Rhinitis and Sleep Apnea

Maria T. Staevska, MD, Mariana A. Mandajieva, MD,

and Vasil D. Dimitrov, MD, PhD

Address
Clinic of Asthma, Allergology, and Clinical Immunology, Medical
UniversitySofia, University Hospital Alexandrovska, 1, St. George
Sofiisky str., 1431, Sofia, Bulgaria.
E-mail: marista@rtb-mu.com
Current Allergy and Asthma Reports 2004, 4:193199
Current Science Inc. ISSN 1529-7322
Copyright 2004 by Current Science Inc.

The nose and pharynx begin the upper airway system and
represent a continuum. This is the biologic basis for the
mutual influences of rhinitis and obstructive sleep apnea
(OSA). Sleep-disordered breathing has a large differential
diagnosis that includes snoring, upper airway resistance
syndrome, and severe OSA. Nasal obstruction is an independent risk factor for OSA, but there is no correlation of
daytime nasal resistance with the severity of OSA. However, nasal resistance was an independent predictor of
apneahypopnea index in a recent study of nonobese OSA
patients. Rhinitis alone is associated with mild OSA, but
commonly causes microarousals and sleep fragmentation.
Reduction of nasal inflammation with topical treatment
improves sleep quality and subsequent daytime sleepiness
and fatigue. Patient compliance with the nasal continuous
positive airway pressure (nCPAP) device is relatively low, in
part due to adverse nasal effects.

Introduction
Allergic rhinitis (AR), the most prevalent allergic disorder,
and nonallergic rhinitis affect more than 25% of the population [1]. AR is characterized by local symptoms, such as
nasal obstruction, itching, sneezing, rhinorrhea, and postnasal drip, as well as daytime sleepiness, fatigue, headaches, and malaise [1]. The latter systemic symptoms are
especially related to poor performance and concentration
at school and work, and to overall impairment of quality
of life. It is generally accepted that complaints of sleepiness, fatigue, and malaise are secondary to the action of
high levels of inflammatory mediators, such as tumor
necrosis factor (TNF)-, interferon (IFN)- , and other
cytokines on the hypothalamus [2]. There is an increasing
body of evidence, however, that the disabilities might be
partially due to nasal congestion and sleep-disordered
breathing [35].
Obstructive sleep apnea syndrome (OSAS) is characterized by: 1) complete or partial collapse of the upper air-

ways during sleep, with consequent cessation of breathing,

despite ongoing respiratory effort; and 2) coexistent daytime somnolence. OSAS is an important health problem,
given its associated adverse consequences and its prevalence of least 4%. Two kinds of clinical sequelae are associated with the disorder. Neuropsychiatric complications
include sleepiness; depression; cognitive dysfunction; disruption of professional, family, and social life; and inattention that can result in road and industrial accidents.
Cardiovascular complications include pulmonary and systemic hypertension due to chronic sleep-related hypoventilation, congestive heart failure, coronary heart disease,
myocardial infarction, and stroke [6].
Obesity, increased neck circumference, aging, male sex,
acromegaly, hypothyroidism, and relatively rare craniofacial abnormalities are strong risk factors for sleep-disordered breathing (SDB). Currently, the most important
clinical risk factors are those of high prevalence that potentially can be modified [7]. Rhinitis meets these criteria,
because it is a syndrome of high and increasing prevalence
with relatively easily modified nasal congestion as a major
contributing factor. Although earlier studies failed to demonstrate a linear correlation between nasal resistance and
the severity of OSA [79], in 2000, Lofaso et al. [10] used
stepwise multiple regression analysis to show that daytime
nasal obstruction represented an independent risk factor
for OSAS. Rhinitis had a weaker correlation than cephalometric landmarks, obesity, and male sex, but was stronger
than age. Recently, several reviews discussing the role of
nasal obstruction in the genesis of SDB have been published [11,12,13].
Finally, OSA might be a chronic inflammatory condition characterized by high levels of cytokines and inflammatory mediators that are similar to those of allergic
rhinitis and asthma. Asthma might be more severe and difficult to control if OSA is present. Nasal continuous positive airway pressure (nCPAP) therapy can improve both the
OSA and asthma [14,15]. The inflammatory mediators
generated by OSA could possibly account for the cardiovascular and asthmatic complications [16]. The cause of the
OSA-related inflammation and its role in rhinitis are still
open to debate.

Scope of Sleep-disordered Breathing

Sleep-disordered breathing is a large entity encompassing a
variety of conditions of sleep-related regular respiratory

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Rhinitis

disturbances. One could represent it as a continuum [17]:

Intermittent snoring Persistent or habitual snoring
Upper airway resistance syndrome Mild OSAS Severe
OSAS Obesityhypoventilation syndrome.
The mildest form is snoring, ranging from intermittent
to persistent, with lack of any detrimental effect on individual health. Snoring affects 35% of the middle-aged population, with a distribution of 44% men and 28% women.
It becomes more common with age [18]. Snoring is produced by vibration of the soft palate and partially collapsed pharyngeal walls due to turbulent airflow. States
causing nasal obstruction, such as nasal polyps, hypertrophied turbinates, and nasal septal deviation are often
involved in this process. Recently, a population-based
cohort study showed that nasal congestion at night is a
strong independent risk factor for habitual snoring with an
odds ratio of 4.9 [18].
At the other end of the spectrum is Pickwick or obesityhypoventilation syndrome. This is the most severe form of
SDB, and is characterized by persistent hypoxia and hypercapnia, high morbidity, and mortality.
In the middle of the continuum is OSAS. Some additional terms are needed to outline this disorder. Apnea is
defined as cessation of airflow for at least 10 seconds. It
could be central, obstructive, or mixed. Central sleep
apnea, which is rare and beyond the scope of this review, is
due to absence of brainstem-derived respiratory efforts.
Obstructive sleep apnea is much more common and
results from complete obstruction of the upper airways,
despite persistent ventilatory effort. Hypopnea results from
incomplete upper airway obstruction, and is defined by at
least a 30% reduction of airflow. The apneahypopnea
index (AHI) is the average number of apnea and hypopnea
events per hour of sleep. AHI less than 5 is considered normal. OSA is characterized by an AHI of 5 or higher, and is
associated with a 4% decrease in oxygen saturation. OSA is
divided into three severity levels: mild with AHI of 5 to 15;
moderate with AHI of 15 to 30; and severe with AHI higher
than 30. Apnea and hypopnea always cause arousal. These
repetitive arousals underlie sleep fragmentation, resulting
in daytime sleepiness. OSA, together with daytime sleepiness, constitutes OSAS [19].
Subgroups of patients have excessive daytime sleepiness because of repetitive nocturnal arousals, without
apnea, hypopnea, or oxygen desaturation. In these cases,
the airflow channel of the nocturnal polysomnogram
shows less severe inspiratory flow limitation. Inspiratory
esophageal pressures show repetitive, increased upper airway resistance. The respiratory efforts aimed at overcoming
this increased upper airway resistance result in transient
arousals. The term respiratory effort-related arousal
(RERA) is applied to this event.
Guilleminault et al. [20] noted that the repetitive
RERAs were pathognomonic for the condition and introduced the term upper airways resistance syndrome
(UARS). Because nasal resistance is responsible for at least

40% of total airway resistance, its increase could result in

UARS. UARS is the mildest form of SDB and shows better
sleep fragmentation responses with treatment of nasal congestion than other OSA patients [12,21]. Like OSA, UARS
is characterized by excessive daytime sleepiness and fitful
sleep. However, snoring is not present in all patients.
Although UARS was often placed between snoring and
OSAS, it could be a distinct disorder [22]. Unlike OSA,
UARS patients are predominantly nonobese, younger
women with histories of fainting, cold extremities, low
blood pressure, and postural hypotension [22]. These
patients frequently complain of sleep-onset insomnia,
fatigue, headaches, depression, irritable bowel syndrome
(IBS), bruxism (teeth grinding), gastroesophageal reflux
disease, and rhinitis [23]. The arousal threshold for
increased inspiratory effort is elevated in OSA, but is lower
than normal in UARS. As a result, UARS patients wake up
very easily in response to even mild increases in respiratory
effort. Guilleminault and Chowdhuri [22] hypothesize
that different functional arousal pathways are dysfunctional in the two syndromes. Blunted mechanoreceptor
responses predominate in OSA patients, whereas UARS
patients have intact or even increased sensitivity of mechanoreceptor systems.
Electroencephalograms (EEGs) show that delta sleep
and the percentage of sleep spent in alpha rhythms are relatively increased in UARS patients. Delta sleep is decreased
in OSA patients. UARS patients have evidence of alpha
delta sleep. This is the appearance of waking alpha
rhythms that intrude into the slow-wave delta rhythm that
characterizes deep sleep. This EEG finding is not a feature
of OSA. Curiously, alphadelta sleep is widespread in
disorders characterized by chronic fatigue. These include
chronic fatigue syndrome, fibromyalgia, migraine/tension
headache syndrome, IBS, and temporomandibular joint
syndrome (TMJ). Gold et al. [23] demonstrated a correlation between UARS and increasing prevalence of alpha
delta rhythm, IBS, headache, and sleep-onset insomnia.
Patients with OSA had low correlations with these conditions. Rhinitis was present in approximately 30% of UARS
patients in this study.
Levander [24], in a recent review on the pathophysiology of dysfunctional disorders, discussed the concept of
sensory sensitization dysfunctional disorder that could
be applied to the functional somatic syndromes mentioned earlier and to dry eyes and mouth syndrome
(SICCA syndrome), gastralgia, interstitial cystitis, chronic
prostatitis, vestibulitis syndrome, and nonallergic rhinitis.
Nonallergic rhinitis shows a significant overlap with
chronic fatigue syndrome: 76% of chronic fatigue syndrome patients have significant rhinosinusitis complaints
[25]. It is tempting to speculate that UARS is part of the
spectrum of sensory sensitization dysfunction disorders.
Coexisting nonallergic rhinitis could be an additional
aggravating factor for UARS, resulting in increased inspiratory effort due to nasal obstruction.

Rhinitis and Sleep Apnea Staevska et al.

Pathophysiology of
Sleep-disordered Breathing
The pharynx is a complex structure with opposing functions, such as breathing and swallowing, as well as phonation. It consists of three main compartments: the
nasopharynx, oropharynx, and laryngopharynx. The
nasopharynx is the area between the nasal turbinates and
hard palate. The oropharynx is the space between the hard
palate and epiglottis. The laryngopharynx is also called the
hypopharynx. It is situated between the base of the tongue
and the larynx. The narrowest portion of the pharynx is
the retropalatal region of the oropharynx, or velopharynx.
The oropharynx has no bony structural support and is the
most easily collapsible part of this airway. The normal
pharynx has an elliptical cross-sectional area with a major
lateral diameter. The pharynx walls are made up of muscles (dilators and constrictors), lymphoid tissue, and pharyngeal mucosa. There are also parapharyngeal fat pads in
the velopharynx and in the retroglossal part of the
oropharynx [17,26,27]. Dilator muscles maintain upper
airway patency. Normally, their activation precedes the
activation of the diaphragm and ensures upper airway
patency, despite the negative intraluminal pressure during
inspiration [28,29]. The constrictor muscles participate in
expiration. During sleep, the dilator muscles are hypotonic. This results in a normal narrowing of the pharynx.
This is normally compensated by the relative hypoventilation and higher PaCO2 setpoint for chemoreceptors during
sleep. These factors make upper airway stability vulnerable
during sleep.
Remmers et al. [30] first identified the oropharynx as
the exact location of collapse in OSA patients. He proposed
that this is caused by imbalance of the negative intraluminal pressure and opposing forces originated by the pharyngeal dilator muscles. Unlike normal subjects, OSA patients
have narrower pharyngeal airways due to genetic or obesity-related structural abnormalities. Furthermore, the
longest diameter of the pharyngeal cross-sectional area is
anteriorposterior, making it more round and susceptible
to lateral-wall collapse. Other factors that tend to narrow
the pharyngeal airway include neck flexion, jaw opening,
gravidity, and surface adhesive forces. There are data that
OSA patients maintain their anatomically narrower airway
through higher activity of their dilator muscles [31]. However, the physiologic dilator muscle hypotonia that occurs
during sleep fails to prevent nocturnal pharyngeal obstruction. Environmental factors that can further attenuate dilator muscle activation are alcohol, sleep deprivation,
sedatives, and anesthesia.
King et al. [32] showed that pharyngeal obstruction is
the primary defect in OSA, as opposed to reflex or arousal
response abnormalities. These can be illustrated if the
pharynx is represented as an elastic tube. The tubes
patency is determined by its transmural pressure (Ptm).
Ptm is defined as the difference between the negative
intraluminal pressure (Pil) and the pressure created by the

195

surrounding dilator muscles (Psurr) (Fig. 1). Healthy subjects succeed in maintaining positive transmural pressures
of approximately 0 to +10 cm H2O during sleep, despite
the lower dilator muscle tone (Fig. 1B) [31]. Apneics, however, fail to maintain positive pressure during sleep and
develop airway collapse due to negative transmural pressure (Fig. 1C). This model can be further simplified. If
there is no flow through the airway, Pil = 0 = atmospheric
pressure. In this situation, the absolute values of the transmural pressure and of the pressure of the surrounding tissue would be equal, but their mathematic signs would be
opposite (Ptm = 0 Psurr Ptm = - Psurr). Hence, healthy
people can maintain positive transmural pressure by maintaining negative surrounding tissue pressures. The specific
value of Psurr at the time of collapse is called the critical
closure pressure (Pcrit). Pcrit exceeds -41 cm H 2 0 in
healthy, awake subjects. In OSA patients, it ranges from -41
to -17 cm H20 [6]. The dilator muscle hypotonia during
sleep causes Pcrit to rise to -13 cm H20 in normal subjects
[6], to -6.5 cm H20 for asymptomatic snorers [6], -4.0 cm
H20 in UARS patients [27], -1.6 cm H20 for patients with
hypopneas but no apneas [6], and to +2.5 cm H 2 0 for
patients with frank apneas [6]. As a result, OSA could be
considered to be a condition resulting from pathologically
elevated Pcrit during sleep. Pcrit is an important index,
because it defines the lowest level of nCPAP that will keep
the upper airways patent [6].
The Starling resistor model can be applied to the
upper airways. Under conditions of flow limitation, the
maximal inspiratory flow is determined by the change in
pressure between the upstream (ie, nasal passage) pressure
and that at the most collapsible site of the upper airway.
The downstream (tracheal) pressure generated by diaphragmatic inspiration does not affect this relationship
(Fig. 1). That means that in the beginning of an inspiratory
effort, the pattern of airflow will increase in proportion to
the increase in the intraluminal pressure. However, when
the critical intraluminal pressure is reached, airflow will
remain constant, regardless of any continuing increase of
the diaphragmatic driving pressure. This plateau leads to
the characteristic flattened shape of the pressureflow
curve. Airway flow limitation is a very sensitive marker of
elevated intraluminal resistance. The maximal intraluminal pressure depends on two factors. The first is the transmural pressure discussed earlier. The second is the
resistance of the upstream segmentthat is, the nasal and
nasopharyngeal part of the upper airways. An increase in
airflow velocity in an attempt to maintain the intraluminal
pressure actually results in paradoxical pharyngeal collapse
due to the Bernoulli effect [28].
Any pathologic event that increases nasal resistance can
limit maximal upper airway airflow and contribute to OSA
or UARS. This includes all obstructive conditions of the
nasal cavity, such as nasal septum deviation, hypertrophy
of the inferior turbinates, stenosis of the nasal valve, nasal
polyps, the nasal congestion characteristic of rhinitis, and

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Rhinitis
Figure 1. Schematic
representation of the
pharynx as a collapsible tube enclosed in a
chamber. A, If intraluminal pressure (Pil) is
equal to the pressure of
the surrounding tissue
(Psurr), transmural
pressure is 0 (Ptm = Pil
Psurr = 0 Pil =
Psurr). B, If Psurr is
greater than Pil in absolute value, Ptm is positive (Ptm = Pil Psurr
>0 Pil > Psurr Pil is
less negative than
Psurr). C, If Psurr is
smaller than Pil in
absolute value, Ptm is
negative (Ptm = Pil Psurr < 0 Pil is more
negative than Psurr.)

adenoidal hypertrophy [33]. One response to nasal airflow

obstruction is to switch to unstable oral breathing. However, this eliminates nasal reflexes and could facilitate
sleep-disordered breathing [11].
Complete closure of upper airway causes apnea. Apnea
leads to hypoxia and hypercapnia. These chemical changes
stimulate increased respiratory efforts that can provoke an
arousal from sleep. The arousal itself stimulates pharyngeal
dilator muscle activity that can restore airway patency. The
repetitive nature of these events leads to fragmented sleep,
disrupted sleep architecture, intermittent hypoxia and
hypercapnia, and adrenergic stimulation [16]. The periods of high airway resistance result in a significant number
of cortical arousals, sleep fragmentation, and subsequent
daytime sleepiness.

Artificially Induced Nasal Obstruction

Early studies of partial or complete nasal obstruction identified the positive relationship between nasal obstruction
and SDB. Zwillich et al. [34] observed that acute viral rhinitis caused poor quality of sleep and OSA in some infants.
They investigated the sleep of 10 healthy men who had
intranasal balloon cannula inserted to artificially induce
nasal obstruction. They compared full night recordings of
sleep stages and breathing rhythms before and during
nasal obstruction. They found significantly reduced time
spent in deep sleep and, conversely, a significant increase
in stage 1 nonrapid eye movement (REM) light sleep.
They also demonstrated a twofold increase in cortical
arousals and awakening as a consequence of the increased
number of apneas. Apneas were also significantly more frequent during nasal obstruction. Oxygen saturation was
studied in four subjects using an ear oximeter. Desaturation with SaO2 less than 90% was found 255 times during

obstructed sleep compared with 27 times during control

sleep. Olsen et al. [35] investigated eight normal subjects
randomized in a cross-over fashion to have their noses
obstructed by nasal packing. Sleep records were compared
between nights with open and obstructed nasal passages.
There was prolongation of stage 1 non-REM sleep, and significant increases in obstructive hypopneas and apneas.
Taasan et al. [36] investigated the effect of nasal packing on
seven patients who had undergone nasal polypectomy or
septoplasty. They found that all patients had significantly
increased number, frequency, and duration of cortical
arousals during the night of nasal packing. Lavie et al. [37]
studied the effects of partial or complete unilateral and
bilateral nasal obstruction in 10 normal young adults. They
demonstrated a significant increase in the number of
apneas in the setting of bilateral nasal occlusion. They also
found a significant increase of nonapneic breathing disorders resulting in microarousals and the amount of waketime during sleep. Suratt et al. [38] used gauze impregnated with petrolatum to induce acute bilateral nasal
obstruction. They found a statistically significant increase
in sleep latency, REM latency, and a trend toward lighter
sleep and less slow-wave and REM sleep. The number of
apneas, hypopneas, and minutes of obstructive events per
hour of sleep were also significantly increased.

Studies Evaluating Nasal Resistance in

Obstructive Sleep Apnea Patients
To test the hypothesis that the nose serves as a Starling
resistor, Blakley and Mahowald [9] compared nasal resistance by anterior rhinomanometry in 37 normal subjects
and 53 patients with OSA. Nasal resistance was increased
in OSA patients compared with the normal group,
although there was no linear correlation with apnea severity. In contrast, there were no differences in nasal resistance
in 71 OSA patients and 70 non-OSA heavy snorers [8]. This
might have been because chronic nasal congestion is a
strong risk factor for snoring [18]. Duchna et al. [39]
assessed 56 SDB patients who had either normal or
impaired nasal patency. They found significantly more
subjective night-time dyspneic episodes and higher apnea
index scores in those with nasal obstruction, but no significant differences in the numbers of hypopneas or SaO 2.
Young et al. [7] used anterior rhinomanometry to examine
a population-based sample of 911 subjects and failed to
demonstrate a linear correlation between nasal resistance
and sleep indices. In post hoc analysis, the subset with
allergic nasal congestion was 1.8 times more likely to have
an AHI higher than 1 than were nonallergic subjects.
In 2000, Lofaso et al. [10] proved that nasal obstruction was an independent risk factor for OSA. The investigators performed posterior rhinomanometry in the awake
state and sleep polysomnography in a prospective study of
541 unselected, consecutive snorers. The authors rigorous
criteria for OSA (AHI > 15) was met by 259/541 (48%).

Rhinitis and Sleep Apnea Staevska et al.

OSA patients had significantly higher nasal resistance than

the non-OSA patients. Subjects with nasal resistances 3
hPa/L/s or more were more prevalent in the OSA group,
with a significant odds ratio of 2.2. Stepwise multiple linear regression analysis ranked the explained variances (R2)
of AHI as hyoid bone position 6.2%, obesity 4.6%, male
sex 3.0%, nasal obstruction 2.3%, increasing age 1.3%,
and mandibular characteristics 0.9%.
De Vito et al. [33] used anterior rhinomanometry in the
seated and supine positions and demonstrated that 44% of
36 consecutive OSA patients had nasal obstruction. Again,
there was no significant correlation between nasal resistance and the degree of OSA. Virkkula et al. [40] found
an association between nasal resistance and the cross-sectional area of the pharyngeal airway at the base of the
tongue in the supine position. Nasal resistance and the
change into a relaxed mandibular position during recumbency were independent predictors of AHI among patients
with normal body mass index (BMI). The authors considered the possibility that there are several subtypes of OSA
with different pathogenic factors. In some, nasal mucosal
receptors might regulate pharyngeal dilator muscle activity.
Impaired nasal breathing could lead to OSA.
Physical examination of 202 subjects showed a higher
prevalence of nasal obstruction in OSAS compared with
non-OSAS subjects [41]. The relative risk of OSA with a
high Mallampati class (3 and 4) was 1.95 for all OSA
patients and 2.45 if nasal obstruction was present. They
concluded that Mallampati score was associated with OSA
only if there was concomitant nasal obstruction. These
findings endorsed the hypothesis that impaired nasal and
oral patency were risk factors for OSA.

Studies on Patients with Allergic Rhinitis

The influence of disordered nasal breathing on sleep was
first investigated in 14 allergic rhinitis patients [3]. All
showed periodic breathing, hypo- and hyperpneic episodes, and microarousals. The microarousals were 10 times
more frequent than in normal subjects. Increased upper
airway resistance and nasal discharge were thought to
cause these problems. Several of these patients had difficulties falling asleep, nocturnal awakenings, and excessive
daytime sleepiness. Changes during and after the ragweed
season were evaluated in seven seasonal AR subjects [42].
Nasal resistance and the number of obstructive apneas
were significantly higher during ragweed season compared
with after the season. Males had a correlation between the
seasonal change in nasal resistance and the corresponding
frequencies of obstructive sleep apnea episodes. Rhinitisinduced apneas were associated with only mild decreases
in SaO2. The number of obstructive apneas in AR patients
was still fewer than in the typical OSAS patient. They conclude, however, that nasal resistance due to allergic rhinitis
could be an important factor in the pathogenesis of OSA.
This led to a comparison of allergic rhinitis patients with or

197

without mild OSA [43]. Nasal obstruction was measured

by acoustic rhinometry before and after topical nasal
decongestion. The minimal cross-sectional area at the anterior nasal valve was significantly smaller in the OSA than
the non-OSA group (P = 0.03). The non-OSA patients had
a significant subjective improvement in nasal congestion
after vasoconstriction, whereas the OSA patients did not.
This indicated that reversible, allergic nasal obstruction
was associated with mild OSA.

Effect of Local Treatment of Nasopharynx on

Sleep-disordered Breathing
Sleep fragmentation and microarousals can unfavorably
influence daytime energy levels, mood, and daytime function [44]. Nasal steroids were used to treat 20 perennial
allergic rhinitis patients in a double-blind, placebo-controlled trial [4]. Subjective scores of nasal congestion and
sleep were significantly improved in the topical corticosteroid-treated patients compared with placebo group. Daytime sleepiness also improved, but did not achieve
significance (P = 0.08). Unfortunately, no objective measurements of sleep and nasal obstruction were included in
the study. Azelastine was also found to significantly
improve subjective sleep scores in 24 allergic rhinitis subjects [45]. However, there were no differences in nasal congestion and daytime sleepiness. The effects of nasal
fluticasone on OSA related to adenoidal and tonsillar
hypertrophy were assessed in 13 children [46]. AHI
decreased significantly from 10.7 to 5.8. The frequencies of
hemoglobin desaturation and respiratory movement/sleep
arousals were also improved compared with the placebo
treatment. There were no changes in adenoid sizes. The
effects of budesonide were assessed using the Epworth
Sleepiness Scale, Functional Outcomes of Sleep Questionnaire, Rhinoconjunctivitis Quality of Life Questionnaire, and a daily diary for nasal symptoms, sleep
problems, and daytime fatigue records [47]. Budesonide
significantly improved daytime fatigue, somnolence, and
quality of sleep

The Impact of Obstructive Sleep Apnea on the

Nose: Does Obstructive Sleep Apnea Impact
Nasal Mucosa?
Rubinstein [48] demonstrated that patients with OSA
without clinical symptoms of rhinitis have nasal inflammation. They had a significantly increased number of cells,
percentages of neutrophils, and higher concentrations of
bradykinin and vasoactive intestinal peptide (VIP) in nasal
lavage fluid. Intracellular adhesion molecule-1 (ICAM-1),
interleukin-6 (IL-6), IL-8, and monocyte chemoattractant
protein-1 (MCP-1) are also elevated. Exhaled air condensates also showed increased indicators of inflammation
and oxidant stress including nitric oxide, pentane, and 8isoprostane in OSA patients compared with normal con-

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Rhinitis

trol subjects [16,49]. All these changes can be reversed by

application of nCPAP therapy. Similar mediators act in
allergic rhinitis and asthma. There is some evidence that
OSA is associated with more severe asthma, and that both
improve with nCPAP therapy [14,15]. A proinflammatory
effect of OSA could also be related to the cardiovascular
complications of sleep apnea [16].

The Impact of Continuous Positive Airway

Pressure on Nasal Mucosa
Night ventilation with nCPAP is the gold standard for treatment of moderate and severe OSA. The flow generator provides air under positive pressure through a nasal or facial
mask. This provides a pneumatic splint of the upper airways. Polysomnography is used to measure Pcrit, which sets
the necessary pressure within a range of 4 to 20 cm H2O
[16,50]. Compliance with nCPAP treatment is relatively low
because of undesirable side effects. These include nasal congestion, rhinorrhea, crusted nose, epistaxis, sneezing, and
dryness. Although nasal disturbances are very common in
OSA, nCPAP treatment can aggravate their rhinitis. Nasal
congestion depends on the temperature and humidity of the
air being breathed. Cold, dry air can induce inflammatory
mediator release. Heated, humidified air often reduces the
nasal complaints and improves compliance. Nasal steroids,
decongestants, anticholinergic agents, allergy shots, and surgical correction of nasal cavity anatomical obstructions
might still be necessary to obtain satisfactory compliance
with nCPAP therapy [16,50].

Conclusions
Obstructive sleep apnea is largely the result of nasal and pharyngeal abnormalities. The full differential diagnosis and
pathogenic factors have not yet been fully discerned. The
influence of the nose on pharyngeal collapse is apparent
from the Starling resistor model of the pharynx as a collapsible tube. Nasal reflexes could play a role in maintaining
pharyngeal patency, but this is controversial. Studies showed
that artificial nasal obstruction clearly induced SDB. However, there was no linear correlation of nasal resistance with
apnea severity in either OSA or non-OSA patients. Overall,
nasal obstruction is an independent but relatively weak risk
factor for OSA. However, increased nasal resistance was a
stronger, independent predictor of the AHI in a nonobese
subgroup of OSA patients with less severe sleep disorders
[40]. Also, within the continuum of SDB is UARS [20].
UARS can be subdivided into two main subtypes: obese,
heavy snorers at risk for OSA, and nonobese, nonsnoring
patients who might have functional somatic syndromes. The
latter group appears to have a strong link with nonallergic
rhinitis. Nasal steroid therapy and CPAP appear to be capable of reducing nasal inflammation and improving sleep
quality, nocturnal arousals, daytime sleepiness, and fatigue.

Allergic rhinitis subjects with coexisting OSA also improve

after successful immunotherapy.

Acknowledgments
The amount of literature in the area is extremely large. We
apologize for omitting some important studies for lack of
space. We would like to thank Dr. Dora Popova for her
indispensable help in reviewing the manuscript and Dr.
Alexander Simidchiev, for his valuable help with the literature search.

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