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43. Pornsriniyom D.Sleep apnea: A novel risk factor in acute stroke and transient ischemic attack.
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Ear, Nose, andThroat (ENT) Aspects
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ofObstructive Sleep Apnea (OSA)
CasaleManuele andMoffaAntonio
11.1 Introduction
Sleep-disordered breathing (SDB) encompasses a broad spectrum of sleep-related
breathing disorders, including obstructive sleep apnea (OSA), central sleep apnea,
sleep-related hypoventilation, and hypoxemia. OSA is characterized by recurrent
events of upper-airway (UA) collapse during sleep and affects nearly one billion
people worldwide. About 9% of women and 24% of men between 30 and 60years
old have an AHI>5in polysomnography (PSG), and between 2% and 4% are associated with excessive daytime sleepiness (EDS), an incidence that increases with
age [1]. OSA is considered a decisive risk factor for cardiovascular diseases, and its
inuence on the development of pulmonary arterial hypertension, cardiac arrhythmias, atherosclerosis, type 2 diabetes, cognitive dysfunction, and structural brain
changes has been shown.
It is well known that OSA is a complex disease characterized by the collapse at
the UA during sleep: the velopharynx, the lateral pharynx, and/or the tongue base.
More often, the collapse is multilevel. However, it is equally true that OSA could
have severe consequences on ENT districts.
In particular, recent evidence suggests that OSA might be associated with alterations in the auditory and vestibular systems [2], increasing the risks of hearing loss
(HL), tinnitus, and dizziness [3]. It is estimated that over 41% of patients with mild
to severe OSA showed HL.The incidence rate for peripheral vertigo, including
benign paroxysmal positional vertigo (BPPV), Meniere’s disease, vestibular neuritis, and other peripheral vestibulopathy, is 149.86 per 10,000 OSA subjects [4]. HL
11
C. Manuele · M. Antonio (*)
School of Medicine, Campus Bio-Medico University, Rome, Italy
Integrated Therapies in Otolaryngology, Fondazione Policlinico Universitario Campus
Bio-Medico, Rome, Italy
e-mail: m.casale@policlinicocampus.it; a.moffa@unicampus.it
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_11
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and peripheral vestibular disorders (PVD) are prevalent conditions associated with
adverse health-related consequences such as falls, cognitive decline, and incident
dementia. While aging is the most decisive risk factor for these conditions, identifying modiable risk factors, such as OSA, may have signicant public health implications [5].
Moreover, OSA could cause damage to other ENT organs by altering sensitive
and motor functions of the pharynx and larynx. Dysphagia is one of the most common problems symptoms in OSA patients. Although the pathophysiology of dysphagia in OSA is not clearly understood, the literature suggests that dysphagia in
OSA may result from sensory and motor changes of the pharynx and altered swallowing–breathing integration. Moreover, OSA patients are much more prone to
developing laryngopharyngeal reux (LPR), with an overall incidence of 45.2% of
LPR positivity in OSA patients [6].
The rst-line therapy for moderate–severe OSA is continuous positive airway
pressure (CPAP); however, more than 50% of patients with OSA had interrupted
treatment 1year after the prescription [7]. It is uncomfortable to wear, and can cause
many side effects such as dermatitis, mask leak, aerophagia, barotrauma, and claustrophobia. Moreover, OSA patients with CPAP usually complain of nasal obstruction, rhinorrhea, nasal dryness, sneezing, and mouth or throat dry.
For these reasons, in the last years, OSA and snoring surgical management
underwent signicant evolution to obtain therapeutic success and avoid CPAP therapy in selected patients. Newer intrapharyngeal remodeling surgical procedures,
less invasive or morbid, improving patients’ compliance, makes OSA surgery a reasonable alternative [8] with promising results and minimal side effects However, the
managing of acute postoperative pain from these procedures remains a signicant
challenge. Usually, in the postoperative period, patients also experience throat
phlegm, nose regurgitation, dry throat, and throat lump. Most of these tend to
resolve within a few days.
The chapter aims to provide a brief overview of the major OSA consequences on
the ear, nose, and throat (ENT) organs showing etiopathogenetic mechanisms, clinical evidence, and management strategies.
C. Manuele and M. Antonio
11.2 Hearing Functions inOSA Patients
11.2.1 Mechanisms That Could Explain Auditory andVestibular
System Damage inOSA Patients
Chronic intermittent hypoxia is one of the key OSA features and a signicant contributor to adverse OSA consequences [9]. Usually, OSA is characterized by short
episodes of intermittent and high-frequency hypoxemia (for 15–60s) with a cyclic
pattern during sleep. The episodic hypoxemia is followed by a reoxygenation or
reperfusion state after each episode [9]. Hypoxemia induces chemoreex stimulation and consequent vasoconstriction that persists even during normal breathing
daytime wakefulness in OSA patients. Intermittent hypoxia results in an increased
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production of reactive oxygen species, vascular inammation, endothelial dysfunction, and elevated blood pressure. These vascular changes may induce direct damage to the inner ear, which is very sensitive to circulatory alterations since it is
supplied by a single terminal artery and lacks adequate collateral blood supply [10].
Moreover, it is an organ requiring a large amount of energy, but the PO2 level near
the cochlea and vestibule is among the lowest throughout the body. Therefore, when
blood PO2 is reduced, or there is insufcient blood transport, cochlear and vestibular
functions may be severely damaged [11]. In OSA, the base of the cochlea that
receives high frequencies is more sensitive to damage than the apex (coding for low
frequencies), something similar to what is seen in noise exposure and ototoxic
drugs. In particular, the level of natural glutathione was signicantly lower in basal
outer hair cells than in apical outer hair cells, supporting a higher susceptibility of
the basal cell population to free-radical damage. For these reasons, high frequencies
represent the rst and mostly damaged frequencies by snoring and OSA.
For the vestibular system, an induced OSAS vascular inner ear deciency can
cause a change in the otolith’s chemical composition leading to BPPV and abnormal
endolymph homeostasis, causing Meniere’s disease. In vestibular neuritis, although
the etiology of acute unilateral peripheral vestibular decit remains unclear, it may
suggest that the chronically repeated hypoxic episodes would affect the neuronal
activities of the vestibular nucleus and immune responses to herpes virus [12].
The chronic hypoxic state seen in OSA results in the progressive reduction in the
peripheral vestibular system, which consequently becomes asymmetrical. However,
the central vestibular system initially tends to correct this disequilibrium between
the two sides.
Chronic hypoxemia and consequent impairment in blood ow are not the only
mechanisms producing inner ear damage induced by sleep apnea. Recently, another
important contributing factor has been proposed: the noise exposure from snoring
sounds leads to hearing dysfunctions in snorers and their bed partners [13]. In particular, the repeated loud snoring sound from the vibration of an overly long or
oppy soft palate transmits through the Eustachian tube and conductive mechanism,
causing acoustic trauma, particularly at the base of the cochlea, which corresponds
to high-frequency hearing. The persistent acoustic trauma may explain the poor
response to steroid treatment at a high-frequency in patients with OSA and sudden
sensorineural hearing loss (SSNHL) [14]. Snoring also has detrimental effects on
the bed partners. In particular, Sardesai MG etal. [13] observed a unilateral highfrequency pattern of HL consistent with noise-induced HL in the bed partners.
These results pointed out how snoring is not just a “cosmetic” problem, but it can
cause damage to the cochlea.
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11.2.2 Research Studies Linking OSA andHearing Loss
It has been shown that moderate OSA can cause a loss of high-frequency hearing
functions and speech discrimination scores. In contrast, severe OSA has signicant
effects on all hearing functions, as reported by the study by Kayabasi etal. [15]
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Pure-tone and speech recognition thresholds were positively correlated with AHI
and ODI and negatively correlated with min. Oxygen saturation. Speech discrimination scores on both ears were negatively correlated with AHI and ODI and positively correlated with min. Oxygen saturation [15]. Martines etal. [16] did not
detect hearing impairment in simple snorers. In contrast, in patients with moderate/
severe OSA, signicant hearing impairment was shown in the high-frequency range
above 6kHz, especially in the extended high-frequency zone of 10–16kHz. Also,
our group [17] reported cochlea impairment in patients affected with severe OSA,
showing a pure tone average signicantly higher than the control group, and lower
transient evoked otoacoustic emission (TEOAE) reproducibility and distortion
product otoacoustic emissions (DPOAE) amplitude, and prolonged mean latencies
of waves I, III, and V.It is widely known that the otoacoustic emission (OAE) is the
direct reection of the cochlear active mechanisms, attributed to the active process
of outer and inner hair cells; the reduction of the OAE levels can be attributed to a
vulnerability of the hair cells to oxygen blood level. OSA can cause “subliminal”
hearing damage without alteration of hearing thresholds [17]. Many studies showed
a signicant reduction in OAE amplitude in OSA patients without hearing loss
modications. OAE is a kind of sound energy produced in the cochlea, which can
be recorded in the external auditory canal and reect the functional status of outer
hair cells in the cochlea. A possible explanation for this phenomenon is that chronic
hypoxia of the cochlea in OSA patients may damage the outer hair cells, which are
more vulnerable than the inner hair cells, thereby affecting cochlear function. Inner
hair cells transform the sound vibrations from cochlea’s uids into electrical signals
relayed via the auditory nerve to the auditory brainstem. In contrast, the outer hair
cells mechanically amplify low-level sound that enters the cochlea. It has also been
observed that the DPOAE change in amplitude was earlier than that of hearing
thresholds. For these reasons, DPOAE could be used to monitor the cochlear function of OSA patients [18].
C. Manuele and M. Antonio
11.2.3 Tinnitus
Regarding tinnitus, some studies proposed that OSA-induced hypoxemia might
have a negative impact on auditory function, leading to chronic tinnitus [19].
Secondly, tinnitus and SDB are closely associated with anxiety, depression, and
short sleep duration; thus, they might be comorbidities or etiologically related [20,
21]. Many recent studies showed that the risk of tinnitus was found to be signi-
cantly higher among middle-aged and elderly OSA patients [22]. In addition, tinnitus can be considered an “alarm bell” for apnea and may prompt doctors to
diagnose OSA early. In conclusion, OSA patients with Idiopathic SSNHL had signicantly poorer responses to steroid treatment than patients without OSA, especially at high frequencies (4000 and 8000Hz) [14]. There is conicting evidence
regarding middle ear function: one study indicated an increase in middle ear pressure (MEP) [23], and another showed a decrease in this parameter [24]. In contrast,
two studies revealed no changes in MEP in OSA patients [25, 26]. MEP also
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increases in OSA patients during sleep, with the increased pressure proportional to
the number of hours slept [27]. Using a seven-question subjective questionnaire—
the Questionnaire-7 (ETDQ-7)—patients were asked if they experienced symptoms
like ear pain or pressure. One study reported statistically worse Eustachian tube
Dysfunction symptoms in OSA patients despite an unequal sample size (31 OSA vs.
99 healthy controls) [28]. In contrast, another study revealed no difference in
Eustachian tube dysfunction and nasal symptoms compared to the control [29].
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11.2.4 Regarding theTreatment
There are no effective treatments for SNHL except for hearing aids, cochlear
implants, and glucocorticoid treatment for sudden SNHL.The rst-line therapy for
moderate–severe OSA patients is CPAP.However, its failure in long-term adherence is well known, reaching 25%–50% of cases [8]. Through correction of hypoxia
and improvement in cerebral blood ow and central oxygenation, CPAP therapy
directly improves inner ear microcirculation and indirectly could improve auditory
and vestibular functions. Chi JC etal. [30] investigated the effects of CPAP application to SNHL patients with OSA, suggesting that CPAP treatment for 6–12months
may improve pure tone audiometry threshold at low, medium, and average frequencies, when adjusting for age, gender, smoking, alcohol, coronary artery disease,
hypertension, and AHI.Moreover, Alessandrini etal. [31] highlighted that postural
instability and dizziness-related conditions due to OSA improved after 12months
of CPAP treatment. Some evidence investigated whether CPAP would effectively
manage vertigo and hearing loss in Ménière’s disease patients showing signicant
improvement in dizziness handicap inventory (DHI) and audiometric testing [32].
Further investigation is required to determine whether early application of CPAP
can serve as a valid strategy for preventive or therapeutic purposes. Intriguingly,
there is only a single study [33] evaluating the effects of uvulopalatopharyngoplasty
(UPPP) on the auditory functions showing an improvement of transient-evoked otoacoustic emissions after surgery. However, to date, no other similar studies in the
literature support an improvement in hearing functions after the “new” intrapharyngeal remodeling surgeries that are notoriously associated with better results and
fewer complications in compared with the “old” UPPP [34].
11.3 Nose andThroat inOSA Patients
11.3.1 Pharyngeal andLaryngeal Alterations inOSA Patients
Dysphagia is often an underreported OSA complication. Furthermore, the pathophysiology associated with dysphagia in OSA patients remains poorly understood.
A recent review estimated prevalence range from 16% to 78% [35]. Evidence suggests repeated trauma and tissue stretching resulting from low-frequency snoring
vibrations can lead to palatal-pharyngeal injury. Further, this may be associated
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C. Manuele and M. Antonio
with sensory impairments, contributing to not only upper-airway collapse but also
swallowing dysfunction as well. Moreover, OSA perturbs the rhythmic swallowing–breathing coordination, as supported by study ndings of increased duration of
swallow-related respiratory cessation in patients with OSA.An additional factor to
be considered is LPR.Caparroz etal. [36] studied the association of dysphagia and
LPR in patients with moderate/severe OSA.Many authors are convinced that OSA
and gastroesophageal reux coexist because of shared risk factors like obesity or
because one condition aggravates the other. The incidence of LPR is approximately
10% in the general population, whereas, in OSA patients, the incidence ranges from
30.6% to 89.2%. A few studies have suggested that OSA treatment relieves
LPR.During OSA episodes, there is a change in the pressure dynamics inside the
airway with a decrease in intrathoracic pressure and an increase in transdiaphragmatic pressure [37]. This could trigger gastric reux mainly if there is transient
lower esophageal sphincter relaxation. On the other hand, reux is known to cause
airway irritation and bronchospasm through direct or indirect (vagal) mechanisms.
The more severe the apnea is, the higher the degree of reux. This should be considered when treating this group of patients.
Other studies by Nguyen AT etal. [38] showed that upper-airway mucosal sensory function is impaired in the oropharynx and larynx of OSA patients than normal
controls. This could arise from of mechanical injury due to trauma from vibration,
suction collapse, and upper-airway tissue distortion during obstructed respiratory
efforts. Reux of gastric acid and proteases into the laryngopharynx, which has
been reported in OSA, could be a factor [39]. Tissue hypoxia may also play a role.
These insults could produce direct injury to the upper-airway mucosa and may lead
to damage from the production of reactive oxygen species, inammatory cell inltration, and cytokine release. These ndings, therefore, support the study hypothesis
that mucosal sensory function is impaired at multiple levels of the upper airway in OSA.
OSA has been associated with upper-airway inammation, thickened pharyngeal
walls, hypertrophic tonsils, or a thickened and slack soft palate, which may adversely
affect voice production and resonance and contribute to abnormal voice features
[40, 41]. Moreover, it has been suggested that altered structure (including excess
fatty inltration into parapharyngeal tissues) narrows the upper airway and may
contribute to hyperfunctional voice patterns related to efforts to overcome excess
upper-airway resistance. Likewise, chronic snoring may cause dryness and inammation in the upper respiratory system, which may adversely affect the health of the
vocal folds and contribute to disturbances in phonation [42]. Expanding literature
suggests that alterations in upper-airway structure and function may contribute to
unexplained chronic cough (CC), diurnal breathing problems, and voice disorders.
This triad of symptoms is commonly referred to as “irritable larynx syndrome”
(ILS) or more recently “laryngeal hypersensitivity syndrome” (LHS), suggesting
that the larynx becomes hypersensitive or hyperresponsive following overexposure
to a variety of irritants that contribute to “hyperkinetic laryngeal dysfunction” [43].
Descriptions of ILS and related laryngeal motor dysfunction vary considerably, but
most include: [1] dysphonia within the context of a structurally normal larynx
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(combined with excess perilaryngeal muscle activation) [2], transient inspiratory
dyspnea (with lateromedial glottic and/or supraglottic laryngeal narrowing), and [3]
CC, throat clearing, or globus sensation. The exact mechanisms underlying ILS are
unknown (and are likely multifactorial), but laryngeal hypersensitivity possibly
related to sensory neuropathy and/or upper-airway inammation is often proposed
[44, 45].
Further studies will be required to elucidate the mechanisms underlying sensory
and motor impairment and the potential role in the impaired defense of upperairway patency during sleep, which characterizes OSA.
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11.3.2 The Effects ofCPAP Treatment onUpper Airway
Currently, CPAP therapy is the gold standard for treating moderate and severe
OSA.The efcacy of CPAP in an ideal setting is apparent, but adherence to CPAP
may limit its effectiveness in the home setting. It is well known that acceptance and
compliance are often suboptimal in CPAP treatment. It is estimated that 30% to
80% of OSA patients can be classied as nonadherent when using CPAP for less
than 4h per night [46]. Several factors have been linked to CPAP rejection, including patient characteristics (e.g., age, race, and smoking status), disease characteristics (e.g., symptom severity), experienced side effects (e.g., skin irritation, dryness
in the nose or mouth, and abdominal bloating), treatment titration procedures, and
psychosocial factors (e.g., skills at coping with challenging situations, mental health
problems, self-efcacy, and social support). The main complaints are dry nose,
mouth, or throat [47]. In particular, dry mouth can be the reason patients are nonadherent to CPAP therapy. The absence of saliva in the mouth causes an unpleasant
and scratchy sensation, difculty swallowing, bad breath, and the growth of fungi
and bacteria in the mouth with mucosal lesions because saliva’s antimycotic and
antibacterial action is lacking. It is thought that dry mouth is caused by an inux of
air that dries up the oral mucosa. This would seem to be the case when using a fullface CPAP appliance or if a patient’s mouth remained open when using a nasal-only
CPAP appliance [48]. In most cases, the salivary ow rate in OSA patients was
close to normal; only 20% of examined persons had objective signs of hyposalivation. Most cases are associated with mouth breathing but not with salivary gland
hypofunction. CPAP’s role in voice disorder development and maintenance remains
a source of controversy. It is unclear whether CPAP improves or worsens voice
function. For instance, two studies have concluded that CPAP has adverse effects on
voice related to drying of the upper airway and vocal fold mucosa from “nonhumidied” airow [49, 50]. In contrast, Atan D etal. [51] showed that phonatory
function improved in the OSA group after 1month of regular humidied CPAP use.
Likewise, 11 CPAP-adherent participants reported a trend toward voice improvement (as measured by the Voice Handicap Index 10; VHI-10) and a signicant
reduction of reux symptoms after 6months of regular humidied CPAP use [52].
Thus, the relationship between duration, consistency, type of CPAP use, reux
symptoms, and voice problems remains unclear. To improve sleep and quality of life
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of these patients and in particular dryness in the upper respiratory tract, it is recommended that the humidity and temperature of inspired air should be increased by
heated humidication. During spontaneous breathing and mouth leakage, the relative humidity was reduced from 80% to 40%, and heated humidication improved
the relative humidity to 60% [53]. Moreover, positive airway pressure can lead to
nasal complaints, such as nasal obstruction, rhinorrhea, nasal dryness, and sneezing
in up to 44%–65% of CPAP users [54, 55]. Balsalobre etal. [56] showed CPAP use
by awake healthy individuals resulted in worsening of nasal obstruction, which was
more evident in those with a known history of Allergic Rhinitis. Nasal complaints
present prior or secondary to CPAP have also been identied as predictors of CPAP
adherence. For these reasons, nasal obstruction surgical and medical therapy can
still play an essential role in facilitating the treatment of patients with OSA by
improving tolerance and compliance with CPAP.
It is the treating physician’s role to understand the problems related to CPAP use
to maximize adherence. However, due to the high incidence of noncompliance
CPAP, otolaryngologists must offer other treatment options, including various surgical interventions, for these patients so that untreated OSA with its potentially
severe consequences does not go untreated.
C. Manuele and M. Antonio
11.3.3 Postoperative Discomfort, Short andLong-Term
Complications After Intrapharyngeal Surgery
Over the years, the surgeons’ attention has turned to intrapharyngeal surgery, evolving from the older uvulopalatopharyngoplasty (UPPP) to the newer reconstructive
palatal techniques [34]. Several studies have shown that UPPP and other older palatal surgery techniques were associated with a high incidence of unfavorable postoperative complications and comorbidities such as dysphagia, rhinolalia,
velopharyngeal insufciency, and nasopharyngeal regurgitation, phlegm in the
throat, and abnormal scarring with velopharyngeal stenosis [57]. So, compared to
the older techniques, these newer palatal surgery techniques, including Barbed
Pharyngoplasty (BP) based on reconstructive principles respecting the lateral pharyngeal walls and preserving some or part of the uvula, are expected to have fewer
long-term postoperative complications and comorbidities. The palate/pharyngeal
mucosa has profuse tactile and pain innervations and is prone to considerable discomfort. Despite the belief that all of these surgeries lead to severe postoperative
pain, pain the intensity varies according to different techniques [58]. It is typically
present during the rst postoperative days and tends to gradually disappear over
1week. That the postoperative pain was signicantly less in the patients if low temperature plasma surgery was employed [59]. These new intrapharyngeal surgical
procedures, in particular the different Barbed Pharyngoplasties proposed, are very
sure with signicant short- and long-term complications. A recent review [34] found
that thread/knot extrusion was the most frequent short-term complications.
Concerning long-term complications, these patients infrequently experienced dry
throat, throat lump, throat phlegm, mild and moderate dysphagia, rhinolalia, nose
regurgitation, foreign body sensation, and a sensation of sticky mucus in the throat.
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11.3.4 Postoperative Discomfort, Short- andLong-Term
Complications After Hypopharyngeal Surgery
Hypopharyngeal obstruction is prevalent, and its presence is associated with
increased OSA severity. Failure to address hypopharyngeal obstruction can lead to
residual OSA and suboptimal treatment outcomes. Hence, sleep surgeons need to
complete their armamentarium corrective treatment for hypopharyngeal obstruction. One of the most common surgical procedures is epiglottoplasty with or without tongue base reduction. Hypopharyngeal surgery is a safe and well-tolerated
procedure for the treatment of OSA.Potential postoperative complications include
hemorrhage, dyspnea due to tongue or residual epiglottic edema, infection of the
cartilaginous stump of the epiglottis, aspiration, or dysphagia. Usually, patients who
underwent epiglottoplasty with or without tongue base reduction proved to have a
reasonable short-term swallowing outcome with no long-term sequelae [60]. OSA
patients with initial swallowing difculties, particularly during the pharyngeal
phase of swallowing, are not candidates for epiglottic surgery. If there is a question
regarding this, a barium swallow should be performed to rule out aspiration on penetration before considering the procedure.
11.3.5 Side Effects ofMandibular Advancement Devices
forSnoring andSleep Apnea
Mandibular advancement devices (MAD) are the most common oral appliances
used to treat snoring and OSA.Although there are several MAD designs, all devices
protrude the mandible and induce changes in the anterior position of the tongue, soft
palate, lateral pharyngeal walls, and mandible, resulting in improved UP patency
[61]. However, the response to MAD is variable and typically depends on the MAD
design and patient characteristics. MAD is also associated with several side effects.
In the short term, a patient could complain of the Temporomandibular Joint (TMJ)
pain, myofascial pain, tooth pain, salivation, TMJ sounds, dry mouth, gum irritation, and the morning after occlusal changes. Most of these can be managed or even
prevented with conservative behavioral therapy. In the long-term, the main side
effects reported are represented by dentoskeletal changes, which are not clinically
relevant [62, 63].
11.4 Conclusions
OSA is a complex disease with well-known adverse effects on multiple human body
systems. It might affect ENT organs such as hearing and balance disorders, sensory
and motor impairment of the upper airway, problems related to CPAP use, and
short- and long-term side effects after OSA surgery. Otolaryngologists should be
aware of these consequences while preventing or improving multiorgan damage in
OSA patients.
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