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surgery shows a success rate when Friedman’s classication is grade 1 or 2, which
corresponds to the nonobese subject, with low Mallampati, and hypertrophic tonsils
[26]. The shape of the ogival palate and modied Mallampati 3 or 4 were shown to
be associated with AHI [26].
Skeletal craniofacial alterations can be evaluated by physical examination and
conrmed by cephalometry. Related to the diagnosis of sleep apnea are maxillary
and mandibular hypoplasia. In addition, a narrow and ogival hard palate may predispose to OSA [3]. Recently standardized facial photographs have been added to identify facial phenotypes that correlate to skeletal craniofacial alterations and presence
of OSA [27].
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4.3 Complementary Exam intheDiagnosis ofOSA
4.3.1 Nasofibrolaryngoscopy
This exam is critical to evaluate the upper airway and locate possible obstructive
sites involved in the origin of respiratory disorders. Usually used in the ENT ofce,
it allows visualization of tumors and anatomical anomalies [3, 19]. It is fundamental
to mention that the exams are performed during wakefulness and usually in seated
patients.
A complete evaluation of the nasal cavities in detail, the nasopharynx, oropharynx, the soft palate up to the larynx. There is observation of the size of the tonsils,
uvula, lingual tonsils, the base of the tongue and the epiglottis. The Muller Maneuver
research—forced inspiration—allows to simulate the tendency of airway collapse,
but the subjectivity of research and interpretation make its standardization difcult.
Also, aspects suggestive of laryngopharyngeal reux could be investigated.
4.3.2 Drug-Induced Sleep Endoscopy
Drug-induced sleep endoscopy (DISE) has been used for the diagnostic evaluation
of the site of airway obstruction [28] allowing exploration of anatomical sites for a
possible therapeutic intervention. May it be for upper airway surgery (UAS) [29,
30], or mandibular advancement device (MAD) [31]. In addition, sleep endoscopy
is part of the protocols for hypoglossal nerve stimulation implant surgery [32]. It is
also proposed to explore the upper airways for patients who do not tolerate CPAP,
due to the possible identication of structural changes during the use of positive
pressure equipment, for example, patients with an epiglottis that closes the laryngeal inlet while using positive pressure machines [33]. This exam provides a
dynamic assessment of the upper airway [34].
There is a discussion about the best drug to induce sleep, or sedation. Studies
have shown differences between drugs. Comparatively to propofol, midazolam produces greater collapse in the velopharynx and base of the tongue than propofol. The
comparison between propofol and dexmedetomidine showed that propofol increases
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collapse in the entire airway compared to the last one. The disadvantages of using
dexmedetomidine would be the longer onset of action, half-life, and cardiovascular
effects such as bradycardia [34].
On the other hand, when sleep architecture was evaluated, only the use of midazolam for more than 90min of examination allowed an architecture similar to natural sleep, with non-REM and REM sleep [35]. Propofol showed an increase in N3,
a reduction in N1, and the absence of REM sleep [36]. Thus, the evaluation of sleep
endoscopy lasting between 15 and 30 min makes it possible to reliably assess
obstructions occurring in N1 and N2 [34]. Still, there is no clarity about the use of
sleep endoscopy in patients with REM-related OSA.
Given the risks caused by respiratory and cardiological changes, DISE must be
performed under monitoring. It is widely performed in the operating room. Ideally,
monitoring the level of sedation through the bispectral index (BIS) [30]. The
interobserver agreement is linked to the experience in performing DISE, requiring a
learning curve to obtain reliable observations [37].
While evaluating DISE ndings related to the severity of OSA, the lateral collapse of the oropharyngeal region and the anteroposterior region of the base of the
tongue and the BMI were considered predictors of the severity of apnea [38]. A
meta-analysis [39] describes ndings when evaluating the sites of obstruction in 2
points, 92% present obstruction in the soft palate and 58% obstruction at the base of
the tongue. When 4 different levels are evaluated: 84% have obstruction in the soft
palate, 32.8% in the palatine tonsils, 52% for the base of the tongue, and 34.3%; in
the epiglottis. In this study, obstruction at the tongue base correlates with the mean
AHI (Fig.4.4).
E. Zancanella et al.
4.3.3 Biomarkers
A polysomnography exam conrms the nal diagnosis and severity degree of
OSA.However, this laboratory exam is costly, is not readily available, and is timeconsuming. Therefore, there are other tools that expand the diagnosis providing
screening, diagnosis, severity, evolution, and prognosis. Biomarkers could be an
alternative tool. However, OSA is correlated to several metabolic dysfunctions and
comorbidities, making it challenging to identify a high specicity biomarker. Strong
evidence is based on small studies performed in sleep centers or participants with
complaints of snoring and tiredness. There isn’t a population cohort where this
association could be tested.
Meta-analysis have shown that some inammatory biomarkers such as C-reactive
protein, tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin 8
(IL-8), intercellular adhesion molecule (ICAM), vascular cell adhesion molecule
(VCAM), and Selectins. On this M-A, it is possible to highlight that IL-6 is two
times higher in apneic patients than in controls, ICAM 3 times, and IL-8 4 times
higher [40]. Another M-A [41] appointed that plasma IL-6 and IL-10 are suitable
biomarkers to identify adults with or without OSA; this conclusion is inuenced by
the high sensitivity and specicity reported by Li et al. respectively, 100% and
ac
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b
Fig. 4.4 (a) Sleep endoscopy showing retropalatal area obstruction. (b) Sleep endoscopy showing
hypopharynx obstruction. (c) Sleep endoscopy showing larynx collapse (type closing door). (d) Sleep
endoscopy showing larynx collapse (type closing book). [Salzano G, Maglitto F, Bisogno A, et al.
Obstructive sleep apnoea/hypopnoea syndrome: relationship with obesity and management in obese
patient. Acta Otorhinolaryngol Ital 2021;41:120–130. https://doi.org/10.14639/0392-100X-N1100]
d
100% for IL-6 and 100% and 97% for IL-10. Other possible biomarkers that could
be cited are acid uric, PTH, and vitamin D, but the level of evidence does not support clinical use [40, 41].
4.4 Polysomnography andSleep Monitoring
In Sleep Medicine, the patient’s report on objective data about his night of sleep is
often impaired. With polysomnography (sleep monitoring)—perhaps still the only
complementary examination available—it is important to highlight the frequent
complaint of patients submitted to in laboratory polysomnography, and the subjective impression of the evaluated night of sleep does not correspond to the nights
at home.
Understanding the different monitoring modalities and characteristics of each
patient and the pathology may allow a better understanding of the disease. Therefore,
the quality of polysomnography is fundamental for the follow-up of any patient.
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E. Zancanella et al.
4.4.1 Polysomnography—Sleep Monitoring
Polysomnography is still the “gold standard” for the diagnosing Sleep Breathing
Disorders and other sleep-related disorders [1]. It should be performed at night in
the sleep laboratory for at least 6 h under the supervision of a trained technician.
The quality of the test is fundamental for the diagnosis and therapeutic planning,
and post treatment control. Therefore, it is essential to emphasize the need for a new
polysomnography study after the implementation of treatment to measure the real
impact of the proposed treatment.
Sleep monitoring techniques have been systematically updated over the years,
with the incorporation of new technologies [42]. Since the rst standardization for
sleep interpretation in 1968 [43], almost 30 years have passed for a signicant
review of these criteria [44]. The American Academy of Sleep Medicine published
in 2007, and updated in October 2020 (version 2.6) the technical criteria for sleep
monitoring, updating the rules for sleep and respiratory parameters analysis [45].
The minimum parameters to be used in polysomnography are
– Electroencephalogram: electrodes F4–M1, C4–M1, and 02-M1
– Electrooculogram: bilateral
– Electromyogram: chin, tibial anterior bilateral
– Nasal and oral airow recorded by thermistor or thermocouple sensors
– Recording of nasal pressure obtained by a pressure transducer
– Record of thoracic and abdominal movement
– Electrocardiogram
– Oximetry digital
– Hoarse record
– Body position record
Data captured on a polysomnography night should be interpreted by a physician
with a specialization in Sleep Medicine following American Academy of Sleep
Medicine criteria. Reading and interpretation training requires specic training. The
polysomnographic tracing is read in periods of 30s for sleep staging with differentiation of Stages REM and N1, N2, N3, and marking of respiratory and limbs events.
The entire night study is checked by the polysomnographic tracing [44].
The nal report of the polysomnography must provide the following data
• Parameters used for monitoring
• Sleep architecture:
– Total record time—TRT
– Total sleep time—TST
– Efciency: >85% (TST/TRT)
– Latencies: NREM and REM
– Total time awake after sleep onset
– Time at each stage
– Percentage of TST at each stage
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• Arousal:
– Total number
– Index
It is important to have a differentiation between those associated with respiratory
events and those associated with limbs movements: total number and index.
• Cardiac events:
– Frequencies
– Arrhythmias
• Lower limbs movements
– Periodic movements of members
– Awakenings associated with movements
• Respiratory events:
– Hypopnea–apnea index (AHI)
– Oxyhemoglobin desaturations: average, minimum, and desaturation index
per hour
– Predominant decubitus during sleep and in the presence of respiratory events
– Presence of snoring
• Conclusion:
– Description of exam ndings
– EEG abnormalities
– Non-ECG abnormalities
– Behaviors observed during sleep (somniloquism, sleepwalking, etc.)
– Hypnogram (optional)
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4.4.2 Portable Sleep Monitoring—OCST (Out ofCenter
Sleep Testing)
In 1994, the Practical Parameters of the American Association of Sleep Disorders—
the current American Academy of Sleep Medicine [46]—were published for the
evaluation of OSAS with Portable Monitoring, dening the types of Sleep Study—
Table 4.1—and discussing the technical criteria and limitations for its application.
A rational protocol for the indication of home studies, detailing their indications
and limitations, has been delineated over the years. The points listed are for diagnostic suspicion, that entail groups of patients and criteria of use. Undoubtedly,
patients with Sleep Breathing Disorders are the main beneciaries. Collop et al.
[47] describe a owchart rationalizing the indication of Home Monitoring, concluding that this tool should be integrated into a broad program of evaluation and follow up of the patient and conducted by a sleep specialist physician.
This monitoring can be assisted or not by a polysomnography technician and
allows the examination to be recorded in the patient’s home. Its limitation is the loss
of monitoring channels due to failure or loosened channel issues, which has been
estimated between 4 and 33%, and the signicant variability of equipment and
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Table 4.1 Studies for sleep apnea assessment (minimum 06-h monitoring)
Level II
Comprehensive
Level I Standard
polysomnography
Parameters Minimum of seven,
including EEG
(C4-A1 or C3-A2),
EOG, chin EMG,
ECG, airow,
respiratory effort,
oxygen saturation
Body
position
Leg
movement
Personnel In constant
Interventions Possible Not possible Not possible Not possible
EEG electroencephalogram, EOG electrooculogram, EMG electromyogram, ECG
electrocardiogram
Documented or
objectively
measured
EMG or motion
sensor desirable but
optional
attendance
portable
polysomnography
Minimum of seven,
including EEG
(C4-A1 or C3-A2),
EOG, chin EMG,
ECG or heart rate,
airow, respiratory
effort, oxygen
saturation
May be objectively
measured
EMG or motion
sensor desirable but
optional
Not in attendance Not in
Level III
Modied
portable sleep
apnea testing
Minimum of
four, including
ventilation (at
least two
channels of
respiratory
movement, or
respiratory
movement and
airow), heart
rate or ECG,
oxygen
saturation
May be
positively
measured
May be
recorded
attendance
E. Zancanella et al.
Level IV
Continuous
single- or
dualbioparameter
recording
Minimum of
one
Not measured
Not recorded
Not in
attendance
technologies involved. Studies discuss the diagnostic failure of sleep monitoring,
both in the gold standard and in-home monitoring, observing rates of 20% of AHI
failure below 15/h and variations between 15 and 25% in consecutive night studies.
With an interval of 30days, only 45% of the cases presented night-to-night differences less than or equal to 5 events/h.
Type II monitoring allows the identication of different sleep phases with a demonstration of statistics and calculations of AHI/h of sleep. It has the limitation of the
technician going to the patient’s residence to t and remove the equipment the next
day. There is no relocation of registration channels if they are disconnected during
the exam.
Type III monitoring does not assess sleep phases nor differentiate whether the
events occur at wakefulness or during sleep. It gives information and determines
only respiratory events, not allowing the diagnosis of other events such as limb
movement. Some equipment allow the patient to assemble it at home without the
need for the technician to move.
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Type IV monitoring captures 1–2 channels, and one of them is mandatorily
oximetry. It does not evaluate the sleep phases and does not differentiate the types
of apneas but evidences the desaturations. However, it does not allow for the evaluation of any sleep-related data.
Peripheral Arterial Tonometry (PAT) [48] is a new method proposed to diagnose
OSA. This technology uses a sensor (modied digital plethysmography) that eliminates the venous pulse and continuously measures changes in arterial volume in the
nger. Changes in the arterial volume are regulated by α-adrenergic innervation and
reect the sympathetic activity. Events of apneas or hypopneas lead to arousals and
therefore increased sympathetic activity and peripheral vasoconstriction, resulting
in attenuation of the PAT signal. Watch-PAT® is a portable device that detects
obstructive events by noticing changes in sympathetic activity associated with the
end of events. This equipment also aims to analyze, in addition to AHI and RDI,
total sleep time and sleep phases [49].
All portable sleep monitoring should also issue a report showing the type of
monitoring. The parameters used to obtain the data, and a report of the possible
records performed. Version 2.6 of the American Academy of Sleep Medicine
Manual denes the items to report. The clarication of these data will allow the
evidence of objective respiratory data per hour of sleep or monitoring time.
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4.5 Obstructive Sleep Apnea Syndrome
The initial description of Obstructive Sleep Apnea Syndrome was made by
Guilleminault in 1976. The denition of clinical parameters of normality with the
“cutoff” in 5 events/h was described in 1985.
Obstructive sleep apnea is characterized by repetitive episodes of upper airway
obstruction (respiratory events) resulting in oxygen desaturation and awakenings.
The respiratory events are described as:
– Apnea Respiratory pauses of at least 10s, baseline decrease in at least 90% with
respiratory effort in chest brace or abdomen.
– Hypopnea is characterized by partial airway obstruction. They have the same
consequences as apneas. They consist of a decrease in nasal pressure baseline by
30%, minimum duration of 10s and desaturation of 3% or arousal.
– Increased airway resistance is characterized by the same symptomatology of
OSAS but without apnea or hypopnea in polysomnography, with the presence of
RERA: awakening associated with respiratory effort. It consists of an event last-
ing at least 10s with increased respiratory effort leading to an awakening. It can
be evaluated on the ow sensor by a attening on the ow curve extending the
inspiratory period.
The publication of the International Classication of Sleep Disorders—3rd.
Edition 2014—Table 4.2—seeks to highlight, in addition to complaints or symptoms,
the presence of comorbidities and adds the possibility of sleep monitoring being
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Table 4.2 Sleep apnea diagnostic criteria
Diagnostic criteria
((A and B) or C)+D must be met
A.The presence of one or more of the following:
1. The patient complains of sleepiness, fatigue, insomnia, or other symptoms leading to
impaired sleep-related quality of life.
2. The patient wakes with breath-holding, gasping, or choking
3. The bed partner or other observer reports habitual snoring or breathing interruptions
during the patient’s sleep
B.Polysomnography (PSG) or home sleep apnea test (HSAT) demonstrates:
1. Five or more predominantly obstructive respiratory events (obstructive and mixed
apneas, hypopneas, or respiratory effort-related arousals) per hour of sleep during a
PSG or per hour of monitoring (HSAT).
C.PSG or HSAP demonstrates:
1. Fifteen or more predominantly obstructive respiratory events (obstructive and mixed
apneas, hypopneas, or respiratory effort-related arousals) per hour of sleep during a PSG
or per hour of monitoring (HSAT).
D. The symptoms are not better explained by another current sleep disorder, medical disorder,
medication or substance use.
American Academy of Sleep Medicine. International Classication of Sleep Disorders. 3rd ed, text
revision. Darien: IL: American Academy of Sleep Medicine; 2023
E. Zancanella et al.
performed outside the laboratory (OCST). It includes the possibility of the respiratory
event index being described “by monitoring time,” in addition to “per hour of sleep”
as traditionally described validating monitoring without recording sleep data.
4.5.1 Criteria forSeverity ofOSA
The OSA severity criteria were empirically created in 1999 with a publication by the
American Academy of Sleep Medicine (AASM) [50]. This publication created severity categories based on the apnea-hypopnea index (AHI) of polysomnographic examination. The rationale for this classication derived from data from the Wisconsin sleep
cohort [51], a large cross-sectional study that correlated The AHI with the isolated
measurement of blood pressure made on the night of polysomnographic examination.
This study concluded a linear increase in blood pressure with increased AHI and highlighted that the risk of hypertension became substantial with an AHI of around 30 or
more. Therefore, the AASM created the categories of mild, moderate, and severe
OSA, noting that there were no data to differentiate the mild and moderate categories.
However, despite this recognized lack of evidence, this classication remains in vigor
and is widely used in research and clinical practice [52].
According to AHI, OSA in adults is classied as
1. Normal: AHI from 0 to 4.9/h of sleep.
2. Mild: AHI from 5 to 14.9/h of sleep.
3. Moderate: AHI from 15 to 30/h of sleep.
4. Accentuated: AHI above 30/h sleep.
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Note that in this classication, the moderate category includes the AHI limit
values of 15 and 30.
Despite the evolution of the sensors used in polysomnography, and several
changes that occurred in the interpretation of the tracings—particularly in the way
of marking a hypopnea [53, 54]—this classication remains unchanged. In addition, this same classication is used for all types of examinations that record respiratory events during sleep, that is, polysomnography (examination with objective
sleep quantication) and polygraphs (examination without objective quantication
of sleep). Some sleep laboratories record, in addition to apneas and hypopneas, a
third respiratory event known as “RERA” (respiratory effort related arousal: awakening associated with respiratory effort). The index that sums apneas, hypopneas
and RERAs is known as respiratory disorder index (RDI). The numerical criterion
of severity used for the RDI is the same used for the AHI above.
For the population under 18years of age, the most used OSA severity classication involves obstructive AHI (AHIo) [53]. In obstructive AHI, obstructive and
mixed apnea events and obstructive hypopneas are added, excluding apneas and
hypopneas of a central nature. It should be emphasized that this classication of
severity for children has even less scientic evidence than that used in adults and
reects little on the overall well-being of the child. According to AHIo, OSA in
children is classied as:
1. Normal: AHIo from 0 to 1/h of sleep.
2. Mild: AHIo from 1.1 to 5/h of sleep.
3. Moderate: AHIo from 5.1 to 10/h of sleep.
4. Accented: AHIo above 10/h of sleep.
Although widely used, a simple numerical criterion is not sufcient to categorize, nor reect, the various clinical presentations of patients with OSA. The oximetry values, although they point to the intensity of OSA, have not yet been effectively
incorporated into any classication of the severity of this disease. It is believed that
the spectrum of OSA is better understood when considering, in addition to polysomnography, the symptomatic aspects (such as daytime sleepiness and sleep quality) and the comorbidities present in each individual. However, incorporating this
information into a new classication of severity of OSA has not yet occurred.
The evaluation of snoring remains without objective parameters for its measurement during sleep monitoring.
Take-Home Message
• Diagnosis of OSA is performed with a complete clinical history, sleep question-
naires, and a complete physical examination.
• Complementary physical examination includes a Nasoberolaryngoscopy, Drug-
induced sleep endoscopy (DISE), and Biomarkers.
• There is a need to perform a Sleep test. There are diverse types of sleep tests,
with Polysomnography being the “Gold Standard”. However, the limitation of
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E. Zancanella et al.
possibilities to perform this test has made it necessary to perform more simpli-
ed sleep tests.
• According to AHI, OSA in adults is classied as:
• Normal: AHI from 0 to 4.9/hour of sleep.
• Mild: AHI from 5 to 14.9/hour of sleep.
• Moderate: AHI from 15 to 30 /hour of sleep.
• Severe: AHI above 30/hour sleep.
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