Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Contents
- •Contributors
- •1.6 Mixed Disorders
- •1.7 Isolated Symptoms
- •1.7.1 Snoring
- •1.7.2 Catathrenia
- •1.8 Summary
- •References
- •1.1 Introduction
- •1.2 Obstructive Sleep Apnea
- •1.2.1 Obstructive Sleep Apnea, Adult
- •1.2.2 Obstructive Sleep Apnea, Pediatric
- •1.3 Central Sleep Apnea
- •1.3.5 Primary Central Sleep Apnea
- •1.5 Sleep-Related Hypoxemia Disorder
- •2.7 Summary
- •References
- •3: Health Consequences of Obstructive Sleep Apnea
- •3.1 Cardiovascular Consequences
- •3.1.1 Chronic Heart Failure
- •3.1.2 Systemic Hypertension
- •3.1.3 Coronary Heart Disease
- •3.1.4 Arrhythmias
- •3.1.5 Cerebrovascular Disease
- •3.2 Respiratory Consequences
- •3.2.1 Asthma
- •3.2.3 Pulmonary Embolism
- •3.2.4 Pulmonary Hypertension
- •3.3.1 Diabetes Mellitus
- •3.3.2 Metabolic Syndrome
- •3.3.3 Sexual Dysfunction
- •3.4 Gastrointestinal Consequences
- •3.4.2 Nonalcoholic Fatty Liver Disease
- •3.5 Obstetric Outcomes
- •3.5.2 Gestational Diabetes
- •3.5.4 Maternal Surgical Complications
- •3.6 Perinatal Outcomes
- •3.6.1 Impaired Fetal Growth
- •3.6.2 Preterm Birth
- •3.6.4 Stillbirth
- •3.6.5 NICU Admission
- •3.7 Perioperative Outcomes
- •3.8 Accident-Related Consequences
- •3.9 Cancer-Related Outcomes
- •3.10 Survival Outcomes
- •3.10.1 Overall Mortality
- •3.10.2 Cardiovascular Death
- •3.10.4 Perioperative Mortality
- •References
- •4.1 Patient Case
- •4.2 Introduction
- •4.3 History
- •4.4.1 Oxygen
- •4.4.2 Vascular
- •4.4.3 Endocrine
- •4.6.1 Attention & Executive Function
- •4.6.4 Visual-Spatial
- •4.7 Summary
- •References
- •5.1 Introduction
- •5.2 Obesity
- •5.3 Hypertension
- •5.4 Diabetes Mellitus
- •5.5 Fatty Liver Disease
- •5.6 Conclusions
- •References
- •6.1 Background
- •6.2 History Taking
- •6.3 Physical Examination
- •6.4 Conclusion
- •References
- •Further Reading
- •7.1 Background
- •7.2.2 Screening Tools
- •7.2.3 Diagnostic Tests
- •7.2.7 Clinical Guidelines
- •7.3 Home Sleep Apnea Test (HSAT)
- •7.3.1 Advantages
- •7.3.2 Disadvantages
- •7.3.3 Patient Selection
- •7.3.4 Data Obtained
- •7.3.8 Recommended Follow-Up
- •7.3.9 Clinical Outcomes
- •7.4 Polysomnography (PSG)
- •7.4.1 Patient Selection
- •7.4.4 Follow-Up
- •7.5 Conclusions
- •Further Reading
- •8.1 Introduction
- •8.4 CBCT and OSA
- •8.5.1 CPAP
- •8.5.2 Oral Appliances
- •8.5.3 Maxillomandibular Advancement
- •8.6 Upper Airway Stimulation
- •8.7 Summary
- •References
- •9.1.1.1 Cranial Base Lengthening
- •9.1.1.2 Cranial Base Flexion
- •9.1.5.3 Tongue Growth
- •References
- •10.2.1.1 Cranial Base
- •10.2.1.2 Facial Height
- •10.2.1.4 Pharyngeal Airway Space
- •10.2.1.6 Hyoid Bone Position
- •10.3.1 Maxillary Expansion
- •10.3.1.4 RME for OSA
- •References
- •11.2 Pathophysiology
- •11.3 Clinical Exam
- •11.5 Treatment
- •11.6 Summary
- •References
- •12.1 Introduction
- •12.5 Mask Options
- •12.6.1 Dry Mouth
- •12.6.2 Tangled Tubing
- •12.6.3 Condensation
- •12.6.4 Headgear Problems
- •12.6.6 Ramp
- •12.6.7 Cleaning Equipment
- •12.6.8 Skin Irritation
- •12.6.9 Nasal Congestion
- •12.6.10 Aerophagia
- •12.7 Cleaning Equipment
- •12.7.1 Travel Options
- •References
- •13: Oral Appliance Therapy
- •13.1 Introduction
- •13.2 Terminology
- •13.3.2 Device Designs
- •13.4 Methodology
- •13.7.2 Device Design
- •13.7.5 Non-anatomical Traits
- •13.7.6 Disease Severity
- •13.7.7 Supine Dependency
- •13.12.3 Adherence
- •13.12.4 Mean Disease Alleviation
- •13.13 Long-Term Outcomes
- •13.16 Guidelines
- •References
- •14.1 Introduction
- •14.2 Positional Therapy
- •14.2.1 Weight Loss
- •14.2.2 Nasal EPAP Therapy
- •14.2.3 Oral Pressure Therapy
- •14.2.4 Hypoglossal Nerve Stimulation
- •References
- •15.1 Introduction: Background Information
- •15.4 Preoperative Assessment
- •15.4.1 Physical Examination
- •15.4.2 Polysomnography
- •15.4.3 Clinical History
- •15.5 Preoperative Consent
- •15.6 Preoperative Assessment
- •15.6.1 Surgical Setting
- •15.8 Instrumentation
- •15.8.1 Tonsillectomy
- •15.8.2 Adenoidectomy
- •15.9 Postoperative Management
- •15.9.1 Pain
- •15.9.2 Diet
- •15.9.3 Follow-Up
- •15.10 Expected Outcomes by Population
- •15.10.1 General Population
- •15.10.2 Complex Children
- •15.10.2.1 Obese Children
- •15.10.2.2 Down Syndrome
- •15.10.2.3 Craniofacial Syndromes
- •15.10.2.4 Synchronous Airway Lesion
- •15.11.3 Cardiovascular Parameters
- •15.13 Conclusion
- •References
- •Further Reading
- •16.1 Introduction
- •16.3.1 Anatomic Factors
- •16.8 Summary
- •References
- •17: Palatal Surgery for OSA Patients
- •17.1 Introduction
- •17.2.2 Nasopharyngeal Endoscopy
- •17.2.3 Cephalometrics
- •17.3.1.1 Success Rate of UPPP
- •17.3.1.2 Limitations of UPPP
- •17.3.1.3 Impact of UPPP
- •17.3.1.4 Complications of UPPP
- •17.3.2.2 Z-Palatopharyngoplasty
- •17.3.2.3 Expansion Sphincter Pharyngoplasty
- •References
- •18: Hypopharyngeal Surgery for OSA Patients
- •18.1 Introduction
- •18.2 Historical Perspective
- •18.3 Patient Selection
- •18.4 Physical Exam
- •18.5 Imaging I
- •18.5.1 Imaging
- •18.6 Drug-Induced Sedated Endoscopy
- •18.7 Treatment Algorithm
- •18.8 Procedures
- •18.8.1 Transoral Robotic Surgery
- •18.8.2 Radiofrequency Ablation (RFA)
- •18.8.3 Genioglossus Advancement
- •18.8.4 Tongue Base Suspension
- •18.8.5 Hyoid Suspension
- •18.8.7 Hypoglossal Nerve Stimulators
- •18.9 Future Directions
- •References
- •Suggested Reading
- •19.1.1 Imaging
- •19.2.1.1 Pierre Robin Sequence
- •19.2.1.2 Craniofacial Microsomia
- •19.2.2.1 Crouzon’s Syndrome
- •19.2.2.2 Apert Syndrome
- •19.2.3.1 Treacher Collins Syndrome
- •19.2.3.2 Goldenhar Syndrome
- •19.3 Surgical Correction
- •Bibliography
- •20.1 Introduction
- •20.4.2 Surgical Technique (DOME)
- •20.4.4 Consolidation Phase
- •20.6 Discussion
- •References
- •21.3.3 Maxillomandibular Setback
- •References
- •22.1 Introduction
- •22.3 Results
- •22.3.1 Success Rate
- •22.4 Cases
- •22.5 Discussion
- •22.6 Conclusion
- •References
- •23.1 Patient Evaluation
- •23.1.1 Patient Concerns
- •23.1.4 Facial Evaluation
- •23.1.5 Lateral View
- •23.1.6 Oral Examination
- •23.1.7 Periodontal Evaluation
- •23.1.8 Tongue Assessment
- •23.1.9 Temporomandibular Joint
- •23.1.10 The Nose
- •23.1.11 Oropharyngeal Airway Assessment
- •23.2 Radiographic Evaluation
- •23.2.2 Lateral Cephalometric Radiograph
- •23.2.5 Cephalometric Analysis
- •23.3 Dental Model Analysis
- •23.3.1 Arch Length Measurements
- •23.3.2 Tooth Size Analysis
- •23.3.3 Tooth Position
- •23.3.4 Arch Width Analysis
- •23.3.6 Cuspid-Molar Position
- •23.3.7 Tooth Arch Symmetry
- •23.3.10 Ankylosed Teeth
- •23.4 Summary
- •References
- •24.1 TMJ Articular Disc Displacement
- •24.3 Reactive Arthritis (ReA)
- •24.5 Trauma
- •24.6 TMJ Ankylosis
- •24.7 Other End-Stage TMJ Conditions
- •24.8 Summary
- •References
- •25.1 Background
- •25.2 Treatment Planning Maxillary Surgery
- •25.2.1 Bone Anatomy
- •25.2.2 Vascular Anatomy
- •25.5 Adjunct Procedures
- •25.6 Complications
- •References
- •26: Mandibular Surgical Procedures
- •26.1 Genioplasty Procedures
- •26.2 Osseous Genioplasty
- •26.2.1 Anteroposterior Augmentation
- •26.2.2 Surgical Procedure
- •26.2.3 Anteroposterior Reduction
- •26.2.4 Vertical Augmentation (Downgraft)
- •26.2.5 Vertical Reduction
- •26.3 Alloplastic Augmentations
- •26.3.1 Surgical Procedure
- •26.4 Genioplasty Complications
- •26.5 Mandibular Subapical Procedures
- •26.5.3 Possible Complications
- •26.6 Mandibular Body Surgery
- •26.7.1 Nonunion or Malunion
- •26.7.3 Infections
- •26.7.4 Periodontal Defects
- •26.7.5 Nerve Damage
- •26.8 Mandibular Ramus Surgery
- •26.9 Vertical Ramus Osteotomy
- •26.11.1 Early Relapse
- •26.11.2 Condylar Sag
- •26.11.4 Unfavorable Splits or Fractures
- •26.11.6 Periodontal Defects
- •26.11.8 Nerve Injury
- •26.11.9 Infections
- •26.11.10 Nonunion
- •26.11.11 Bleeding Problems
- •References
- •27.1 Occlusal Plane Alteration
- •27.1.1 History
- •27.2 Corrected Frankfort Horizontal Plane
- •27.3 High Occlusal Plane (HOP) Facial Type
- •27.3.6 MRI Evaluation
- •27.3.7 TMJ Disc Displacement
- •27.3.9 Reactive Arthritis
- •27.3.11 Other End-Stage TMJ Pathologies
- •27.6 Summary
- •References
- •28: Maxillomandibular Advancement
- •28.1.1 Symptoms
- •28.1.3.1 Noninvasive Treatments
- •28.1.3.2 Surgical Interventions
- •28.4.1 Preoperative Medical Assessment
- •28.5 Procedure
- •28.5.1.2 Plates Vs. Screws
- •28.7 Post-MMA Follow-Up Care
- •28.8 Conclusion
- •References
- •29.2.1 CASS Adoption Widespread
- •29.2.2 Overall CASS Accuracy
- •29.2.2.1 Soft-Tissue Prediction Simulators
- •29.2.3 Cost
- •29.4.1 Overall CASS Process
- •29.4.1.1 Step 1: Patient Referral
- •29.4.1.7 Step 7: Procedure
- •29.4.4 Case 3
- •29.5 Conclusion
- •References
- •30.1 Introduction
- •30.2 Preoperative Considerations
- •30.2.1 Surgical Facility
- •30.2.2 Medical Clearance
- •30.2.3 Anesthesia Considerations
- •30.3 Inpatient Postoperative Management
- •30.3.1 Immediate Postoperative Course
- •30.3.2 Acute Pain Management
- •30.3.5 DVT Prophylaxis
- •30.3.6 Nutrition
- •30.3.7 Antibiotics
- •30.4.1 Follow-Up Regimen
- •30.4.2 Postoperative Occlusal Guidance
- •30.5 Conclusion
- •References
- •31.1 Paradigm
- •31.2 Preoperative
- •31.3 Acute Post-surgical
- •31.4 Long-Term Post-surgical
- •References

76
M. P. Mansukhani et al.
7
7.1 Background
Obstructive sleep apnea (OSA) is characterized by complete or partial closure of the upper airway during sleep
and is the most common form of sleep-related breathing
disorders. OSA is highly prevalent in the community;
In this chapter, we describe the testing modalities
that are currently available for the diagnosis of OSA in
adults. Diagnosis of OSA in children and other sleeprelated breathing disorders such as central sleep apnea
syndromes and sleep-related hypoxemia/hypoventilation
is beyond the scope of this chapter.
recent epidemiologic data suggest that 14% of men and
5% of women in the general population have OSA that
is associated with excessive daytime sleepiness. Certain
7.2 Diagnosis ofOSA
high-risk populations such as those with resistant
hypertension, pulmonary hypertension, coronary artery
7.2.1 History andExamination
disease, congestive heart failure, cardiac arrhythmias,
stroke, and diabetes mellitus type 2 have signicantly
higher rates of OSA.
OSA is associated with several adverse individual and
population health consequences. Hypoxemia, hypercapnia, sympathetic dysregulation, intrathoracic pressure
swings, and increased arousals from sleep are thought
to be the pathophysiologic mechanisms underlying these
increased risks. OSA has been shown to be linked with
adverse neurocognitive, cardiovascular, and metabolic
sequelae. These include excessive daytime somnolence,
enhanced risk of motor vehicle and work place accidents,
mood disorders, and dementia. There is a heightened
risk of systemic and pulmonary hypertension, coronary
artery disease, congestive heart failure, arrhythmias, and
stroke. OSA is associated with metabolic dysregulation
and increased risk for diabetes. Additionally, OSA is
linked with increased healthcare utilization.
OSA is generally well treated with continuous positive
The evaluation of OSA starts with a comprehensive
sleep evaluation, comprising of a detailed history for
symptoms suggestive of OSA, and to assess for the possibility of other sleep disorders, and presence of comorbid conditions. Physical examination should include an
assessment of the body mass index (BMI), neck circumference, blood pressure, focused ear, nose, and throat
examination (e.g., the presence of nasal septal deviation,
nasal turbinate hypertrophy, nasal mucosal erythema/
discharge, nasal polyps, nasal valve collapse, micro- and/
or retrognathia, maxillary hypoplasia, high-arched palate, overbite, cross-bite, overjet, Friedman palatal position, decreased anteroposterior and lateral dimensions
of the oropharynx, macroglossia, ankyloglossia, dental
marks on the tongue, and tonsillar hypertrophy) as well
as an examination of the cardiovascular and respiratory
systems. See 7
Chap. 6 for further information on the
clinical evaluation of OSA.
airway pressure (CPAP) and has been shown to decrease
symptoms, rate of motor vehicle accidents, the adverse
medical consequences noted above, and healthcare uti-
7.2.2 Screening Tools
lization as well as improve quality of life. However, a
CPAP device may be cumbersome and difcult to tolerate for many patients. Oral appliance treatment is used
as an alternative therapeutic option. Generally, this is
less efcacious than CPAP in terms of eliminating disordered breathing events, but may be more acceptable
to some patients. Oral appliance treatment is benecial
in reducing daytime sleepiness and blood pressure to a
degree equivalent to CPAP.
Thus, OSA is a common medical disorder that
is associated with signicant injurious health consequences and increased healthcare costs. A false-negative
test may leave symptomatic patients untreated, adversely
affect their quality of life, and increase the risks of poor
health outcomes. On the other hand, treatment of OSA
may be difcult for many patients to tolerate. A falsepositive test may expose patients to unnecessary inconvenience and expense. Therefore, it is imperative that the
diagnosis of OSA be established as accurately as possible. Access to testing, ease and cost of the diagnostic
procedures are other relevant factors that are important
to consider from the patient perspective.
Screening questionnaires and prediction algorithms
are not sufcient to make the diagnosis of OSA as they
have been found to have a low accuracy when compared to traditional diagnostic tests in several studies.
Many of these studies were performed in high-risk
populations for OSA such as the elderly, bariatric surgery candidates, and commercial vehicle drivers and
thus may not be generalizable to other patient groups.
In general, the specicity of these screening tools was
noted to be low, resulting in a large number of false
positives. Furthermore, the rate of predicted false
negatives was more than 1in 10, which would render
these measures as unacceptable for the purposes of
diagnosing OSA.The most recent American Academy
of Sleep Medicine (AASM) clinical practice guideline
for the diagnostic testing for adult OSA recommended
that these tools may be used in clinical settings, but
not as a substitute for objective sleep testing. Examples
of questionnaires and algorithms used in screening
for OSA include the Epworth Sleepiness Scale, Berlin
Questionnaire, Stop- BANG, sleep apnea clinical score,

Diagnostic Testing forObstructive Sleep Apnea
77
7
Kushida Index, OSAS score, OSA50, Multivariable
Apnea Prediction Questionnaire, and morphometric
models.
7.2.3 Diagnostic Tests
The diagnosis of OSA involves measurement of
respiratory parameters in sleep. Attended or in-laboratory polysomnography (PSG) is considered the
gold- standard test for making the diagnosis of OSA
and requires the simultaneous measurement of eight
or more physiological parameters during sleep, including electroencephalography (EEG), electrooculography
(EOG), electromyography (EMG), electrocardiography,
air ow (with an oronasal thermistor and nasal pressure
transducer), chest/abdominal muscle effort (usually with
respiratory inductance plethysmography), pulse oximetry, heart rate, snoring (with a microphone), and body
position. Time-synchronized audio and video recording
is generally available as well. Due to issues with access
to in-laboratory PSG requiring the presence of skilled
personnel and associated cost, home sleep apnea tests
(HSATs) have emerged as a viable option for the diagnosis of OSA in well-selected patients.
peripheral arterial tonometry to diagnose OSA have
emerged. The SCOPER (sleep, cardiovascular, oximetry,
position, effort and respiratory parameters) classication, proposed by the AASM more recently after a comprehensive technology evaluation, is an alternative and
more complex classication system that includes these
newer technologies.
7.2.5 Denition ofOSA
The International Classication of Sleep Disorders,
Third Edition, denes OSA as being present if a respiratory index (RDI) of ≥5 per hour is noted on PSG or
HSAT, associated with typical symptoms of OSA, that
is, loud snoring, choking/gasping/breath-holding episodes, witnessed apneas, unrefreshing sleep, sleepiness,
fatigue, insomnia, and/or a diagnosis of mood disorder,
cognitive dysfunction, hypertension, coronary artery
disease, stroke, congestive heart failure, atrial brillation, stroke, or type 2 diabetes mellitus. Alternatively, an
RDI of ≥15 per hour on PSG or HSAT in the absence
of these symptoms or comorbid medical conditions is
sufcient to make the diagnosis of OSA.
7.2.6 Scoring ofRespiratory Events
7.2.4 Types ofSleep Studies
The RDI comprises apneas, hypopneas, and respira-
Sleep studies are traditionally classied as types I–
IV (. Table 7.1). Type I is attended in-laboratory
PSG. Unattended sleep studies are categorized into
types II–IV.Type II studies are similar to type I except
that they are unattended studies and can be performed
outside of the sleep laboratory. Type III studies utilize
oximetry, two respiratory, and one cardiac channel. Type
IV studies use only one or two sensors, for example, airow or oximetry and pulse rate. There is considerable
device variation even within the same sleep study category. In addition, since this original classication was
devised, newer technologies such as those incorporating
. Table 7.1 Types of sleep studies
Tech EEG EOG EMG ECG Airow Resp effort SpO
Type 1 X X X X X X X X
Type 2 X X X X X X X
Type 3 X X X X
Type 4 X
tory effort-related arousals (RERAs) per hour of sleep,
whereas the apnea-hypopnea index (AHI) includes only
apneas plus hypopneas per hour of sleep. The criteria
for dening hypopneas have changed over the years, rendering an evaluation of the medical literature regarding
the diagnosis and outcomes of OSA difcult. The AHI
(and therefore the RDI) may be considerably different
in an individual person depending upon which denition of hypopnea is employed. The most recent AASM
Manual for the Scoring of Sleep and Associated Events
version 2.4, 2017, recommends scoring hypopneas in
adults when there is a≥30% reduction in nasal pressure
2
Abbreviations: tech sleep technologist, EEG electroencephalography, EOG electrooculography, EMG electromyography, ECG electro-
cardiography, Resp respiratory, SpO
pulse oximetry
2

78
M. P. Mansukhani et al.
signal excursion (alternative hypopnea sensor if this is
7
unavailable) or positive airway pressure (PAP) device
ow for at least 10seconds accompanied by a≥3% oxyhemoglobin desaturation or arousal. However, many
laboratories are also using ≥4% desaturation criterion
(with no arousal criteria), along with a≥30% or≥50%
reduction in nasal pressure excursion, in keeping with
the patient to leave the home or healthcare setting due
to complexity of cares. Aside from being able to sleep
in a familiar environment, generally, fewer sensors are
applied during a HSAT, which may also serve to enhance
patient comfort. In one RCT in which both HSAT and
PSG were performed in the same patient, over three-
fourths of the subjects preferred HSAT.
the “acceptable” denition of hypopneas in the current
scoring manual and the denition in the older version
of the manual from 2007 respectively. This is largely
7.3.2 Disadvantages
due to the lack of reimbursement from certain medical
insurance companies (mainly Centers for Medicare and
Medicaid Services) for OSA diagnosed based on the latest recommended scoring criteria and paucity of data
demonstrating a difference in long-term clinical outcomes with the different criteria in use.
HSAT is less accurate when compared to PSG in the
diagnosis of OSA and tends to underestimate severity.
Usually, EEG is not recorded; therefore, the degree of
sleep fragmentation secondary to OSA cannot be deter-
mined. Other sleep disorders cannot be assessed on a
HSAT. Furthermore, central sleep-disordered breath-
ing (SDB) events may not be well differentiated from
7.2.7 Clinical Guidelines
obstructive events, and in most cases, RERAs cannot be
detected. There is no opportunity to titrate positive airThe AASM published practice parameters for the indications for PSG in 2005 and initial clinical guidelines for
the use of HSATs in 2007. In some geographic areas,
there has been a signicant upswing in the number of
HSATs performed relative to PSGs for the diagnosis of
OSA; there are a number of potential reasons for this
including changes in payor policies. As noted above,
AASM published an updated clinical practice guideline
for the diagnostic testing for adult OSA in 2017, incorporating a meta-analysis of 87 randomized controlled trials (RCTs) and observational studies from 2005 to 2016
evaluating the accuracy of diagnosis of OSA using clinical prediction rules, HSAT, and PSG as well as relevant
way pressure (PAP) and assess response to this or trou-
bleshoot in the home setting. Chain of custody issues
may arise, for example, in a commercial vehicle driver or
pilot, in ensuring that the patient for whom the study is
being ordered is the one undergoing the test. Lastly, if the
HSAT is negative for OSA, a PSG is indicated for further
evaluation in the patient with suspected moderate- to-
severe OSA (assuming they were appropriately selected
for HSAT). In this situation, one study suggested that
there were a signicantly high proportion of patients
who did not follow through with the recommended sec-
ond round of testing with PSG, thus leaving their OSA
untreated with potential attendant long-term risks.
clinical outcome measures. Four recommendations in
this guideline were graded “strong” based on the quality
of the evidence, benets versus harms, patient values and
7.3.3 Patient Selection
preferences, and utilization of resources. The remaining
two recommendations were rated “weak.” These recommendations will be discussed throughout the chapter.
The AASM recommends that HSAT be performed in an
uncomplicated patient with an increased clinical pre-test
probability of moderate-to-severe OSA.
An uncomplicated patient is one that does not have
7.3 Home Sleep Apnea Test (HSAT)
a condition that would place them at a greater risk of
nonobstructive SDB, such as central sleep apnea, sleepThis type of sleep study is one that can be conducted
outside of the sleep laboratory setting in the absence of
a trained sleep technologist during the recording period.
related hypoxemia, or hypoventilation (e.g., cardiopul-
monary disease, potential respiratory muscle weakness
due to a neuromuscular condition, history of stroke, or
current chronic opioid medication use). Patients with
signicant safety-related issues such as driving or work-
7.3.1 Advantages
place accidents due to sleepiness may also best be studied
by PSG. If a screening oximetry suggests the presence
Potential benets of performing a sleep study in the
home setting include greater convenience and comfort
to the patient, increased access to testing and possibly
decreased cost. HSAT may be particularly advantageous in some situations where it might be difcult for
of signicant hypoxemia and/or hypoventilation or the
patient has other risk factors for hypoventilation for
2
example, a BMI in excess of 40 kg/m
, PSG would be
preferable. In some geographic areas, third-party payors have their own criteria for coverage of HSAT versus

Diagnostic Testing forObstructive Sleep Apnea
79
7
PSG.In patients in whom there is a suspicion for other
sleep disorders that require evaluation (e.g., central disorders of hypersomnolence, parasomnias, sleep-related
movement disorders) or can interfere with the conduct
or accuracy of HSAT (e.g., insomnia), PSG is the recommended test. Other situations that may preclude the
conduction of HSAT may involve personal (e.g., cognitive dysfunction, physical limitations) or environmental
(unsuitable living conditions) factors that can limit the
acquisition and interpretation of data.
There is very limited medical literature evaluating
the validity of HSAT in patients with signicant cardiopulmonary/neuromuscular conditions, insomnia, and
those on opioid medications or at high risk of hypoventilation. HSAT may result in an inaccurate assessment
of SDB in these situations, and thus PSG is the recommended test of choice. If there are other extenuating circumstances, such as an inability to leave the hospital or
home setting, then it may be reasonable to proceed with
HSAT than to perform no testing at all.
According to the recent AASM clinical practice
guideline for the diagnostic testing for adult OSA, an
increased pretest probability of moderate-to-severe
OSA is indicated by the presence of excessive daytime
sleepiness with at least two of the following three factors: (1) habitual loud snoring, (2) witnessed apnea, or
(3) hypertension.
7.3.4 Data Obtained
The recording channels usually comprise a combination of respiratory (including oximetry) and pulse rate
parameters. Newer technologies may employ measures
of peripheral arterial tonometry to determine disordered breathing events and estimate sleep time/stages.
All of these technologies generally include snoring and
body position sensors as well.
A technically adequate device per AASM guidelines
is one that has at least nasal pressure (for airow), chest
and abdominal respiratory inductance plethysmography
(for effort), and oximetry. In the case of devices that
utilize peripheral arterial tonometry, these measures in
addition to actigraphy are required. Detailed requirements for the sensors are described in the most recent
edition of the AASM Manual for the Scoring of Sleep
and Associated Events.
Typically, sleep staging channels such as EEG, EOG,
and EMG are not present in HSAT, thus the number
of disordered breathing events is calculated per hour
of recording time and not sleep time. To reect this difference, the HSAT usually reports severity of SDB as a
“respiratory event index” (REI), as opposed to an RDI
or AHI.The REI represents a potential underestimation
of events that might be calculated on PSG.Secondly, due
to the absence of sleep staging, respiratory events resulting in cortical arousals per current recommended scoring
criteria cannot be determined, which may also result in a
lower severity of SDB than that gauged by PSG.
7.3.5 Conduct andInterpretation ofTest
It is recommended by the AASM (and required by most
third party payors) that the HSAT be administered by
an accredited sleep center under the supervision of a
board-certied or board-eligible Sleep Medicine physician. Similarly, the test should be interpreted by a boardcertied or eligible Sleep Medicine physician.
A single HSAT is conducted over one night. Studies
of single versus multiple nights of recording have demonstrated a marginal increase in accuracy and increased
probability of insufcient information with multiple
recordings compared to a single night of data. It should
be noted that the recordings in these studies utilized only
a single channel (nasal pressure transducer or oximetry)
and efciency of care as well as long-term clinical outcomes were not assessed.
Based on available studies, a technically adequate
HSAT requires a minimum of 4hours of recorded data
obtained for a duration that includes the patient’s habitual sleep period. This includes a minimum of 3hours
of oximetry data and 2hours of airow information.
There is no literature regarding the accuracy of results
obtained from less than 4hours recording on a HSAT
compared to PSG and the inuence of the number of
recording hours on any long-term clinical outcomes.
7.3.6 Accuracy ofResults
There is moderate evidence of the potential for misclassication of severity of SDB in either direction, based
on 27 studies that assessed the accuracy of HSAT versus
PSG.This is partly due to night-to-night variability of
OSA and possibly due to different hypopnea denitions
used in the two test types.
The accuracy of type II and III studies compared to
PSG (AHI cut-off of ≥5 per hour or≥ 15 per hour) is
in the range of 80–90%, for patients thought to be at
high risk for OSA.The accuracy deteriorates in low-risk
groups. The use of single-channel oximetry has signicantly high false-positive and false-negative rates when
compared to PSG (more than 1 in 5). Three studies
assessed HSAT using peripheral arterial tonometry and
actigraphy against PSG.These studies showed a misdiagnosis rate of about 1in 10in high- as well as low-risk
patients, a low specicity of about 0.45 for an AHI of
≥5 per hour and ranging from 0.77–1.0 for AHI cutoffs
of ≥15 or≥30 per hour.

80
M. P. Mansukhani et al.
7
7.3.7 Discussion ofResults
After a positive HSAT, the patient can be commenced
on auto-titrating PAP (APAP) if thought to be appropriate by the treating provider. Alternatively, the management pathway may include titration PSG after a positive
HSAT.If the results are complex, then an in- laboratory
split-night PSG (described below) or titration PSG may
be required, depending upon the individual patient.
Based on currently available literature, the chance of
a technically inadequate study is approximately 20%. If
the HSAT is negative, inconclusive, or technically inadequate in a patient with a high pretest probability of
OSA, then attended PSG is recommended as the next
step rather than a repeat HSAT. This is because evidence from one study suggested that the likelihood of
a second inconclusive or technically inadequate is about
40%. Furthermore, in this study, the rate of nonadherence with the recommended next step of a PSG was high
of treatment of OSA in this group of patients. False
negatives with HSAT that leave patients untreated with
downstream costs relating to adverse health consequences and healthcare utilization, the cost of retesting
with PSG in the setting of negative, inadequate, inconclusive or complex HSAT results, and the potential for
false positives with unnecessary treatment may tilt the
balance in favor of PSG.Conversely, in the one RCT
that evaluated the expense associated with HSAT versus
PSG, there was a 25% lower cost with HSAT.
If HSAT is utilized in appropriately selected patients
and within the care management pathway described
above, it is likely to be more cost-effective than if the
recommended guidelines are not followed. From the
provider perspective, cost may not always be lower with
the HSAT pathway because a large number of components are required to ensure that the quality of the
HSAT pathway-mediated care for OSA is similar to a
PSG pathway.
(approximately 20%); to maximize the rate of a denitive diagnosis in this situation after a failed rst study,
PSG is the recommended test. However, patient prefer-
7.3.11 Summary ofHSAT
ence, available resources, and clinician judgment regarding the possibility of a second failed HSAT will need to
be taken into account before making this decision in an
individual patient.
The use of HSAT in an uncomplicated patient with a
high pretest probability of moderate-to-severe OSA,
using a technically adequate device and recording
period, under the supervision of personnel with the requisite expertise and with a clear management pathway
7.3.8 Recommended Follow-Up
in place, can provide similar clinical outcomes as PSG
when used in the diagnosis of OSA.
Early follow-up is recommended following the initiation of APAP after HSAT. Most RCTs examining the
HSAT- APAP pathway included a follow-up APAP visit
7.4 Polysomnography (PSG)
within 2–7days after HSAT with skilled technical staff.
It should be noted that these RCTS were conducted in
tertiary care or academic settings comprising of highly
skilled medical and technical personnel teams.
In-laboratory PSG, consisting of the simultaneous monitoring of multiple physiological parameters in sleep, in
the presence of skilled technical personnel, is the current gold-standard recommended test for the detection
of OSA.
7.3.9 Clinical Outcomes
In seven RCTs, after CPAP was commenced, patientreported outcomes (sleepiness, quality of life, and PAP
adherence) did not differ between HSAT and PSG
groups. Information regarding cardiovascular and other
outcomes is currently not available.
7.3.10 Cost-Eectiveness
The overall cost-effectiveness of an HSAT versus PSG
pathway of management of OSA is not fully clear. In
the long term, the PSG pathway has been noted to be
more benecial in patients with moderate-to-severe OSA
in some studies due to the favorable cost- effectiveness
7.4.1 Patient Selection
Currently available evidence includes only patients with
comorbid heart failure and chronic obstructive pulmonary disease. The utility and validity of HSAT in patients
with other comorbidities, environmental and personal
factors that can affect testing have not been systematically studied. In the research that has been conducted to
date, the specicity of HSAT in identifying central SDB
or hypoventilation was low or not evaluated. Since these
respiratory abnormalities are potentially associated with
signicantly increased risk of morbidity and mortality,
and may not be adequately assessed by HSAT and/or
require treatment modalities other than CPAP/ APAP,

Diagnostic Testing forObstructive Sleep Apnea
81
7
PSG is recommended for the diagnosis of SDB in
patients with the comorbidities or complicating factors
described above.
7.4.2 Number andDuration ofTests
A split-night protocol (where PAP is applied after the
diagnostic portion of the study) is generally appropriate and may be used instead of a full night diagnostic
study for the purposes of detecting OSA. For a splitnight study, a moderate-to-severe degree of OSA needs
to be observed during a minimum of 2hours of recording time on the diagnostic portion of the PSG and at
least 3 more hours should be available for PAP titration.
The accuracy of split-night PSG has been found
to be comparable to full night diagnostic PSG, even in
those with milder degrees of OSA.Many of these investigations were not RCTs and the types of sensors utilized were inconsistent across studies. Currently, there is
no denitive data regarding the optimal AHI threshold
at which to initiate PAP after the diagnostic portion of
the PSG.
The split-night protocol, in theory, leads to decreased
cost and increased efciency of care by facilitating diagnosis and treatment of OSA during a single night’s
recording. One study did demonstrate lower cost with
the split-night PSG protocol compared to the full night
pathway, based on cost per quality of life year gained.
However, further research regarding cost-effectiveness
is needed. It is worth noting that the studies evaluating
split-night versus full night diagnostic PSG excluded
certain patient groups such as those with severe insomnia, claustrophobia, and other suspected sleep disorders.
Thus, individual patient factors determining eligibility for
the split-night pathway are not fully known at this time.
Additionally, if the diagnostic and/or titration portions
of the study are inadequate or inconclusive, these may
need to be repeated; alternatively, in the case of an inadequate/inconclusive titration, APAP may need to be used
if thought to be appropriate by the treating clinician.
Most studies have shown no signicant differences in
patient-related outcomes such as the rates of adherence to
CPAP or the residual AHI on CPAP treatment in subjects
who underwent split-night or full night diagnostic PSG.
7.4.3 Conduct andInterpretation
oftheStudy
As with HSAT, it is recommended that PSG be administered by an AASM accredited facility with appropriately
trained personnel and the study interpreted by a physician who is board-certied or board-eligible in Sleep
Medicine.
7.4.4 Follow-Up
After undergoing PSG for the diagnosis of OSA, discussion of the results must take place within a reasonable
time frame after the study and the patient commenced
on treatment if appropriate.
7.4.5 Discussion ofResults
If the results of PSG are negative for OSA and there
is still a high clinical suspicion for OSA, it is recommended that a second PSG be considered for the
diagnosis of OSA. There are a few studies of twonight versus one- night PSG that have shown signicant night-to-night variability in AHI in a subset of
patients, although there were no overall differences in
AHI between the groups. Up to a third of individuals
had a change in the classication of severity of their
OSA in either direction after the second study. Body
position was not noted, but an increased proportion
of rapid eye movement sleep was noted on the second
PSG in one of these studies. The available evidence
indicates that 8–25% of symptomatic patients with an
initial negative PSG will have OSA diagnosed after the
second PSG.
A false-negative study may exclude a patient from
therapy and expose them to increased morbidity in
the long term. On the other hand, repeat PSG after an
initial negative study carries with it the potential for
increased expense and inconvenience to the patient and
the possibility of a false-positive test. If the patient is
symptomatic, the potential benets of this approach
may outweigh the risks, but the evidence supporting this
recommendation is weak. A thorough discussion with
the patient is warranted in this situation so that they can
make an informed choice about undergoing a second
PSG.
7.4.6 Repeat Testing intheLong Term
There is a general lack of evidence regarding the performance of repeat PSG in patients with OSA with stable
symptoms, weight, and comorbidities who are adherent
to PAP, in terms of whether this affects classication of
type or severity of SDB in an individual patient or has
any inuence on long-term clinical outcomes. According
to current Centers for Medicare and Medicaid Services
(CMS) coverage criteria for PAP devices in the United
States, a repeat diagnostic and/or titration PSG showing
an AHI ≥5/hour is required if more than 10years have
elapsed since the time of the original diagnostic study
and the patient has not obtained a new PAP device in
this time frame,.

82
M. P. Mansukhani et al.
If there is a signicant change in medical comor-
7
bidities (and there is a suspicion for change in type/
7.6 Summary Box
severity of SDB or PAP device type/pressure requirements) or≥10% change in body weight from the time
of the diagnostic or titration study, repeat PSG could
Based on the AASM Clinical Practice Guideline for
the Diagnostic Testing for Adult OSA
be considered. CMS requires a titration PSG demonstrating adequate control of SDB (AHI <10/hour)
on PAP titration PSG before nocturnal supplemental oxygen treatment can be prescribed for persistent
hypoxemia.
7.4.7 Summary ofPSG
PSG is considered the gold-standard test for the diagnosis of OSA.While HSAT may be appropriate in certain
situations, PSG is recommended for the evaluation of
OSA in patients with coexisting cardiopulmonary/neuromuscular comorbidities and/or other complicating
medical, environmental, or personal factors, and when
other sleep disorders are suspected.
7.5 Conclusions
More accurate screening tools may help identify
which patients are candidates for testing with HSAT
or PSG for the diagnosis of OSA. The advent of
biomarkers that can screen for OSA and/or identify
patients at increased risk for adverse outcomes may
also help with the prioritization and individualization of testing and treatment for OSA.Research on
the factors inuencing inadequate/inconclusive/negative/complex (“failed”) HSAT in patients with a high
pretest probability of moderate-to-severe OSA as
well as patient preferences regarding mode of testing
is needed. Further studies are required regarding the
accuracy and long-term outcomes of HSAT versus
PSG in more diverse patient populations, including
No. Recommendation Strength
of evidence
1 Questionnaires, clinical prediction
tools and algorithms should not
be used (in the absence of PSG or
HSAT)
2 PSG should be used, or HSAT
with a technically adequate device
in an uncomplicated patient with
increased clinical pretest probability of moderate-to-severe OSA
3 PSG should be performed in the
event of a single negative/inconclusive/technically inadequate
HSAT
4 PSG should be performed instead
of HSAT in patients with signicant cardiopulmonary/neuromuscular conditions, suspected
hypoventilation, chronic opioid
medication use, history of stroke
or severe insomnia
5 Split-night rather than full night
PSG should be performed if clinically appropriate
6 A second PSG can be considered
if the initial PSG is negative and
there is still a clinical suspicion
for OSA
Abbreviations: AASM American Academy of Sleep
Medicine, OSA obstructive sleep apnea, No number,
PSG polysomnography, HSAT home sleep apnea test
Strong
Strong
Strong
Strong
Weak
Weak
more female and ethnically/racially diverse populations, those with signicant comorbid cardiopulmonary and neuromuscular conditions, and patients with
other complicated environmental/personal factors.
The accuracy, clinical implications and cost-effectiveness of portable monitoring or “HSAT”s versus
PSG performed in the hospital setting, single versus
multiple-night HSAT, PSG versus repeat HSAT for a
failed HSAT, split-night versus full night PSG, second
versus no PSG when the rst one is negative and the
role of repeat PSG in chronic disease management
needs clarication.
Further Reading
1. Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra
R, Ramar K, Harrod CG.Clinical Practice Guideline for Diag-
nostic Testing for Adult Obstructive Sleep Apnea: An American
Academy of Sleep Medicine Clinical Practice Guideline. J Clin
Sleep Med. 2017;13(3):479–504. Most recent and comprehensive
update from the American Academy of Sleep Medicine regard-
ing diagnostic testing for OSA.
2. Collop NA, Tracy SL, Kapur V, Mehra R, Kuhlmann D, Fleish-
man SA, Ojile JM.Obstructive sleep apnea devices for out-of-

Diagnostic Testing forObstructive Sleep Apnea
83
7
center (OOC) testing: technology evaluation. J Clin Sleep Med.
2011;7(5):531–48. A comprehensive review and classication of
home sleep apnea test device technologies.
3. Kushida CA, Littner MR, Morgenthaler T, Alessi CA, Bailey D,
Coleman J Jr, Friedman L, Hirshkowitz M, Kapen S, Kramer
M, Lee-Chiong T, Loube DL, Owens J, Pancer JP, Wise M.Practice Parameters for the Indications for Polysomnography and
Related Procedures: An Update for 2005. Sleep. 2005;28(4):499–
521. Clinical practice guidelines for the indications and conduction of polysomnography.
4. Berry RB, Brooks R, Gamaldo CE, et al. For the American
Academy of sleep medicine. The AASM manual for the scoring
of sleep and associated events: rules, terminology and technical specications version 2.4. Darien, IL: American Academy
of Sleep Medicine; 2017. Most recent version of the American
Academy of Sleep Medicine manual for the scoring of events on
polysomnography and home sleep apnea tests.
5. Duce B, Milosavljevic J, Hukins C.The 2012 AASM respiratory
event criteria increase the incidence of hypopneas in an adult
sleep center population. J Clin Sleep Med. 2015;11(12):1425–31.
Article discussing the impact of varying hypopnea denitions on
the diagnosis of OSA.
6. Flemons WW, Littner MR, Rowley JA, Gay P, Anderson WM,
Hudgel DW, McEvoy RD, Loube DI.Home diagnosis of sleep
apnea: a systematic review of the literature. An evidence review
cosponsored by the American Academy of Sleep Medicine, the
American College of Chest Physicians, and the American Thoracic Society. Chest. 2003;124(4):1543–79. Review article discussing the feasibility and utility of home sleep apnea testing for
the diagnosis of OSA.

85
Cone-Beam CT Use forAirway
Imaging
JuanMartinPalomo, TarekElshebiny, andKingmanStrohl
Contents
8.1 Introduction – 86
8.2 Accuracy andReliability ofMeasuring theAirway
Using CBCT–87
8.3 Evaluation ofUpper Airway Using CBCT – 87
8.4 CBCT and OSA – 89
8.5 Evaluation ofOSA Treatment Approaches Using CBCT – 92
8.5.1 CPAP – 92
8.5.2 Oral Appliances – 93
8.5.3 Maxillomandibular Advancement – 94
8
8.6 Upper Airway Stimulation – 95
8.7 Summary – 102
References – 102
© Springer Nature Switzerland AG 2021
K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_8

86
J. M. Palomo et al.
8.1 Introduction
become a well-accepted oral and maxillofacial diagnostic imaging, providing a three-dimensional view of hard
Imaging as always was a key concept in craniofacial
diagnosis and treatment planning. Airway imaging
techniques used in the diagnosis of obstructive sleep
apnea (OSA) have greatly improved especially with
understanding OSA pathophysiology [1]. Treatment
planning and evaluation of surgical and nonsurgical
therapies which target-specic areas of obstruction are
now possible with newer imaging modalities. Airway
imaging can be done using numerous techniques such
as nasal pharyngoscopy, cephalometric radiographs,
uoroscopy, conventional and electron beam computed tomography (CT), acoustic reection, magnetic
resonance imaging (MRI), and cone-beam computed
tomography (CBCT) [2].
The importance of the third dimension for airway
8
assessment has been emphasized highlighting important
limitations of two-dimensional studies. The high radiation dose of conventional CT devices might have been
a limiting factor for its use, but the evolution of a new
technology, CBCT, took a signicant turn. CBCT has
and soft tissues of the head and neck with low doses
of radiation. CBCT studies allow us to examine areas,
volumes, and complex hollow structures, including the
airway channel (.
Fig.8.1) [3–5]. Several CBCT manu-
facturers currently use pulse technology where radiation
only occurs when taking images, allowing the creation
of a three-dimensional (3D) image with less radiation to
the patient than a panoramic radiograph [6].
The purpose of this chapter is to describe the possible use of CBCT technology for airway evaluation
in OSA patients. Since a CBCT does not provide any
information on neuromuscular tone, susceptibility to
collapse, or actual function of the airway, one cannot
use a CBCT to diagnose sleep apnea alone. A CBCT
may be used for monitoring conditions or for treatment
considerations, such as the location of the maximum
constriction, so the clinician can decide between expansion, if it is located in the nasal area, and mandibular
advancement devices, if it located in the oropharynx, for
example.
. Fig. 8.1 Different views of a CBCT volume showing the upper airway using two different software packages
Соседние файлы в папке Библиотека им академика М.И. Перельмана
