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A. Dardeer et al.
26.7 Obstructive Sleep Apnea (OSA)
andPostoperative Complications
According to a recent meta-analysis, patients having OSA who are undergoing
non- cardiac surgery are more prone to cardiorespiratory complications compared
to non-OSA patients. These complications include, but are not limited to, desaturation in the postoperative phase, respiratory failure, cardiac events, and unplanned
transferals to ICUs [84]. It is the effect of the hypnotic sedative agents used in
general anesthesia or sedation that causes these patients to have such complications. The pharyngeal muscles are prone to collapse, closing the airway, which
might be augmented by the sedative effect of anesthesia, leading to respiratory
complications. This periodic collapse/reopening of the airway causes hypoventilation and acidosis, sympathetic activation, and hypoxia, which eventually leads to
the various cardiovascular complications associated with OSA [82–84]. The risk of
OSA may not normalize for several nights postoperatively, with the greatest risk on
postoperative night three. Later, the disturbance and rebound in Rapid Eye
Movement (REM) sleep, caused by administration of high doses of opioids in the
postoperative period, which suppress REM, causes sleep deprivation and related
consequences [85].
26.8 Conclusion
OSA is associated with a number of upper airway anatomical and physiological
changes that pose a signicant challenge to perioperative care. The effects of sedatives, analgesics, and anesthetics can worsen OSA airway and ventilation. OSA has
a three-to-four-fold higher risk of DI when compared to non-OSA patients. Acute
and chronic pathologies of the epiglottis that cause OSA, despite being uncommon,
mandate attention from both anesthetist and surgeon, as they impose certain challenges to both diagnosis and management. The golden rule in an OSA patient is the
maintenance of airway control either by the patient or by the anesthetist. Extubation
is a critical time in the management of OSA patients and should be well planned
ahead with multiple layers of safety.
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27
MohamedAbdelwahab, RakhaAbdelwahab,
andRobsonCapasso
27.1 Introduction
27.1.1 The Problem
Obstructive sleep apnea (OSA) is a prevalent yet treatable chronic condition affecting over a billion subjects globally [1]. Subjects with OSA are reported to be up to
38% of the US population [2]. However, when we evaluated subjects with insurance
coverage, this percentage was only 4.34% of all enrolled subjects, indicating that
over 80% of the population likely remain undiagnosed [3]. Beyond debilitating
quality of life daytime symptoms and possible partner sleep issues, associated oxygen desaturations seem to lead to worsened cardiovascular outcomes, including systemic hypertension, increased incidence of stroke, heart failure, atrial brillation,
and coronary heart disease [4–8].
Managing OSA can be difcult, as phenotyping respiratory drive and airway col-
lapsibility remains a challenge [5, 6]. Anatomical (including the craniofacial
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-34992-8_27. The videos can be accessed individually by click-
ing the DOI link in the accompanying gure caption or by scanning this link with the SN More
Media App.
M. Abdelwahab
Sleep Surgery Division, Department of Otolaryngology Head and Neck Surgery, Medical
University of South Carolina, Charleston, SC, USA
R. Abdelwahab
Department of Otolaryngology, Head and Neck Surgery, School of Medicine, Mansoura
University, Mansoura, Egypt
R. Capasso (*)
Division of Sleep Surgery, Department of Otolaryngology-Head & Neck Surgery, Stanford
University Medical Center, Stanford, CA, USA
e-mail: rcapasso@stanford.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
M. Delakorda, N. de Vries (eds.), The Role of Epiglottis in Obstructive Sleep
Apnea, https://doi.org/10.1007/978-3-031-34992-8_27
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M. Abdelwahab et al.
skeleton, neck dimensions, and airway soft tissue anatomy) [9, 10] and physiological (including the loop gain, arousal threshold, and transmural pressure) [11] phenotypes of OSA have been extensively studied. [12, 13] While our group has dened
and continued to improve the comprehensive approach to OSA management since
1986 [14–16], an important step is to dene the pattern, level, and triggers of airway
collapse. This collapse occurs most commonly at the level of the Velum, but may
involve the Oropharynx (lateral pharyngeal wall), tongue base and less commonly
the Epiglottis (therefore the acronym VOTE), or a combination of any of the above
[17–19]. The VOTE classication based on drug-induced sleep endoscopy (DISE),
describing the dynamic airway obstruction, has guided and warranted reproducibility of our understanding of airway collapse during sleep.
Laryngeal obstruction in OSA results from collapse of the laryngeal inlet, formed
by the epiglottis, aryepiglottic folds, the arytenoids, and the overlying mucosa. This
may be primary (also known as “oppy epiglottis”) (Fig.27.1) or secondary, when
the epiglottis is retro-displaced by the tongue base (Fig.27.2). Epiglottic collapse
may be difcult to treat with conservative therapies, such as oral appliances [20]
Fig. 27.1 An example of
a oppy epiglottis on sleep
endoscopy
Fig. 27.2 An example of
a retrodisplaced epiglottis
on sleep endoscopy

27 Future Directions
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and CPAP, [21] and has shown to be a predictor of OSA persistence after surgical
treatments [22].
However, prior to considering a surgical intervention, it is important to investigate the following: when does the epiglottic collapse (based on DISE) requires
treatment beyond positional measures, and the type of intervention required that
could minimize risks of immediate and long-term swallowing dysfunction and aspiration due to a modied supraglottic anatomy.
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27.1.2 Relevant Anatomy
The epiglottis is a leaf-like sheet of elastic brocartilage that is curled-out and laterally attached to the aryepiglottic folds. The laryngeal inlet is usually wide to avoid
its collapse with inspiration according to the Bernoulli’s phenomenon. The lower
narrow part, the petiole, is attached to the posterior surface of the thyroid alae at
their junction just above the anterior commissure. The anterior surface is separated
from the hyoid and thyrohyoid membrane by pre-epiglottic space. It projects
upwards and backwards behind the tongue and the hyoid bone, separated from the
tongue by the vallecula. The aryepiglottic ligaments and overlying mucosa (folds)
form the sides of the laryngeal inlet between the apex of arytenoid & the upper free
edge of epiglottis on both sides [23, 24].
The shape can be classied into: (1) omega-shaped (sharply curved if the
angle between its lateral parts was less than 90° at the central portion) epiglottis;
(2) normally curved epiglottis shape; and (3) at epiglottis. An epiglottis was
classied as at if its medial part lacked the characteristic anterior convexity
[25]. In most cases of obstruction at epiglottis and/or tongue base, the epiglottis
was at (type 3), where it was lacking the typical anterior convexity in its upper
part. The hypothesis was that the change of its shape is a result of degeneration
of the suspensory apparatus that maintains the convexity of the epiglottis and
maintains it in position. This may help identify patients with narrowing at this
level [25]. Another nding was that subjects with isolated epiglottic collapse
have lower mandibular plane to hyoid distance and tend to have a bigger angle of
their epiglotic curvature [26]. For full details on anatomy, please review Chap. 5.
Epiglottic collapse can vary based on the phenotype from a oppy epiglottis
(primary) to a retro-displaced epiglottis by the tongue base (secondary) and from
partial to complete collapse. The epiglottis can also collapse into two different
patterns: one where it is retro-displaced in an antero- posterior (AP) direction,
thereby obstructing the laryngeal inlet. This is also known as the trapdoor phenomenon. Alternatively, it can collapse in a lateral direction (omega-shaped pattern), thereby resulting in obstructing at the level of the hypopharynx or laryngeal
inlet [17–19].
In pediatric cases with laryngomalacia, the epiglottis is omega-shaped, and the
aryepiglottic folds are medially posed resulting in a narrow laryngeal inlet
(Fig.27.3). This narrow inlet results in collapse with inspiration presenting with

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Fig. 27.3 An example of
an endoscopic view of an
omega shaped epiglottis in
a 2-day old newborn with
laryngomalacia
M. Abdelwahab et al.
stridor and/or OSA.The former being the main symptom due to increasing negative
pressure according to Bernoulli’s effect [23, 24, 27, 28].
27.1.3 Diagnosis
Non-invasive imaging techniques such as magnetic resonance imaging (MRI) and
computed tomography (CT) scan have been described to detect anatomic and functional impairments of the upper airway in OSA patients during wakefulness [29].
However, these techniques are not suitable for clinical practice due to cost and the
challenge of having adequate imaging during natural sleep. While it has some limitations, DISE is the most commonly used tool for detecting the level(s), severity,
and patterns of airway collapse [25]. This can guide the surgical intervention,
towards either the palate, the pharynx, or the larynx.
In our practice at Stanford, we rely on manual-controlled propofol infusions.
Preoperatively, the patient is given nasal decongestant (oxymetazoline). As sedation
is started and before the patient is sleepy, the surgeon places the distal chip-on-tip
exible scope into the nares on the side with least obstruction. The scope is preferably passed through the middle meatus, on top of the inferior turbinate, and inferior
to the middle turbinate, and advanced posteriorly until the posterior wall of the
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