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19 Ophthalmology: Neuro-Ophthalmological
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Anesthesia Considerations in
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Obstructive Sleep Apnea
AbigailAlmaguerValadez, BeliaGarduño,
LiliaMayorgaPadilla,
andDanielaAlejandraBecerrilGaitan
20.1 Introduction
Obstructive sleep apnea (OSA) is a condition in which the upper airway is periodically, partially, or completely obstructed during sleep, causing hypoxia, hypercarbia, sleep disorders, and various medical complications, including daytime
sleepiness and an increased risk of hypertension, diabetes, and cardiovascular disease [1, 2].
The name obstructive sleep apnea–hypopnea syndrome was adopted by consensus using the acronym OSA.OSA is characterized by recurrent episodes of apnea or
hypopnea that generate desaturations and microarousals due to upper airway collapse during sleep. These events produce inammatory, cardiovascular, neurocognitive, and metabolic responses that increase the patient’s morbidity and mortality
[1, 3, 4].
The prevalence of OSA in the general population varies from 3% to 7% for adult
men and 2% to 5% for adult women, depending on the population studied and the
diagnostic criteria used [1]. The prevalence is greater in surgical patients, between
24% and 41% [5]. The main risk factors associated with the development of OSAHS
are obesity, male sex, and increased age [2, 3].
Senaratna etal. in 2017 published a systematic review that reported patients with
an apnea–hypopnea index (AHI) ≥5 events/hour with a prevalence in the general
20
A. A. Valadez (*) · B. Garduño · L. M. Padilla
Jose Eleuterio Gonzalez University Hospital, Monterrey, Mexico
D. A. B. Gaitan
Hospital Universitario Jose Eleuterio Gonzalez, Monterrey, Mexico
Hospital Angeles Valle Oriente, San Pedro Garza García, Mexico
© 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_20
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A. A. Valadez et al.
population of 9% to 38%, a predominance in men, and a proportional increase with
age. This factor was found in some groups of elderly adults, reaching 90% in men
and 78% in women. The prevalence of OSA was also greater in obese men and
women [6].
These studies demonstrate that OSA is associated with increased perioperative
morbidity and mortality. These patients have a greater risk of cardiovascular and
respiratory compromise and a possible transfer to intermediate or intensive care in
the immediate postoperative period.
20.2 Physiopathology
Upper airway obstruction that leads to obstructive apnea occurs when negative pressure generated by the inspiratory muscles exceeds the pressure of the dilator muscles of the pharynx [2, 7]. These muscles have tone and are driven by mechanoreceptors
and chemoreceptors. OSA occurs when the muscles of the soft tissues of the pharynx, such as the tongue, palate, uvula, or lateral walls, relax, causing airway narrowing, vibration, tremor of the soft tissues, and/or partial or total closure that causes
breathing to stop momentarily [8, 9].
The shape of the mandible, adipose tissue, the area of the palate, the uvula, and
the size of the tongue form the upper airway (Fig.20.1) [10]. In addition to the anatomical structures, the central nervous system coordinates airway opening; for
Fig. 20.1 PatilAldreti test
20 Anesthesia Considerations in Obstructive Sleep Apnea
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example, when we talk or swallow during the day. At night, pharyngeal muscle tone
decreases and, therefore, favors collapse. The diaphragm, which continues to be
active, must work harder to overcome the increased upper airway pressure [1, 9,
11]. This effort can cause microarousals that coincide with airway opening and
normalization of breathing. The succession of microarousals during the night disrupts the sleep cycle causing nonrestorative sleep [9].
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20.2.1 The Cardiovascular Mechanism inPatients withOSA
Patients with apnea–hypopnea syndrome suffer intermittent hypoxia with periods of
decreased oxygen saturation and increased CO2. These changes increase sympathetic tone, which causes vasoconstriction and raises arterial pressure [12]. Hypoxia
releases vasoactive substances such as endothelin, which increases blood pressure.
When intermittent hypoxia occurs with sleep disruption, inammatory mediators
related to cardiovascular diseases, such as C-reactive protein, cytokines 6 and 8, and
tumor necrosis factor, are released. Therefore, systemic inammation, sympathetic
activation, and oxidative stress produce endothelial damage and, as a result, cardiovascular disease [13]. It is frequent to see patients with OSA and hypertension. It is
estimated that 35% to 80% of patients with OSA have hypertension, and approximately 40% of individuals with hypertension have OSA [14].
20.3 Clinical Presentation
OSA is a common problem that has been detected more frequently. However,
patients and doctors are not aware of this problem. Physicians do not routinely ask
their patients about sleep symptoms to reach a precise diagnosis, especially before
a surgical procedure [15, 16].
This syndrome is linked to daytime sleepiness, cognitive dysfunction, cardiovascular problems such as hypertension, ischemic heart disease, arrhythmias, pulmonary hypertension, congestive heart failure, metabolic dysfunction, and reduced
quality of life [12].
Risk factors for OSA include obesity, a body mass index greater than 35kg/m2,
male gender, excess alcohol intake, smoking, a neck circumference greater than
40cm, and low physical activity [2, 17].
20.4 Diagnostic andSeverity Criteria
20.4.1 Apnea–Hypopnea Index (AHI)
The apnea–hypopnea index represents the number of respiratory events (apneas,
hypopneas, and microarousals) per hour of sleep. It is used to identify cases, quantify disease severity, and determine disease prevalence in normal and clinical populations. Apnea is when an individual stops breathing for 10 s or more during a
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polysomnogram. Hypopnea is dened when there is a ≥3% oxygen desaturation
from baseline and/or when the event is associated with an arousal. A score greater
than 5 events is diagnostic of OSA [18, 19].
• An AHI≥5 per hour is mild.
• An AHI≥15 but <30 per hour is moderate.
• An AHI≥30 per hour is severe.
A. A. Valadez et al.
20.4.2 Heart Failure andOSA
The apnea–hypopnea index is useful for evaluating patients with heart failure.
Patients with moderate or severe OSA have twice the mortality compared to those
with heart failure without apnea or with mild apnea [20]. For example, a patient
with an AHI greater than 30 per hour has a probability of 58% of developing heart
failure compared to those with 5 events per hour [21]. These patients are also more
likely to have arrhythmias such as atrial brillation and ventricular arrhythmias,
which can cause sudden death.
20.4.3 Arrhythmias andOSA
A series of events such as increased diastolic ventricular pressure plus dilatation
with increased atrial wall pressure plus hypoxemia, hypercapnia, and autonomic
stimulation cause arrhythmias in patients with OSA [22, 23].
The most frequent arrhythmias are atrial brillation in up to 49%. Atrial and
ventricular tachycardia and ventricular extrasystoles are also seen in approximately
40%. Arrhythmia episodes are more frequent at night and increase with the severity
of OSA [22, 23].
Sinus pauses or bradycardias are common, most often during rapid eye movement (REM) sleep when apneas tend to be prolonged. Bradycardias depend on the
number of episodes of apnea and hypoxia, which are more frequent with severe OSA.
The QTc interval is prolonged during apnea and shortens in the postapnea period.
This prolonged QT interval favors ventricular arrhythmias and is directly related to
OSA severity [22].
20.4.4 Pulmonary Hypertension andOSA
This common anomaly in OSA is more marked during REM sleep. It occurs due to
activation of the autonomic nervous system, hypoxic alveolar vasoconstriction, and
increased intrathoracic negative pressure. The latter because of the inspiratory effort
caused by the obstructed airway [20].
Pulmonary hypertension is more common in obese individuals or when chronic
obstructive pulmonary disease is present and is not directly related to the
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apnea–hypopnea index as in cardiovascular disease. OSA is associated with repetitive nocturnal arterial oxygen desaturation and hypercapnia, large changes in negative intrathoracic pressure, and acute increases in pulmonary artery pressure.
Rodents exposed to several hours of brief, intermittent hypoxia to mimic OSA
develop pulmonary vascular remodeling, pulmonary hypertension, and right ventricular hypertrophy. However, it was unclear whether OSA-associated episodic
nocturnal hypoxemia is sufcient to cause similar changes in humans [24].
Recent studies have shown that pulmonary hypertension occurs in 20% of
patients with OSA in the absence of other cardiopulmonary disorders and with pulmonary artery pressure reductions in patients with OSA after nocturnal continuous
positive airway pressure treatment. OSA-associated pulmonary hypertension is
mild and may be due to a combination of precapillary and postcapillary factors,
including pulmonary arteriolar remodeling, hyperreactivity to hypoxia, left ventricular diastolic dysfunction and left atrial enlargement [24, 25].
The development of pulmonary hypertension is a poor prognostic sign in patients
with OSA and affects mortality and quality of life. Although pulmonary hypertension in OSA is traditionally viewed as a result of apneas and intermittent hypoxia
during sleep, recent studies indicate that neither of these factors correlates very well
with pulmonary artery pressure. Human data show that pulmonary hypertension in
the setting of OSA is largely due to left heart dysfunction with either preserved or
diminished ejection fraction. Longstanding increased left heart lling pressures
eventually lead to pulmonary venous hypertension. The combination of hypoxic
pulmonary vasoconstriction and pulmonary venous hypertension with abnormal
production of mediators will result in vascular cell proliferation and aberrant vascular remodeling leading to pulmonary hypertension. These changes are similar to
those seen in other forms of pulmonary hypertension and suggest shared mechanisms. Most patients with OSA are not diagnosed and undertreated. Appreciating
the high prevalence and understanding the mechanisms of pulmonary hypertension
in OSA would lead to better recognition and management of the condition [25].
Changes have been reported in the structure and function of the right ventricle in
patients with OSA; however, their clinical signicance has not been demonstrated.
Right ventricular failure in OSA seems uncommon and is more likely if there is
coexisting left-sided heart disease or chronic hypoxic respiratory disease [24].
Obstructive sleep apnea affects up to 4% of middle-aged adults. The most common complaints are loud snoring, restless sleep, nocturia, and excessive daytime
sleepiness, which can reduce the quality of life. Patients may develop cardiovascular abnormalities because of repetitive snoring, airway collapse, and arousal. Most
patients are overweight and have a short, thick neck. Some are of normal weight but
have retrognathia. Patients with obstructive sleep apnea may go undiagnosed
because they are unaware of their heavy snoring and nocturnal arousals; therefore,
it is helpful to question the bedroom partner or a family member about chronic
sleepiness and fatigue [1, 17, 26].
Polysomnography in a sleep laboratory is the gold standard for conrming the
diagnosis of obstructive sleep apnea; however, the test is expensive and not widely
available. Home sleep studies are less costly but not as diagnostically accurate.
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Treatments include weight loss, nasal continuous positive airway pressure, dental
devices that modify the tongue or jaw position, and upper airway and jaw surgical
procedures in selected patients; however, surgery is restricted because of its invasiveness and expense [26].
A. A. Valadez et al.
20.5 Diagnosis
20.5.1 The Berlin Questionnaire
This questionnaire is frequently used for OSA in primary care. It includes 11 questions organized into three categories. The predictive yield of the Berlin questionnaire for OSA varies according to the diversity of the populations. Sensitivity ranges
from 54% to 86% and specicity from 43% to 87% in primary care patients. The
questionnaire has not been validated in surgical patients (Table20.1) [17, 27].
20.5.2 The ASA STOP Questionnaire
A checklist—the ASA STOP questionnaire—has been recommended as a routine
tool for OSA in the perioperative management of patients with obstructive sleep
apnea. The STOP questionnaire was developed and validated for surgical patients as
a useful tool in individuals with OSA or suspicion of OSA.Some studies have validated the Berlin and ASA-STOP questionnaire as diagnostic tools for OSA in surgical patients [27].
Patients with undiagnosed OSA have increased perioperative morbidity and
mortality. Anesthesiologists require a sensitive instrument to identify patients with
a high risk of OSA.Although several predictive questionnaires have been developed
to identify patients with OSA, none have been validated for surgical patients. The
STOP-BANG questionnaire has been studied the most (Table20.2) [28, 29].
20.5.3 Epworth Sleepiness Scale
Several scales assess excessive daytime sleepiness in patients with OSA.Among
these is the Epworth Sleepiness Scale (ESS), which is frequently used [30]. It is a
self-administered questionnaire with 8 questions that measure daytime sleepiness.
It is based on a 4-point scale (0–3) that measures the subject’s propensity to doze off
or fall asleep in different situations that occur in common daily activities. The ESS
score ranges from 0 to 24. The higher the score, the higher the person’s propensity
in daily life [31].
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Table 20.1 The Berlin questionnaire
Name: ___________________ Date. _____ Age: _____ Gender: _____
Weight: _____ kg Height: _____ cm
1. Has your weight changed in
the last 5years?
A.Increased
B.Decreased
C.Has not changed
2. Do you snore?
A.Yes
B.No
C.Don’t know
3. Is your snoring…?
A.Slightly louder than
breathing
B.As loud as talking
C.Louder than talking
D.Very loud that it can be
heard in the next room
4. How often do you snore?
A.Every night
B. 3–4 times a week
C. 1–2 times a week
D. 1–2 times a month
E.Never or rarely
5. Has your snoring ever
bothered other people?
A.Yes
B.No
C.Don’t know
6. Has anyone noticed that you
stop breathing during your
sleep?
A.Almost every night
B. 3–4 times a week
C. 1–2 times a week
D. 1–2 times a month
E.Rarely or never
Category 1. Questions 2–6: High risk: 2 or more of the underlined answers
Category 2. Questions 7–9: High risk: 2 or more of the underlined answers
Category 3. Question 10: High risk: One yes and/or body mass index greater than 30
7. Do you feel tired or fatigued in the
morning after your sleep?
A.Almost every day
B. 3–4 times a week
C. 1–2 times a week
D. 1–2 times a month
E.Never or rarely
8. Do you feel tired or fatigued during
the day?
A.Almost every day
B. 3–4 times a week
C. 1–2 times a week
D. 1–2 times a month
E.Never or rarely
9. Have you ever felt sleepy or fallen
asleep as a passenger or while
driving a vehicle?
A.Yes
B.No
9.1 If the answer is yes, how often
does this happen?
A.Almost every day
B. 3–4 times a week
C. 1–2 times a week
D. 1–2 times a month
E.Never or rarely
10. Do you have
high blood
pressure?
A Yes
B.No
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Table 20.2 The STOP-BANG questionnaire
STOP-BANG questionnaire
S Snoring Do you snore loudly (loud enough to be heard through a closed
door?
T Tired Do you often feel tired, fatigued, or sleepy during the daytime?
O Observed apnea Has anyone observed you stop breathing during sleep?
P Pressure Do you have or are you being treated for high blood pressure?
B Body mass index Is your body mass index more than 35kg/m2?
A Age Are you older than 50?
N Neck circumference Is your shirt collar 40cm or greater?
G Gender Are you male?
High risk of obstructive sleep apnea syndrome: Yes to 5–8 questions
Intermediate risk of obstructive sleep apnea syndrome: Yes to 3–4 questions
Low risk of obstructive sleep apnea syndrome: Yes to 0–2 questions
A. A. Valadez et al.
20.6 Polysomnography, Home Sleep Apnea Testing,
andDrug-Induced Sleep Endoscopy
20.6.1 Polysomnography
Conventional polysomnography (PSG) is a simultaneous recording of neurophysiological and cardiorespiratory variables that assesses the quantity and quality of
sleep [32] and identies different cardiac, respiratory, and motor events and their
impact on sleep [33].
PSG can be performed at night, or during the subject’s habitual sleep schedule,
with at least 6.5h of recordings and 180min of sleep [4].
There are common parameters recorded in almost all PSG studies, such as electroencephalography (EEG), electrooculography (EOG), surface electromyography
(EMG), and electrocardiogram (ECG) channels, nasobuccal ow, and/or respiratory
bands. Sleep apnea protocols focus on recording respiratory and cardiac parameters,
which include oxygen saturation (SaO2) by pulse oximetry, respiratory effort recordings with thoracic or abdominal bands, snoring sensors, and nasobuccal ow using
pneumotachographs or thermistors [4, 8, 26].
Ambulatory monitoring for simplied diagnosis of sleep apnea (Home PSG).
Home PSG consists of a compact and simple device for home sleep with up to
ve information channels: respiratory effort, pulse, oxygen saturation, nasal ow,
and snoring. This device also provides a longer recording time and storage space
[34, 35].
Parameters
• Central, obstructive, and mixed apnea index.
• Hypopnea index.
• Apnea–hypopnea index.
• Flow limitation with and without snoring.
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• Oxygen desaturation index.
• Probability screening for Cheyne–Stokes respiration to help determine when to
refer patients for further laboratory diagnosis.
• Differentiation between obstructive apnea and central apnea.
20.6.2 Drug-Induced Sleep Endoscopy
Although nocturnal PSG is the study of choice or the “gold standard” for this syndrome, it does not exactly locate the upper airway obstruction [8, 26]. Drug-induced
sleep endoscopy (DISE) is a broendoscopic examination in which sleep is induced.
Airway videoendoscopy is performed to determine where the greatest obstruction
occurs during sleep [36].
DISE is an invasive study that dynamically assesses the anatomical structures of
the upper airway. It is performed with a 4-mm berscope while the patient is sedated
with anesthetic drugs. It must be carried out in the operating or endoscopy room
with essential monitoring (electrocardiogram, pulse oximetry, and noninvasive
blood pressure measurement). It is convenient to measure sedation depth with the
bispectral index (BIS), maintaining adequate sedation with a BIS value between 60
and 70 [37, 38].
The patient is evaluated in three positions, supine, right lateral decubitus, and left
lateral decubitus, with mandibular advancement in the same positions [39]. The
study is used for diagnosis and as a tool in case of planned surgery and when surgery
is indicated for the patient. The soft palate, and the lateral walls of the oropharynx,
including the palatine tonsils, tongue, and epiglottis, are observed as part of the
protocol [38]. The most frequently used anesthetic drugs for this procedure are propofol and dexmedetomidine (Table20.3) [36, 40].
Table 20.3 Differences and effects of anesthetic drugs used for drug-induced sleep endoscopy
Agent
Drug characteristics Alkylphenol Alpha-2 adrenergic
Site of action or
receptors
Use in anesthesia Inductor of anesthesia
Cardiac effect Reduces systemic vascular
Respiratory effect Dose-dependent depression Minimal respiratory depression
Cerebral effect Neuroprotector
Start of anesthetic
effect
Drug elimination 7–10min More than 20min
Propofol
Gamma-aminobutyric acid
(GABA)
Total intravenous anesthesia
(TIVA)
Sedation
resistance
Reduces blood pressure
Anticonvulsant
2–8min After 10min
Dexmedetomidine
Alpha-2 receptors in the locus
ceruleus
Antihypertensive
Sedative
Analgesic
Maintenance of anesthesia
Reduces blood pressure
Reduces heart rate
Neuroprotector
Induces physiological sleep
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