incision is made on both
sides of the nose and connected to a complete
transxion incision. Skin–soft tissue elevation is
achieved along the nasal dorsum in a standard
sub-SMAS plane to the rhinion and a subperiosteal plane from the rhinion to the nasion in order
to allow for proper skin redraping. If a signicant
or exaggerated supratip depression is present, the
graft is simply placed in the supratip depression
and its ends are secured to the caudal-most aspect
of the upper lateral cartilages with a single throw
of 5-0 PDS suture on either side. Once the graft is
xed in position, the skin is redraped and the dorsum is inspected and palpated for irregularities. If
irregularities are noted, the dorsum is reduced
further to create a smooth contour. Frequently,
especially in patients with thin skin, crushed cartilage grafts are placed on the nasal dorsum,
cephalic to the upper edge of the buttery graft,
to camouage the edges of the graft and create a
smooth dorsal contour. Mucosal incisions are
closed with 5-0 chromic suture.
22.5.5 Nasal Valve Flaring Suture
Skin and soft tissue envelope is elevated off the
osseocartilaginous understructure of the nose as
previously described. Once the incisions are
made and the tissues have been elevated, a retractor is placed under the skin ap to expose the
upper lateral cartilages. A horizontal mattress
stitch is thrown from one upper lateral cartilage
to the other and tied tightly over the nasal dorsum. As the suture is tied down, the upper lateral
cartilages elevate outward, thereby widening the
nasal valve angle and area. Nasal valve aring
sutures may be used alone or in combination with
various other techniques in order to maximize the
widening of the valvular airway. Incisions are
closed as previously described.
22.5.6 Maxillary Expansion
Maxillary expansion is a technique to consider in
individuals with maxillary constriction, a narrow
maxilla in the lateral dimension compared to
other facial bones, because maxillary constriction increases nasal resistance. Rapid maxillary
expansion is an orthodontic treatment that can
increase the lateral dimension of the maxilla.
This treatment is most often applied to children
but can also be performed in adults in conjunction with Lefort I osteotomies. Rapid maxillary
expansion has been shown to decrease nasal
resistance [42], and there is encouraging evidence that it can reduce apneas in young adults
with mild to moderate OSA [43, 44]. With regard
to the INV, a recent case series demonstrated an
increase in INV angle and area after surgical
maxillary expansion in adults which was associated with improved daytime sleepiness and subjective nasal obstruction [44].
22.5.7 Medical Treatment
22.5.7.1 Antihistamines
Although rst-generation oral antihistamines
(diphenhydramine, chlorpheniramine, and brompheniramine) was able to effectively treat allergic
rhinitis, these drugs have been associated with
strong sedative effects. Second-generation antihistamines, such as fexofenadine, loratadine, and
desloratadine, did not have these sedative effects.
Several studies have shown improvements in
symptoms associated with allergic rhinitis with
these antihistamines relative to the placebo
group. Because of their low adverse effect prole, these antihistamines are an effective rst-line
therapy for mild to moderate allergic rhinitis,
especially in patients with intermittent symptoms
and children.
These agents were followed by a generation of
nonsedating antihistamines, such as fexofenadine, loratadine, and desloratadine. Several studies have shown marked improvement in
symptom-based outcome data in patients with
allergic rhinitis compared to the placebo group.
The low adverse effect prole of these agents
supports their use as rst-line therapy for mild to
moderate allergic rhinitis, especially in patients
with intermittent symptoms and in children [45].
For chronic rhinitis, no convincing data are available to show treatment efcacy.
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22.5.7.2 Intranasal Corticosteroids
Topical corticosteroid sprays are indicated predominantly for the treatment of allergic rhinitis.
Currently, U.S.Food and Drug Administrationapproved agents are beclomethasone dipropionate, budesonide, ciclesonide, unisolide,
uticasone propionate, mometasone furoate, and
triamcinolone acetonide. These agents have been
shown to treat symptoms of allergic rhinitis (and
conjunctivitis) more effectively than do oral antihistamines. Beclomethasone, budesonide,
triamcinolone, uticasone, and mometasone have
been compared. The symptom-based outcomes
of these studies do not appear to clearly favor one
agent over another [46]. The overall adverse
effect prole of intranasal corticosteroids is
favorable and includes minor symptoms, such as
dryness, stinging, or burning. Epistaxis is the
most frequent major complication, occurring in
about 5% of patients. The risk of septal perforation and epistaxis may be reduced by instructing
the patient to direct the spray tip away from the
septum toward the lateral nasal wall. Adverse
systemic side effects, such as suppression of the
hypothalamic-pituitary axis and growth retardation, are no longer a relevant issue with contemporary agents.
22.5.7.3 Systemic Corticosteroids
Systemic corticosteroids are typically administered intramuscularly or orally. Intramuscular
agents include betamethasone dipropionate,
methylprednisolone acetate, betamethasone
phosphate, and triamcinolone acetonide.
Systemic corticosteroids are third-line agents
when antihistamines and intranasal corticosteroids have failed. These agents suppress endogenous cortisol production to a variable degree for
12 days to 3 weeks but are highly effective.
Axelsson and Lindholm showed symptomatic
improvement in 16 of 17 patients with allergic
rhinitis after administration of a single dose of
triamcinolone acetonide, while only 2 of 21
patients improved in the placebo group. This
relief can last throughout the allergic season [47,
48]. Few data are available to compare oral with
intramuscular corticosteroids. One study showed
plasma cortisol levels to be suppressed beyond
3weeks with oral prednisolone, 7.5mg daily, but
not with intramuscular corticosteroids [49]. With
adequate screening of patients for diabetes mellitus, glaucoma, hypertension, and osteoporosis,
the use of systemic corticosteroids, such as intramuscular triamcinolone acetonide, has become
an important and safe treatment of chronic
inammatory nasal disease.
22.6 Conclusion
An understanding of the nasal valves and how
they relate to nasal physiology is crucial in making good clinical decisions. Without proper functioning of the nose and nasal valves, the air
conditioning and humidifying capacity of the
nose is lost, along with the sense of olfaction—
prominent parts of our daily lives. A loss of any
of these functions leads to a great decrease in
quality of life, so it is important to preserve them.
It is common to treat valve disorders with surgery. Because the functional residual capacity of
the nose is unknown, it is important to practice
great reserve with the reduction of functional turbinate tissue, regardless of technique. Resection
of turbinate bone alone with preservation of all
mucosal and submucosal tissue is an alternative,
though this may also scar the submucosa and
mucosa and lead to additional problems.
Recognition of the nature and location of nasal
valve pathologies allows for adequate correction
and superb functional results in the majority of
cases. Concurrent rhinoplasty and functional
endoscopic sinus surgery can be performed
safely. The evolution of atraumatic surgical techniques has resulted in improved patient comfort
and speedy recovery.
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Nose andSleep Breathing
https://t.me/medicina_free
Disorders
Anne-LisePoirrier, PhilippeEloy,
andPhilippeRombaux
23
Core Messages
• The nose is the input channel for the airow.
Its rigid and erectile structures determine the
outline and the output of the airow in the
upper airway. Nose obstruction, due to reversible or nonreversible factors, produces collapsing forces that are manifested downstream
in the collapsible pharynx. Moreover, nose
pathologies result in unstable oral breathing,
decreased activation of nasal ventilatory reex
and reduced lung nitric oxide. Long-term oral
A.-L. Poirrier
Department of Otolaryngology, CHU-Liège, ULG,
Sart-Tilman B35, Liège, Belgium
e-mail: annelise@poirrier.be
P. Eloy
HNS & ENT Department, CHU-Mont-Godinne,
UCL, Yvoir, Belgium
Department of Otorhinolaryngology, Cliniques
Universitaires Saint-Luc, Brussels, Belgium
Institute of Neuroscience, Université Catholique de
Louvain, Brussels, Belgium
e-mail: philippe.eloy@uclouvain.be
P. Rombaux (*)
Department of Otorhinolaryngology, Cliniques
Universitaires Saint-Luc, Brussels, Belgium
Institute of Neuroscience, Université Catholique de
Louvain, Brussels, Belgium
HNS & ENT Department, Cliniques Universitaires
Saint Luc, Brussels, Belgium
e-mail: philippe.Rombaux@uclouvain.be
breathing impacts the craniofacial growth.
The management of nose pathologies could be
medical, mechanical (nose dilators) or surgical. Nasal management should be integrated
in a multimodal approach, considering the
involvement of a multilevel obstruction, and
truly reecting the complexity of sleepdisordered breathing.
23.1 Introduction
Sleep-disordered breathing (SDB) is a clinical
entity that is more and more recognised by physicians since the 1970s. It consists of a wide spectrum of sleep-related breathing abnormalities.
Those related to increased upper airway resistance include snoring, upper airway resistance
syndrome (UARS) and obstructive sleep apnoea–
hypopnoea syndrome (OSAHS) [1].
Snoring is associated with changes in the calibre of the upper airway which reduce ow and
increase airway resistance and is a manifestation
of increased turbulence in nasal ow [2, 3]. UARS
is caused by sleep-related ow limitation and
increase in upper airway resistance that precipitates arousals. UARS results in fragmented sleep
and excessive daytime sleepiness. Obstructive
sleep apnoea (OSA) syndrome is the complete or
partial collapse of breathing despite ongoing
respiratory effort. In patients with OSA, recurrent
obstruction of the pharynx during sleep results in
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
Ö. Ö. Celebi, T. M. Önerci (eds.), Nasal Physiology and Pathophysiology of Nasal Disorders,
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frequent episodes of airow cessation, leading to
signicant hypoxemia, fragmentation of sleep and
excessive daytime sleepiness. Obstructive sleep
apnoea is a leading cause of neuropsychiatric conditions (e.g. sleepiness, depression, cognitive dysfunction), cerebro- and cardiovascular diseases
(e.g. pulmonary and systemic hypertension, congestive heart failure, myocardial infarction,
stroke), metabolic disorders, sexual dysfunction,
loss in work productivity and increased risk of
motor vehicle accidents. OSA represents a major
public health problem [2].
In the Wisconsin Sleep Cohort, a stratied
random sample of Wisconsin state employees
aged 30–60years, the prevalence of OSA was
9% in women and 24% in men. The incidence
increases with age and tobacco and alcohol use
and is associated with metabolic and anatomical
features (obesity, retrognathia, high anteroposterior cervical diameter, macroglossia, large
tonsils, hypertrophic tongue base, large neck
size, gastroesophageal reux and nasal obstruction) [1, 2].
In the past, snoring was considered mainly as
a common ordinary disorder that only affected
men and was regarded as a social annoyance particularly for the bed partner. Nowadays many clinicians are regarding SDB as a spectrum of
diseases in which a patient can move from a
snorer without apnoea to a snorer with apnoea.
These disorders form actually a continuum. They
share a common physiopathology: a multilevel
airway obstruction [4].
As the nose plays a major role in the physiology of the respiratory tract, it is important to analyse the role of nasal disorders in the pathogenesis
of SDB and the effects of rhinologic treatments on
snoring and OSA.This topic has not yet received
denitive conclusions because of contradicting
reports in the literature. The number of patients
with polysomnography- documented OSA and
treated only by nasal surgery is far less important
than the number of cases treated with other therapies within the last two decades. The reason is
not quite clear, but one could be that the success
rate of nasal management alone for SDB is low
and the prediction of individual success is not
possible [3].
23.2 Nose Anatomy
andPhysiology
The nose is the input channel for the airow and
the “touchable” beginning of the airways. About
70% of the resistance met by the inspired airow
during its passage through the upper and lower
airways is located into the nose [5]. The nose
may be roughly divided into outer and inner anatomy. The outer nose is supported by the nasal
bones, the paired upper lateral and lower lateral
cartilages and the nasal septum and is covered by
the subcutaneous tissue and skin. The inner nose
includes the nasal septum on the medial wall of
the nasal cavity and the turbinates and the osteomeatal complex on the lateral wall. During inspiration, air is spinning into the nose through the
nasal valve. It can be divided into external and
internal nasal valves [6, 7].
The external nasal valve comprises the alar
cartilages, the nasal wing and the columella and
has a shape of an inverted “funnel”. Its role consists of orientating the airow into the nasal cavities without generating any resistance [8]. The
internal nasal valve is formed by the junction of
the upper lateral cartilages with the nasal septum,
the septum, the head of the inferior turbinate and
the piriform aperture (Fig. 23.1). The normal
angle between the upper lateral cartilages and the
septum is about 10–15° and represents the nasal
region with the smallest cross-sectional area and
the greatest resistance to nasal airow, crucial to
determine nasal resistance (RN) [6]. The internal
Nasal bone
Septum
nal nasal valve
External nasal valve
Fig. 23.1 Anatomy of the external nose
Upper lateral car
Lower lateral cartilage
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nasal valve plays a major role in the physiology
of the nose and particularly in air conditioning.
Its functioning depends on the shape of the cartilages, the tonus of the dilator muscles and the
degree of congestion of the nasal mucosa. The
airstream is rst directed upward through the
internal nasal valve, then bends about 90° posteriorly and ows via the nasopharynx to the lower
airways.
The diameter of the valve inuences directly
the velocity of the airow. On gentle inspiration,
the nasal valve is usually patent. During deep
inspiration (exercises or snifng), the airow
could create a Bernoulli’s effect, which accelerates the ow in this narrow cleft and decreases
the pressure on each side of the nasal vestibule
leading to the collapse of the nasal wing. Patients
suffering from a valve collapse may experience
nasal obstruction even during normal breathing.
The congestion of the nasal mucosa varies
physiologically, spontaneously and alternatively
from side to side with time. One side is blocked,
while the other side is patent. This alternates
every 3–7h in adults, leading to a spontaneous
cycle phenomenon called nasal cycle.
Surprisingly, thanks to this alternation of resistance on each side, the total nasal resistance
remains constant [9].
The paranasal sinus cavities play also a major
role in the physiology of the nose. The sinonasal
architecture is organised around the ethmoid
bone. The perpendicular plate of the ethmoid
articulates medially to the septal cartilage, while
the outer wall of the ethmoid, including middle
concha, articulates laterally with the vertical
plate (ascending process of the frontal bone) of
the maxilla. On the lateral nasal wall is the osteomeatal complex (OMC). The OMC comprises
the middle turbinate, the uncinate process and the
bulla ethmoidalis. In this particular anatomical
area drain the secretions from the anterior paranasal cavities, such as the anterior ethmoid cells,
the frontal sinus and the maxillary sinus.
Anatomical variations of the different structures
of the OMC have been described in the literature,
such as concha bullosa, paradoxically bent middle turbinate and medially bent uncinate process.
In the past ones believed that these anatomical
variations were associated to chronic rhinosinusitis. Now most authors do not consider these variations to be responsible of the pathogenesis of
chronic sinusitis by themselves.
23.3 Nose Pathologies
All pathologies causing nasal obstruction can
cause or worsen SDB [10]. The reasons for nasal
obstruction are complex and varied, but the
causes can be simplied as nonreversible factors,
such as anatomic deformities, and reversible factors, such as mucosal oedema and congestion
(Table23.1).
23.3.1 Nonreversible Factors
Deformity of the nasal septum and/or the nasal
pyramid can obviously be associated with uni- or
bilateral persistent nasal obstruction. In case of
nasal septum deviation, the patient can complain
of a uni- or bilateral nasal obstruction depending
on the shape, type and location of the deviation
Table 23.1 Causes of nasal obstruction
Nonreversible Internal/external valve collapse
Septal deviation, haematoma,
perforation
Other malformation of the nasal
framework
Vestibular synechiae or scars
Concha hypertrophy
Nasal polyposis, antrochoanal polyp
Foreign body, nasal packing
Benign tumours: angiobroma, inverted
papilloma
Malignant tumours: squamous cell
carcinoma, adenocarcinoma, melanoma
Meningocele
Choanal atresia and other craniofacial
anomalies
Reversible Allergic/nonallergic rhinitis:
NARES-NANIPER
Acute or chronic rhinosinusitis with or
without polyps
Drug-induced or occupational rhinitis
Atrophic rhinitis
Pregnancy
Wegener or other granulomatosis
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