Download SDB and Nasal Obstruction

Sleep Disordered Breathing And
Nasal Obstruction
BY
AHMAD YOUNES
PROFESSOR OF THORACIC MEDICINE
Mansoura Faculty Of Medicine
Functional valvular anatomy
• Nsal airflow follows a parabolic curve directed superiorly through
the nostril, upwards through the nasal cavity past the turbinates,
and posteriorly to the nasopharynx during inspiration.
• The internal nasal valve area is the narrowest part of the nasal
passage and is the major source of nasal resistance in normal
patients.
• Four structures compose the internal nasal valve: the upper
lateral cartilage superiorly, nasal septum medially, pyriform
aperture inferiorly, and the head of the inferior turbinate posteriorly.
• The narrowest portion of the internal nasal valve area is the
region between the septum and the caudal border of the upper
lateral cartilage. This structure is approximately 10–15 ° in
Caucasian subjects and can be wider in subjects of African and
Asian descent.
• Patients with internal nasal valve angles of <10° are more prone to
internal nasal valve collapse on inspiration.
Functional valvular anatomy
• The external nasal valve is composed of the nares
and the nasal vestibule.
• The nasal vestibule lies just inside the external
naris and is located caudal to the internal nasal
valve area.
• The septum is located medially along with the
columella, and the alar sidewalls are lateral to the
vestibule.
• Vibrissae are located within the vestibule under the
lateral crus and function as a filter for the inspired
air. They also serve to direct the air posteriorly into
the nasal cavity and to slow the inspired air.
Functional valvular anatomy
• The internal and external nasal valves function together to deliver a
smooth air current to the nasal cavities for humidification.
• The nasal valves can have a greater influence during deep inspiration
when the nostrils flare and the diameter of the external nasal valve is
increased.
• The Bernoulli principle is responsible for this effect in that the intraluminal pressure in the internal valve area decreases when the airflow is
increased through it.
• The cartilaginous structure of the nose serves as a counterbalance to
this tendency toward internal nasal valve collapse.
• The investing nasal musculature consists of elevator muscles, including
the procerus, levator labii superioris alaeque nasi and anomalous nasi.
The depressor muscles include the alar nasalis and the depressor septi
nasi while the compressor muscles include the transverse nasalis and
the compressor narium minor. There are also minor dilator muscles. The
alar muscles contract and dilate the internal nasal valve area in order to
keep the lumen open.
• Throughout normal nasal function, the internal nasal valve area should
remain unchanged.
Functional valvular anatomy
• Individuals with a narrow upper cartilaginous vault
have a narrower internal nasal valve and may
exhibit collapse in the resting state.
• Those subjects who possess weak upper lateral
cartilages and/or lateral nasal walls may be more
predisposed to collapse of the internal nasal valve
during inspiration.
• Those patients who have pre-existing or traumatic
septal deviation can suffer nasal obstruction.
• Insufficient support of the alar rim and alar lobule
may lead to external valve collapse on inspiration.
Causes of nasal obstruction
1- Structural causes: include septal deviation, hypertrophy of the
inferior or middle turbinates and fixed and inspiratory nasal valve
collapse, which may or may not be secondary to prior nasal surgery
or trauma.
• Nasal valve dysfunction may contribute to symptoms in as many as
13% of adults that report chronic nasal obstruction.
• The increased respiratory efforts by OSAHS patients during
episodes of apnea caused by palatal or tongue base obstruction
make these patients more prone to nasal valve collapse.
• In children, in addition to developmental abnormalities like choanal
atresia and craniofacial syndromes (e.g. Pierre Robin sequence),
adenoidal and to a lesser degree – tonsillar hypertrophy also
constitute an important cause for nasal obstruction, both of which
have an important correlation with OSAHS in this patient population.
• Chronic mouth breathing in these patients actually leads to acquired
craniofacial abnormalities (e.g. the ‘ adenoid face ’ ), which further
compromise the stability of the upper airway.
Causes of nasal obstruction
2- Alterations in the nasal mucosa lead to nasal congestion,
which involves the cavernous tissues of the turbinates.
• Common causes of nasal congestion include allergic rhinitis,
vasomotor rhinitis, chronic sinusitis, and upper respiratory
tract viral infections.
• Chronic inflammation, as well as conditions like asthma,
aspirin sensitivity or cystic fibrosis, lead to the development
of nasal or nasopharyngeal polyps, which cause obstruction.
• Intranasal corticosteroid therapy for rhinitis showed
improvement of OSAHS, but not snoring,
3- Facial muscular weakness and impaired nasal reflexes
(especially the ones involved in dilating the nose prior to
inspiration), which occur secondary to neuropathy and facial
palsy, are also important neuromuscular causes of nasal
obstruction.
Diagnostic evaluation of nasal obstruction
1- the history : include whether the obstruction is uni- or
bilateral, intermittent or persistent, seasonal or perennial,
and whether it is worse while in the supine position,
particularly at night.
• A detailed medication history is essential, in order to
document the effects of medications, particularly
decongestants and topical steroids.
• History of previous surgery is also an important aspect that
guides the therapeutic decision making.
• There is no simple way to assess the patient’s nasal airway
during sleep.
• A therapeutic trial of topical decongestants and systemic
steroids may be useful in assessing the effect on snoring
and overall quality of sleep in OSAHS patients.
Diagnostic evaluation of nasal obstruction
2- The physical examination : include an examination of
the internal and external nasal valves and the septum by
means of anterior rhinoscopy.
• The nasal valves are common sites of obstruction in
sleep apneic patients even more than deviated septa.
• Fiberoptic endoscopy enables the surgeon to rule out
the presence of any obstructing masses such as nasal
polyps or nasopharyngeal tumors.
3- Radiologic evaluation; with CT scans may also have a
confirmatory for the preoperative evaluation in select
cases, but is not essential.
Diagnostic evaluation of nasal obstruction
4- Therapeutic trials : help confirm the causes and sites of nasal
obstruction, and also help in determining the potential success of both
medical and surgical interventions.
• Topical nasal steroids, sympathomimetic agents, and antihistamines, as
well as allergic management in the form or desensitization.
• Patients that show significant improvement may choose not to undergo
surgery.
• The impact of decongestants such as oxymetazoline during nighttime
sleep is valuable in assessing the impact of nasal obstruction in
symptoms like snoring and overall in sleep-disordered breathing.
• The role of nasal valve collapse in nasal obstruction can also be
confirmed with a trial of Breathe Right ™ nasal strips which help
maintain the valves open through external dilatation, and prevent
collapse during deep inspiration. Patients that have an adequate
response in the form of reduced snoring and improved breathing are
likely to benefit from nasal valve suspension procedures.
Diagnostic evaluation of nasal obstruction
5- Nasal airflow evaluation:
• Even a thorough clinical evaluation can be unreliable and even
contradictory.
• Patients are often not completely aware of the magnitude of nasal
obstruction they might be experiencing, particularly during sleep.
• In the awake state, patients with atrophic rhinitis secondary to extensive
turbinate resection have a persistent feeling of obstruction in spite of
objective evidence of patency, whereas patients with deviated septa or
nasal polyposis report no obstruction symptoms, despite evidence
against a patent nasal airway.
• The evaluation of nasal airflow is a key element in the evaluation of
improvement after surgical intervention.
• Measurements are performed at baseline and after procedures, in order
to compare values and confirm improvement.
• Nasal airflow tests show a wide variety of normal values, which limits
their use as stand-alone diagnostic tests.
Rhinomanometry
• Rhinomanometry (RM) measures nasal airway resistance
and airflow. It has two phases, passive and active, and it can
be divided into anterior and posterior.
• Active RM requires the patient to generate airflow through
inspiration.
• Passive RM utilizes external generation of airflow through
the nose at a constant pressure.
• Anterior RM reflect the status of the nares, nasal valves, and
nasal cycling, and utilizes a device inserted into the nares.
• Posterior RM, utilizes a sensor inserted into the mouth which
measures the nasopharynx, hence requiring substantial
patient co-operation.
• These tests are also usually performed before and after the
administration of nasal decongestants.
Rhinomanometry
• Features:
1- Frontal & Back Active
Rhinomanometry
2-Automatic or Manual selection of
Respiration cycles.
3-Calculation of Nasal resistance.
4- Easy comparison of the sigmoid
graphics for pre & post
Vasoconstriction .
5-Suitable in Adult and Paediatric
applications.
RHINOSPIR-PRO rhinomanometer
• The RHINOSPIR-PRO rhinomanometer is a PC
based unit, which permits the objective assessment
of nasal airway resistance, allowing the following
tests to be carried out:
1-Active anterior rhinomanometry
2-Active posterior rhinomanometry.
3-Nasal Provocation Test (N.P.T).
Acoustic rhinometry
• Acoustic rhinometry evaluates nasal obstruction by analyzing
reflected sound waves introduced through the nares.
• It is not invasive, is easily reproducible and it does not require
patient co-operation.
• The results are expressed as cross-sectional dimensions of
the nasal cavity.
• The cross-sectional area (CSA) is measured at different points
from the nares to the closest area of narrowing, which
corresponds to the nasal valve area.
• Since a ‘ normal ’CSA varies so much from patient to patient,
an absolute value is not very useful for diagnosis or for
confirmation of nasal valve area obstruction.
• The ratio of the CSA during inspiration to the CSA at rest is
highly diagnostic of nasal valve collapse.
• Normally, deep inspiration should not decrease the CSA. If it
does, it is a sign of nasal valve collapse.
Acoustic reflection
• Sound waves are sent up the
nasal passageway and are
reflected back to accurately map
out the topography of the nasal
airway.
• This allows clear identification of
the location and severity of any
obstruction in the airway.
• The test is completely noninvasive and takes 30 seconds
to complete.
The Eccovision Acoustic Diagnostic
Imaging System
• The Eccovision device uses
acoustic reflection technology
to accurately map out the size,
structure and collapsibility of
the oral and nasal airway.
• The Eccovision is widely used
in ENT, Orthodontic and Sleep
Disorders Dentistry practices
Eccovision® Acoustic Rhinometer
• The Eccovision® Acoustic Rhinometer
allows for quick and easy measurements
of nasal patency.
• The device gathers information using
acoustic reflection. Sound waves are
sent up the nasal passageway and they
are reflected back out in such a way that
the Eccovision® Acoustic Rhinometer
can accurately map out the topography
of the nasal airway.
• This allows us to clearly identify the
location and severity of any obstruction
in the airway.
• The test is completely non-invasive and
takes 30 seconds to complete.
Eccovision® Acoustic Pharyngometer
• The Eccovision® Acoustic Pharyngometer allows
users to quickly and easily measure a patients
pharyngeal airway size and stability from the Oral
Pharyngeal Junction to the Glottis.
• The Pharyngometer graphically displays the
relationship between the cross-sectional area of
the airway and distance down the airway in
centimeters.
• Studies have shown a clear relationship between
the existence of OSA and a narrow, collapsible,
airway.
• The Pharyngometer accomplishes these
measurements using acoustic reflection
technology, similar to a ships sonar.
• Sound waves are projected down the airway and
reflected back out in such a way that the
Pharyngometer software can analyze and quantify
changes in the airways cross-sectional area.
• The test is minimally invasive and takes 2-5
minutes to complete.
Acoustic rhinometry
• Acoustic rhinometry has been
validated against two- and threedimensional CT imaging , MRI
and nasal endoscopy .
• Acoustic rhinometry precisely
locates the nasal minimum crosssectional area, which corresponds
to the head of the inferior
turbinate and nasal valve area .
• Minimum cross-sectional area
correlates with symptoms of nasal
obstruction and regulates airflow .
• This measure is non-invasive (the
instrument rests against the
nostril) and can be completed in
minutes.
Nasal obstruction and sleep disordered breathing
• Nasal obstruction and SDB often co-exist.
• Approximately 15% of patients with SDB also have nasal obstruction, but
there is no correlation between the severity of obstructive sleep apnea
and an objective measure of nasal resistance – acoustic rhinometry.
• Cephalometrics, body mass index and posterior rhinometry showed that
daytime nasal obstruction is an independent risk factor for obstructive
sleep apnea.
• Normal patients have been shown to experience sleep disturbances –
including sleep stage disruption as well as new-onset snoring and even
mild obstructive sleep apnea – after acute, complete bilateral nasal
obstruction such as abrupt occlusion of their nose.
• SDB was related to nasal cross-sectional area objectively assessed using
acoustic rhinometry and both titrated nasal CPAP and the RDI ; however,
these associations were only present in patients with normal BMI.
Nasal obstruction and sleep disordered breathing
• Besides the simple effect of nasal obstruction on
breathing patterns during sleep, the nose is a major
conduit for treatment of obstructive sleep apnea
with positive airway pressure therapy.
• Nasal obstruction can therefore interfere with
treatment.
• Nasal obstruction can increase the required CPAP
in obstructive sleep apnea patients.
• Nasal obstruction can affect positive airway
pressure therapy tolerance and adherence .
Three different theories have been proposed to explain the
relationship between nasal obstruction and SDB.
1-Increased airway resistence: If the extra-luminal
pressure was greater than the pressure of the
downstream segment, flow was related not to
pressure differential across the whole tube, but
rather to inflow pressure minus the extra-luminal
pressure.
• Applying the Starling model to the pharynx maximal
airflow is based on three factors: upstream
pressure, resistance in the upstream segment, and
the extra-luminal pressure.
1-Increased airway resistence
• Nasal resistance matches the impedance of upper
and lower airways to prolong inspiration and
expiration.
• On expiration ,this prolongation has the beneficial
effect of improving pulmonary compliance and
increasing gas exchange.
• On inspiration, nasal resistance can augment
pharyngeal resistance to promote upper airway
collapse.
• The decline in tidal volume and minute ventilation
has been shown in several studies.
2-Unstable oral breathing:
• With nasal obstruction, patients open their mouth. This
reflexive compensation contributes to SDB by narrowing the
pharyngeal lumen in two ways.
• First, the chin and rest of the mandible move posteriorly and
inferiorly with mouth opening to displace the tongue in that
direction. This directly narrows the pharyngeal airway.
• Second, this maneuver decreases the length and tension of
the muscles surrounding the airway, and the compliance of
the pharynx increases.
• It has been shown that opening of the mouth to provide a 1.5
cm separation between incisors moves the angle of the
mandible posteriorly 1 cm, a substantial change.
3- Impaired nasal reflexes:
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Nasal breathing stimulates ventilation,
Not only is minute ventilation higher with nasal compared
to oral breathing, but also that augmented nasal airflow
increases minute ventilation.
Furthermore, the evidence that this response is due to
neural regulation in humans comes from studies which
show that application of topical anesthesia in the nose and
nasopharynx specifically increases nasal and pharyngeal
resistance, and that topical nasal anesthesia actually leads
to increased SDB ,whether this is measured as the number
of apneas, apnea duration, or a decrease in genioglossus
muscle activity.
Effect of treatment:
• Treatment of nasal obstruction has three
potential goals.
1-It can reduce nasal obstruction,
2- reduce the severity of , possibly even
eliminating – SDB, or
3-it can facilitate SDB treatment by allowing the
nose to be used more easily as a conduit for
positive airway pressure therapy.
Effect of treatment:
• A wide variety of treatments have demonstrated benefits
in improving nasal obstruction,
• In contrast, isolated treatment of nasal obstruction does
not successfully treat obstructive sleep apnea for most
patients.
• Medical treatment produced resolution of obstructive
sleep apnea in 9% of patients and surgical treatment in
18%.
• Nasal corticosteroids can produce small changes in
snoring and the Apnea/Hypopnea Index, but the degree
of improvement varies widely.
• Less than 20% of patients achieve a 50% reduction in AHI
with nasal surgery alone.
• A recent report failed to show improvement in snoring
intensity or daytime sleepiness symptoms in a group of
40 patients after nasal surgery for an obstructed nasal
airway, in spite of decreased nasal resistance as
measured by rhinomanometry.
• Patients undergoing nasal surgery alone for the
treatment of OSAHS showed that, despite subjective
improvement in patients undergoing submucous
resection (SMR) of the septum with or without SMR of
the inferior turbinates, an overall improvement in
OSAHS on the basis of polysomnographic data could
not be demonstrated in most patients.
• In fact, when pre- and postnasal surgery AHI have been
compared in mild, moderate, and severe OSAHS
patients, a tendency towards worsening of this
parameter has been observed, although statistical
significance for the postoperative increase in AHI was
only observed in mild OSAHS cases. This paradoxical
effect has been previously described,
• Numerous hypotheses have been proposed for this paradoxical
effect are based on
1- Better subjective sleep quality due to a patent nasal airway is
achieved, which leads to deeper and more comfortable sleep,
resulting in increased apneic episodes due to increased
collapsibility of the upper airway.
2- Another possible explanation for worsening of the AHI from the first
to the second night of study might occur because the patients
experience what is also known as the ‘ first night effect ’ , where
they become adapted to the test environment after the second or
third night of study, and thus are able to sleep better.
3- The increased airflow in a patient’s nasal airway creates more
turbulence by the Bernoulli effect, thus promoting the collapse of
the airway at the site of greatest pressure, which corresponds to
the narrowest point.
• Correction of nasal airway obstruction has been shown to have a
significant impact on OSAHS when performed as a part of a multilevel
approach to treat patients with OSAHS .
Patients with nasal obstruction and OSAHS achieved significantly
better objective and subjective success rates when soft palate
implant insertion for the treatment of snoring and mild to moderate
OSAHS was performed together with nasal surgery .
The lowest oxygen saturation levels (LSaO 2 ) are directly affected by
the patency of the nasal airway, with or without persistent OSAHS.
While the increase in LSaO 2 might be discrete, nasal interventions
might at least maintain adequate blood oxygenation levels.
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Nasal treatments can facilitate the treatment of SDB by decreasing the
magnitude of the positive airway pressure necessary to treat SDB.\
A reasonable improvement (9.3–6.7 cm water) for septoplasty with or
without inferior turbinate reduction, and a smaller effect (8.6–8.0 cm
water) was seen with an external nasal valve dilator device.
Two additional studies have shown that nasal surgery can increase the
adherence to continuous positive airway pressure devices.
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CPAP in itself might promote the development of nasal inflammation,
and in some patients even vasomotor rhinitis, particularly when using
CPAP machines that do not control the temperature of the delivered air
nor humidify it.
Effects of nasal surgery on snoring and sleep apnea
• The location of obstruction in the OSAHS is variable and can often be
localized to several levels in the upper airway.
• In fact, the level of obstruction can vary in the same patient among
consecutive episodes of apnea.
• In normal circumstances, the normal nose contributes to 50% of upper
airway resistance, adding to the resistance provided by both
oropharyngeal tissues and the tongue.
• In fact, resistance at the level of the nose is more constant in both sleep
and awake states, due to the more rigid frame provided by the septum
and the lower and upper lateral cartilages.
• If the upper or lower lateral cartilages are weak, damaged, resected, this
stability is lost. Patients in such cases are subject to an increased
tendency towards collapse during sleep, even with a normal nasal airway
in the awake state.
Effects of nasal surgery on snoring and sleep apnea
• Nasal obstruction interferes with pressure titration in nasal
continuous positive airway pressure (nCPAP) for the
management of OSAHS, and that treatment of such
obstruction improves patient compliance with Ncpap.
• The cause–effect relationship of nasal obstruction and
OSAHS, however, remains unclear.
• The primary sites of nasal obstruction are the nasal
vestibule, the nasal valves, and the turbinates.
• The nasal septum, when deviated, also has a significant
impact on these areas of obstruction.
• Of these three sites, the nasal valve is the site of major
resistance. in fact, nasal valve incompetence may equal, or
even exceed, septal deviation or turbinate hypertrophy as
the prime cause of nasal airway obstruction.
Effects of nasal surgery on snoring and sleep apnea
• During inspiration, particularly during the forced
inspiration that occurs during an apneic episode, the
negative nasopharyngeal and intranasal pressures
increase to generate more flow, creating a transmural
pressure gradient, which, when a critical value is
reached, causes collapse of the upper lateral
cartilages.
• Nasal obstruction leads to mouth opening and
transition to oral breathing, which contributes to airway
flow limitation and collapse, mainly due to inferior
movement of the mandible, a backward fall of the base
of the tongue, resulting in a reduction of the posterior
pharyngeal space and diameter and an increased
respiratory effort that causes collapse of the pharyngeal
tissues due to greater negative pressures.
Conclusions
• The patient population in whom SDB presents will commonly
also show concurrent nasal obstruction.
• Selecting the potential medical and surgical treatment
options requires an understanding of nasal anatomy and
physiology and the combination of history, physical
examination, and accurate diagnosis.
• There are three potential mechanisms for the association
between nasal obstruction and SDB: an increase in airway
resistance; the transition to unstable oral breathing; and the
impairment of nasal reflexes.
• Treatment can effectively reduce nasal obstruction, although
the effects are more variable in the reduction of SDB severity
(when treating nasal obstruction alone) and the facilitation
of SDB treatment.
Conclusions
5- Selected patients who respond to a diagnostic trial of artificial nasal
airway improvement with topical and systemic decongestants and
steroids, along with external nasal dilators (e.g. Breathe Right ™
strips), may also benefit from definitive correction of the nasal
airway, with elimination of snoring and improvement in OSAHS.
6-The majority of patients with nasal obstruction and OSAHS will likely
benefit from a multilevel surgical approach.
7-If nasal surgery is undertaken alone, it is important to inform
patients that it may not only fail to cure, but may even aggravate
snoring and OSAHS in certain cases.
8- Nasal surgery also has a significant impact in improving patients
’subjective symptoms, like daytime sleepiness and quality of sleep.
It also constitutes a valuable intervention in patients that need
nCPAP management for their OSAHS.
Friedman tongue position and the staging of OSAHS
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Nasal, palatal and hypopharyngeal obstruction, acting alone or in concert, are
frequently identified as the cause of snoring and OSAHS.
Even in cases where a single site is primarily involved, the increase in negative
pressure may induce further obstruction in other areas.
When surgical management of OSAHS is considered, a clear understanding of
the complex relationship between the sites of obstruction is essential to surgical
success.
Numerous methods that attempt to predict the location of the upper airway
obstruction include snoring sound analysis, physical examination, computed
tomography, magnetic resonance imaging, cephalometric studies and
fluoroscopy,
The number of methods described is evidence of the lack of agreement that any
single method is perfect.
The most commonly used method is the Mueller maneuver (MM). This methode
is used for the preoperative assessment of sleep-disordered breathing (SDB).
The MM consists of having the patient perform a forced inspiratory effort against
an obstructed airway with fiberoptic endoscopic visualization of the upper
airway.
The test is widely used and simple to perform. Despite this, its use is
controversial and certainly no studies have been able to associate the maneuver
as a tool for patient selection.
Friedman tongue position and the staging of OSAHS
• Friedman tongue positions (FTP) emerged (previously identified as the
Mallampati palate position and subsequently as the Friedman palate
position) has been found to be a simple method to approximate
obstruction at the hypopharyngeal level.
• This classification is based on observations by Mallampati, who
published a paper on palate position as an indicator of the ease or
difficulty of endotracheal intubation by standard anesthesiologist
techniques.
• The Mallampati stages had only been studied in the context of difficult
intubations.
• FTP is based on evaluating the tongue in natural position inside the
mouth.
• FTP included four distinct positions, but now five positions are
necessary to best describe the anatomy.
• FTP has been studied extensively as it relates to OSAHS.
• As there are no studies that have been done on the ‘ Mallampati position
’ in sleep medicine, the use of the term is inaccurate in the context of
OSAHS.
Friedman tongue position and the staging
of OSAHS
• The procedure for identifying FTP involves asking the patient to open
their mouth widely without protruding the tongue.
• The procedure is repeated five times so that the observer can assign the
most consistent position as the FTP.
• FTP I allows the observer to visualize the entire uvula and tonsils or
pillars.
• FTP IIa allows visualization of the uvula but only parts of the tonsils
are seen.
• FTP IIb allows visualization of the complete soft palate down to the
base of the uvula, but the uvula and the tonsils are not seen.
• FTP III allows visualization of some of the soft palate but the distal soft
palate is eclipsed.
• FTP IV allows visualization of the hard palate only.
• Patients with FTP IIb, although they may have been formerly classified
as FTP III in the earlier staging system, share surgical response rates
more characteristic of FTP II.
Friedman tongue position and the
staging of OSAHS
1. The use of FTP enables the clinician to predict the presence of OSAHS.
2. A thorough history is most often the only screening for OSAHS.
Unfortunately, many patients who are in denial about their symptoms
cannot be identified by history alone, and therefore go undiagnosed.
3. Routine use of FTP can be utilized as a cost effective, non-invasive
screening tool that will allow ready identification of patients that may suffer
from OSAHS.
4. Since FTP estimates the presence of hypopharyngeal obstruction,
determining FTP prior to surgical intervention can be instrumental in
guiding the surgical management of OSAHS due to its ability to separate
patients that will likely benefit from uvulopharyngopalatoplasty as a single
modal treatment from those that will require multilevel surgical
intervention.
Friedman tongue position and the staging of
OSAHS
• The primary screening for OSAHS is by a thorough history.
• Patients who complain of snoring, excessive daytime
sleepiness or observed apnea are usually the only ones who
are further tested for OSAHS.
• The obstacles in eliciting history in sleep apnea patients are
1- Because the patient is asleep when the pathology occurs,
they are largely unaware of the problem and often deny
symptoms. In such cases, only a history elicited from a bed
partner can offer sufficient insight into symptomology.
2- symptoms of OSAHS often overlap with other pathologies.
For example, a patient complaining of excessive sleepiness
and fatigue may very likely receive a full work-up for
depression and not OSAHS.
Friedman tongue position and the staging
of OSAHS
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The known physical findings that are associated with OSAHS
include BMI, neck circumference, and tonsil size, are routinely
assessed and are well defined.
Descriptions of hypopharyngeal obstruction have not been
standardized. Often times the similar physical findings are
reported with many arbitrary terms such as ‘ crowded oropharynx
, macroglossia ’ , ‘ retrognathia ’ ,etc. This causes much
confusion in both patient care and in reporting data.
The routine use of FTP in the context of OSAHS can help
standardize the description of hypopharyngeal obstruction.
FTP can be employed in an algorithm that can help identify
patients with OSAHS. This system is based on three readily
identifiable and reproducible physical exam findings and can
provide a simple means for screening patients.
The system relies on calculating the patient’s Body Mass Index
(BMI), along with the assessment of the patient’s tonsil size and
FTP.
Friedman tongue position and the staging
of OSAHS
– Tonsil size and BMI are assessed as follows. Tonsil
size 1 implies tonsils hidden within the pillars.
Tonsil size 2 implies the tonsil extending to the
pillars. Size 3 tonsils are beyond the pillars but not
to the midline. Tonsil size 4 implies tonsils that
extend to the midline.
– The BMI is graded as grade 0 (< 20 kg/m 2 ), grade 1
(20–25 kg/m 2 ) grade 2 (25–30 kg/m 2 ), grade 3 (30–
40 kg/m 2 ), and grade 4 ( > 40 kg/m 2 ).
– OSAHS score = FTP(0- IV) + tonsil size (0-4) +BMI (0-4)
Friedman tongue position and the staging
of OSAHS
• Any value above 8 is considered as a positive OSAHS score,
whereas any value below 4 is considered a negative OSAHS
score.
• A positive score has a positive predictive value of moderate
OSAHS (Apnea/Hypopnea Index (AHI) > 20) of 90%, and was
74% effective in predicting severe OSAHS (AHI > 45).
• A negative score was 67% effective in predicting an AHI of < 20.
• With the use of FTP and the OSAHS score, the number of
undiagnosed cases may also fall.
• In cases where history is unclear, this algorithm may help
identify patients that may have otherwise gone unnoticed. In other
cases, this algorithm may provide the impetus for eliciting a
more detailed history and performing further tests to confirm
suspicion of OSAHS.
PETCO2
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Surgical staging of OSAHS
• Uvulopalatopharyngoplasty (UPPP) is the most common
surgical procedure performed by otolaryngologists for the
treatment of OSAHS.
• Unfortunately, only 40-79% of patients had a ‘ successful ’
surgery defined by an AHI reduction of 50% and a
postoperative AHI < 20 or an Apnea Index (AI) reduced by
50% and a postoperative AI <10.
• The ideal system would identify those patients with a high
likelihood of successful UPPP and separate them from
those with a high likelihood of failure, thus guiding patient
selection and improving outcomes.
• The most common method used to identify patients for
surgery is based on the misconception that patients with
mild/moderate disease are better candidates for UPPP than
those patients with severe disease. Therefore, the
procedure is often recommended for patients with
mild/moderate OSAHS.
Surgical staging of OSAHS
• Severity of disease as determined by clinical
symptoms, polysomnography results, or tools
such as the Epworth Sleepiness Scale has been
shown not to correlate with surgical success.
• Studies have shown that patients with mild SDB
based on clinical and polysomnographic data
have no better chance of successful treatment
with UPPP than patients with severe disease.
• In fact, one study demonstrated that UPPP
performed on unselected patients with mild
OSAHS (AHI<15) not only does not cure disease
in 60% of cases but often makes it worse .
Surgical staging of OSAHS
• It is well known that OSAHS involves obstruction of
the airway at multiple levels.
• Although palatal obstruction accounts for a large
portion of the obstruction, hypopharyngeal
obstruction can also play a significant role.
• UPPP alleviates obstruction at the level of the soft
palate and tonsils, but does not address obstruction
at the level of the hypopharynx. This is clearly a
significant cause of the failure of UPPP.
• Therefore when devising a system that is intended
to predict UPPP outcomes, the anatomical
considerations must be incorporated.
Staging system
Surgical staging of OSAHS
•
Most surgeons have found that patients with BMI <40 have a poor
prognosis for corrective UPPP and therefore these patients are
automatically assigned to stage IV.
• All patients with skeletal deformities such as micrognathia or mid-face
hypoplasia are considered stage IV.
• The rationale for such a staging system is that the success of UPPP is
highly dependent on the anatomical relationship between palatal and
hypopharyngeal obstruction. Stage I patients are those with favorable
tongue position (I, IIa, IIb) indicating minimal hypoglossal obstruction
and large tonsils. They are most likely to benefit from UPPP with
tonsillectomy as hypopharyngeal obstruction does not represent a
significant component of their disease. Stage III patients are on the
opposite extreme of the spectrum with small or no tonsils and unfavorable
tongue position (III or IV) indicating significant hypopharyngeal
obstruction. They are least likely to benefit from UPPP as UPPP will not
address their hypopharyngeal obstruction. Stage II patients are those with
either large tonsils and unfavorable tongue position or small tonsils and a
favorable tongue position. UPPP was most likely achieved in stage I
patients (80.6%) and least likely in stage III patients (8.1%).
Success rate of uvulopalatopharyngoplasty
in treatment of SDB
Success rate of uvulopalatopharyngoplasty
in treatment of SDB
• The use of the anatomic staging system in OSAHS offers a costeffective, non-invasive, reproducible method to stratify patients
based on anatomic variations.
• The use of this system in addition to detailed clinical examination,
cephalometrics and Mueller maneuver can help improve surgical
outcomes in OSAHS.
• Patients with stage I disease have better than an 80% chance of
success with UPPP and should therefore undergo the procedure
when non-surgical treatment has failed. Even patients with severe
SDB had an 80% success rate if they had stage I disease based
on this staging system.
• Patients with stage III disease should never undergo UPPP alone
as a surgical cure for SDB. With an 8.1% success rate, the
surgery is destined to fail.
• They should be treated with a combination of procedures that
address both the palate and the hypopharynx. Patients with stage II
disease do not fall into either extreme but probably can be treated
similar to stage III patients.
Rhinitis and sleep
• Allergic rhinitis affects up to 40% of the population,
and its prevalence appears to be increasing.
• Nasal congestion is a prominent and troublesome
symptom of both allergic and non-allergic rhinitis.
• Additional symptoms of allergic rhinitis include
rhinorrhea, sneezing, and pruritus of the eyes,
nose, and throat, particularly in patients with
perennial allergic rhinitis (PAR).
• Typical sleep-related problems seen include sleepdisordered breathing, sleep apnea, and snoring, all
of which are associated with nasal congestion /
obstruction.
Rhinitis
• Allergic rhinitis can affect the mucous membranes of the nose, eyes,
eustachian tubes, middle ear, sinuses, and pharynx and is usually
triggered by immunoglobulin E in response to an allergen.
• Mediators involved in clinical symptoms include histamine, tryptase,
chymase, heparin as well as leukotrienes.
• Non allergic rhinitis is a term used to describe a variety of diseases
including, infectious, vasomotor, occupational, hormonal, gustatory, and
drug induced rhinitis.
• In non-allergic etiologies, autonomic parasympathetic stimuli lead to
localized nasal swelling and secretions.
• In a recent survey of individuals with allergic rhinitis, 68% of respondents
with perennial allergic rhinitis (PAR) and 48% with seasonal allergic
rhinitis (SAR) reported that their condition interfered with sleep.
• Sleep disturbance can be caused by the mechanical obstruction of nasal
congestion. However, additional symptoms of rhinitis and the release of
inflammatory mediators may influence sleep and resultant daytime
fatigue and somnolence.
• Treatments that improve the symptoms of allergic rhinitis, particularly
those that relieve nasal congestion, have been shown to improve
patients’ sleep and quality of life.
Rhinitis
• Sleep disturbances associated with allergic rhinitis include
sleep disordered breathing (ranging from snoring to
obstructive sleep apnea and/or hypopnea) and microarousals, although one study has suggested that allergic
rhinitis is not a major risk factor for obstructive sleep apnea
syndrome (OSAS).
• Individuals with frequent night-time symptoms of rhinitis
have been shown to be more likely to have chronic
excessive daytime sleepiness or chronic non-restorative
sleep than those who rarely or never have such symptoms.
• Studies using actigraphy have demonstrated objective
evidence that adults with PAR had sleep disturbance when
compared to normal controls.
Mechanisms of sleep impairment :
• The daytime fatigue experienced by patients with allergic rhinitis
could be attributed to sleep impairment resulting from nasal
congestion or other rhinitis symptoms or to the effects of
inflammatory cytokines on sleep or producing fatigue directly.
• The current evidence suggests that symptoms and the underlying
pathophysiologic changes of the disease contribute to reduced
sleep quality, insomnia, hypersomnolence,and daytime
somnolence.
• Nasal congestion is a common and bothersome symptom and
occurs when the cavernous tissues of the nasal turbinates swell as
a result of dilation of the capacitance vessels.
• Nasal congestion reduces the internal nasal diameter, increases
airway resistance to nasal airflow, and can also cause nasal
obstruction.
• The end result of airway resistance is the same irrespective of its
etiology including both allergic and non-allergic etiologies.
• The degree of congestion (nasal patency) can be evaluated
objectively by measures of nasal airflow (such as peak nasal
inspiratory flow), assessment of airways resistance
/conductance (rhinomanometry), and acoustic rhinometry,
which assesses the volume and area of the nasal cavity by
analyzing reflected sound waves .
• Nasal congestion is often worse at night and first thing in the
morning.
• Congestion tends to increase when an individual lies down.
• The normal overnight decline in serum cortisol is likely to
contribute to nighttime worsening.
• Similarly in patients with asthma, lower cortisol levels are
associated with greater airway obstruction, particularly at
night.
• Nasal congestion worsened overnight and peaked at
approximately 6 AM. This shows a clear, large-amplitude,
circadian variation, similar, but slightly delayed from what we
see in asthma .
Circadian rhythms in nasal congestion
demonstrating worsening early in the Morning.
• Approximately half patients stated that congestion was the
most bothersome symptom, that nasal congestion woke them
up during the night, and that it made it difficult to fall asleep.
• These effects were more pronounced for those experiencing
more severe congestion.
• Nasal congestion had a negative effect on emotions and the
ability to perform daily activities. These effects may, in part, be
a consequence of the effects of nasal congestion on sleep.
• Using objective assessments of sleep indicated that nasal
congestion in patients with allergic rhinitis is associated with
an increase in the number of micro-arousals and episodes of
Apnea.
• Simple nasal occlusion by a nose clip in healthy subjects resulted
in an increase in sleep apnea and transient arousals.
• These data support that congestion alone is a major factor
interfering with quality of sleep and congestion alone may cause
disturbance of sleep and daytime somnolence and other poor
outcomes.
• In patients with allergic rhinitis, greater nasal
congestion was associated with obstructive sleep
apnea. Thus, suggesting a direct correlation.
• Subjects with nasal congestion due to allergic rhinitis
were 1.8 times more likely to have moderate to severe
sleep-disordered breathing than subjects with allergic
rhinitis without nasal congestion.
• The switch to oral breathing that occurs as a result of
nasal congestion may be the key factor behind this
association, compromising the airway and leading to
sleep-disordered breathing.
• Other symptoms, such as sneezing, rhinorrhea, and
nasal pruritus, may contribute to reduced sleep quality
and sleep disturbance in allergic rhinitis.
• Rhinorrhea was troublesome to patients with allergic
rhinitis and interfered with sleep.
• Ocular itching has also been demonstrated as a cause
of sleep disturbance .
• The inflammatory mediators, such as histamine and
cytokines released during allergic reactions, may
directly affect the central nervous system, which
contributes to disturbed sleep and fatigue or sleepiness
during the day.
• Histamine is involved in the regulation of the
sleepewake cycle and arousal.
• Higher levels of the cytokines interleukin (IL)-1b, IL-4,
and IL-10 in allergic patients than in healthy subjects
have been shown to correlate with increased latency to
rapid eye movement (REM) sleep, decreased time in
REM sleep, and decreased latency to sleep onset.
• Because the restorative function of REM sleep is
important, its disruption may contribute to daytime
fatigue, difficulty concentrating, and worse performance
in individuals with allergic rhinitis.
• Inflammatory cells and mediators show circadian variation, with
levels peaking during the early morning hours.
• These changes of cytokines could explain the higher level of
allergic rhinitis symptoms upon waking and why overnight sleep is
particularly affected.
• Similar changes in cytokines have also been seen associated with
obstructive sleep apnea with increases noted in Interleukin-1, tumor
necrosis factor (TNF), and IL-6.
• The changes noted may promote a T-helper cell type 2 phenotype
further causing allergic type inflammation leading to increased
congestion.
• Elevation of some of the cytokines seen in both disorders, such as
TNF, IL-6 and IL-1, can cause fatigue and other non-specific
constitutional symptoms during the day.
• The extent that excessive cholinergic activity and the decrease in
adrenergic tone has on the congestion and associated sleep
disturbance is unknown.
• We do know that automonic disturbance is associated with mild
obstructive sleep apnea (OSA).
• The abnormalities noted may be secondary, but may also precede
the OSA and possibly be part of the pathologic mechanism.
Sleep impairment and quality of life
• Individuals with allergic rhinitis suffer impaired cognitive
function and reduced work productivity and performance.
• Allergic rhinitis can affect children’s learning ability and
performance at school and cause somnolence and inability to
concentrate in children. These effects may be a direct result of
allergic symptoms but are likely to be exacerbated by sleep
impairment.
• Sleep disordered breathing and sleep disturbance are known to
be directly associated with decreased quality of life in the
general population. This is made evident by experimentally
induced sleep fragmentation in healthy subjects associated
with impaired mental flexibility and attention, increased daytime
sleepiness, and impaired mood.
• Daytime fatigue, difficulty concentrating, and impaired
psychomotor performance are commonly reported by
individuals with allergic rhinitis and may reduce their ability to
perform the physical and social tasks of daily living.
Disease-specific quality-of-life measures
1-Rhinoconjunctivitis quality of life questionnaire (RQLQ)
include a domain that measures the effects of disease and/or
treatment on sleep. These questionnaires focus on the problems
for which patients seek help, and so are more sensitive to
changes in patients’ quality of life than generic health-status
questionnaires or those specific for obstructive sleep apnea.
2-Nocturnal rhinoconjunctivitis quality of life
questionnaire(NRQLQ) assesses the functional impairments
most problematic for patients with nocturnal symptoms, including
sleep problems, symptoms during sleep time and on waking in
the morning, and problems during waking hours.
General questionnaires that assess daytime sleepiness and
sleep quality
1-Epworth sleepiness scale
2- Pittsburgh sleep quality index,
Poor sensitivity and specificity may limit their use in assessing the
mild-to-moderate sleep disturbance often noted in rhinitis.
Polysomnography
• Polysomnography in seasonal allergic rhinitis and healthy
volunteers showed that there were statistically significant
differences between the 2 groups in sleep parameters, including
increases in the apnea index, hypopnea index ,
apneaehypopnea index, snoring time,amount of REM sleep,
and sleep latency.
• The changes were not clinically relevant, as values remained
within normal limits.
• The study found a statistically significant increase in daytime
sleepiness (assessed subjectively using the Epworth sleepiness
scale) , suggesting the known poor correlation between
subjective and objective measures of sleep disturbance.
Effects of therapy
• Sedating antihistamines are contraindicated in those experiencing
daytime sedation, fatigue, and functional impairment.
• Nonsedating oral antihistamines are widely used to treat allergic
rhinitis and relieve nasal symptoms such as rhinorrhea,
sneezing, and pruritus, but have less effect on nasal
congestion .
• While non-sedating antihistamines are tolerated well and often
improve sleep and quality of life, data have suggested that the
increased sedation secondary to first generation
antihistamines and topical intranasal administration of
sedating antihistamines may exacerbate daytime
somnolence.
Effects of therapy
• Oral decongestants reduce nasal congestion, but may have
adverse effects on sleep because of their stimulatory effects
and their association with systemic side effects, such as
tachycardia and urinary retention. Topical decongestants
appear to improve sleep in patients with nasal obstruction,
but because of the risk of rhinitis medicamentosa
(“rebound” congestion), they should not be used for long
periods .
• The anticholinergic agent ipratropium bromide is not considered
effective in relieving nasal congestion; however, limited data suggest
that sleep and quality of life may be improved following treatment.
• Leukotriene receptor antagonists or a combination of an antihistamine
and a leukotriene receptor antagonist have shown some efficacy in
improving sleep and quality of life in patients with allergic rhinitis or
sleep-disordered breathing.
• The cause of the improved sleep and daytime somnolence may be a
reduction of congestion or a reduction of inflammatory mediators or a
combination of both.
Effects of therapy
•
•
•
•
•
•
•
Intranasal corticosteroids are considered first-line therapy when nasal
congestion is a major symptom.
Intranasal corticosteroids relieve the nasal symptoms, including nasal
congestion, and decrease inflammatory mediators secreted from activated
lymphocytes, epithelial cells, mast cells and other inflammatory cells.
The improvement in nasal congestion is both subjective and objective with
the objective evidence assessed by an increase in peak nasal inspiratory
flow in allergic rhinitis patients treated with intranasal corticosteroids.
Intranasal budesonide reduces nasal congestion, subjective daytime
somnolence, and fatigue and improves sleep quality and patients’ quality
of life.
Another intranasal corticosteroid, flunisolide, improved subjectively
assessed nasal congestion and sleep problems in patients with PAR
compared with placebo, although daytime fatigue and sleepiness did not
show significant improvement.
Flunisolide was superior to azelastine nasal spray in improving nasal
congestion, sleep, and daytime sleepiness in patients with PAR.
Intranasal fluticasone significantly improved subjective assessments of
sleep compared with placebo and decreased daytime sleepiness and
fatigue by more than 10% (although this was not statistically significant).
Effects of therapy
• Fluticasone propionate nasal spray improved nasal
symptoms, quality of life, and verbal memory in children with
SAR.
• Intranasal fluticasone improved allergic rhinitis associated
with OSAS; treatment resulted in a significantly lower
frequency of apnea/hypopnea and subjective improvements
in nasal congestion and daytime alertness, although snoring
noise and sleep quality were unchanged compared with
placebo.
• All intranasal corticosteroids improve quality of life in
patients with allergic rhinitis.
• Intranasal triamcinolone acetonide relieved nasal congestion
and improved health-related quality of life (including sleep),
as assessed using the RQLQ, the NRQLQ, and the
Pittsburgh sleep quality index.
Conclusions
• Sleep impairment associated with rhinitis has a significant impact on
patients’ quality of life.
• Nasal congestion, one of the most common and bothersome symptoms
of these conditions, is thought to be a major cause of sleep impairment
and sleep-disordered breathing.
• The poor sleep associated with nasal congestion is an important
therapeutic target.
• Other rhinitis symptoms, inflammatory mediators released because of
rhinitis can also disturb sleep and lead to an increase in daytime
somnolence and limitations.
• Treatment with intranasal corticosteroids has been shown to significantly
reduce nasal congestion in allergic rhinitis and in those with congestion
should be considered the drug of choice.
• Montelukast may be an alternative therapy in those intolerant to
intranasal corticosteroids.
• Sedating antihistamines should be avoided since they may amplify
the sedation and decrease productivity in those already compromised.
• Immunotherapy has to improve sleep quality and daytime somnolence.
Practice points
1) Sleep impairment associated with rhinitis has a
significant impact on patients’ quality of life with
nasal congestion thought to be a major cause of
sleep impairment and sleep-disordered breathing.
2) Treatment with intranasal corticosteroids has been
shown to significantly reduce nasal congestion in
allergic rhinitis and in those with congestion should
be considered the drug of choice.
3) Sedating antihistamines should be avoided since
they may amplify the sedation and decrease
productivity in those already compromised