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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •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

64
-=
==
[]
()
10
[]
()
()
[]
()
[]
()
()
()
()
R. E. Bourey
. Table 5.5 Diagnosis of hepatosteatosis (fatty liver) and steatohepatitis with brosis (cirrhosis)– see text for details
Citation Cut- off Sensitivity (%) Specicity (%)
Hepatosteatosis
Screening test
Fatty liver index (FLI) [41] ≥30 87 64
NAFLD liver fat score (for liver fat>5.6%) [39] ≥-0.64 86 71
Denitive test
5
Magnetic resonance proton density fat fraction (PDFF) C.f., [42]
Steatohepatitis with brosis
Screening test
Fibrosis-4 (FIB-4) [43, 44] <1.3 85 65
Vibration controlled transient elastography in NAFLD (kPa) C.f., [45] ≥10.3 90 87
Denitive test
Liver biopsy
NAFLD Liver Fat Score (for liver fat dened as >5.6%)
is given by the following calculation [39]:
NAFLD LFS
289118
..
-+
+
045
.yypediabetesyes /no
+[.
015
+
004094..ASTU/L AST/ALT
The FLI has the disadvantage of requirement for measurement of waist circumference, a potentially troublesome
measurement in patients with no waist. Although the
NAFLD liver fat score avoids this measurement, it relies on
assessment of metabolic syndrome and accurate diagnosis
of T2DM. In this calculation, the metabolic syndrome
was dened according to criteria of the International
Diabetes Federation [40]: central obesity (waist circumference ≥94 cm in men and ≥80 cm in women) and at
least two of the following factors: (1) serum triglycerides
≥1.70mmol/L or specic treatment for this lipid abnormality; (2) serum high-density lipoprotein (HDL) cholesterol <1.03mmol/L in men and <1.29mmol/L in women
or specic treatment for this lipid abnormality; (3) systolic
blood pressure (BP) ≥130mm Hg or diastolic BP ≥85mm
Hg or treatment for previously diagnosed hypertension;
and (4) fasting plasma glucose ≥5.6mmol/L or previously
diagnosed type 2 diabetes. Although the requirement to
screen for components of metabolic syndrome seems to
add some complexity to the calculation, data for screening
should be available from standard order sets for automatic
analysis within the EHR.
metabolic syndromeyes /no
t
220
fasting serum insulin mU/L
[]
()
==
]]
-
()
For validated assessment of risk for liver brosis
and cirrhosis in the context of NAFLD, we recommend
additional calculation of Fibrosis-4 (FIB-4) with subsequent study by vibration-controlled transient elastography or biopsy.
Fibrosis-4 (FIB-4) is calculated by the following
equation (McPherson, Stewart, Henderson, Burt, &
Day, 2010; Sterling etal., 2006):
FIB
- 4
A patient with brosis in the context of hepatosteatosis can be expected to have an element of irreversible
liver dysfunction. Treatment to arrest progression and
to reduce fat content of the liver should be aggressive.
Anesthesiologists will need to be aware of the likelihood
of cirrhosis and adjust anesthesia and perioperative
protocols as needed. When in doubt, prudence dictates
consultation with a hepatologist and liver biopsy to fully
dene liver disease and risks.
5.6 Conclusions
5 Recognition of metabolic disease associated with
obstructive sleep apnea allows modication of ther-
apy for sleep apnea to avoid risk of injury to the
patient and to improve chances for a successful out-
come. Specic strategies for management are covered
in parts III and IV of this book.
AgeyearAST U/L
=
PLT/LALT
10 9
é
()
ë
12
ù
û
/

Diagnostic Considerations inMetabolic Disease Associated withObstructive Sleep Apnea
65
5
5 Documentation of associated disease and complex-
ity of care has fast become important to sufcient
reimbursement for services.
5 Diagnosis of obesity and associated morbidities will
allow not only detection of additional metabolic disease such as diabetes and fatty liver, but also requires
recognition of mechanical problems such as arthritis
and anatomical compromise of upper airway by adipose tissue, which in turn justies therapy specic to
obesity.
5 Diagnosis and treatment of hypertension are impor-
tant in the design of therapeutic programs for diet
and exercise, as well as reduction in perioperative
risks associated with surgical therapy.
5 Recognition of prediabetes and diabetes allows reim-
bursement for treatment through multidisciplinary
clinics that specically address metabolic disease,
and allows more accurate calculation of cardiovascular risks associated with exercise or surgical intervention.
5 Recognition of simple hepatosteatosis allows ther-
apy aimed at reversal and prevention of steatohepatitis, irreversible brosis, and hepatic dysfunction.
5 Recognition of steatohepatitis with brosis and cir-
rhosis allows recognition of risk for cardiovascular
disease, metabolic dysfunction, coagulopathy, and
thrombocytopenia, and thereby better management
of perioperative risks.
5 Diagnosis and treatment of metabolic disease can be
easily addressed through efcient use of electronic
health records, problem-generated order sets, and a
multidisciplinary team.
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tro.2017.03.016.

67
Diagnostic
Considerations for OSA
Contents
Chapter 6 Clinical Evaluation of the Obstructive Sleep Apnea
Patient–69
Raman K. Malhotra and Rocio Zeballos-Chavez
Chapter 7 Diagnostic Testing for Obstructive Sleep Apnea–75
Meghna P. Mansukhani, Bhanu Prakash Kolla,
and Kannan Ramar
II
Chapter 8 Cone-Beam CT Use for Airway Imaging–85
Juan Martin Palomo, Tarek Elshebiny, and Kingman Strohl
Chapter 9 Craniofacial Morphology Related to Obstructive
Sleep Apnea: Growth of Craniofacial Bones
and the Upper Airway–105
Su-JungKim andKiBeomKim
Chapter 10 Orthodontics and Sleep-Disordered Breathing–135
KiBeomKim andSu-JungKim
Chapter 11 Obstructive Sleep Apnea in the Setting of Mandibular
Condyle Resorption–165
W.JonathanFillmore

Clinical Evaluation
oftheObstructive Sleep
ApneaPatient
RamanK.Malhotra andRocioZeballos-Chavez
Contents
6.1 Background – 70
6.2 History Taking – 70
6.3 Physical Examination – 72
6.4 Conclusion – 72
69
6
References – 73
© 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_6

70
R. K. Malhotra and R. Zeballos-Chavez
6.1 Background
there are other possible causes of these symptoms that
can be difcult for patients or clinicians to distinguish.
Individuals with obstructive sleep apnea typically present to clinical attention with a chief complaint of excessive daytime sleepiness, snoring, or witnessed apneas
during sleep. Excessive daytime sleepiness (EDS) is
dened as the inability to stay awake and alert during
the major waking episodes of the day, resulting in unintended lapses into drowsiness or sleep [1]. This symptom
is common among the population, with estimates that
more than 30% of the population in the United States
has daytime sleepiness that interferes with their quality
6
of life [2]. The daytime sleepiness may affect important
activities such as work or taking care of children, or may
occur at times that are dangerous such as driving a vehicle. The best initial step in evaluation of patients with
suspected obstructive sleep apnea includes a detailed
history and physical examination [3].
Mood disorders, endocrinopathies, and certain rheumatological disorders commonly cause fatigue. Specically
asking the patient if they actually doze off or fall asleep
in sedentary situations versus not wanting to get up and
do something active can sometimes help determine if
the patient has hypersomnia from a primary sleep disorder or fatigue from another medical cause. Of note, even
with a good history, many patients with sleep disorders
will still describe their sleep disorder with presenting
symptoms of fatigue or lack of energy, so these symptoms should still be taken seriously in the evaluation of
sleep apnea [4]. Obstructive sleep apnea can also cause
symptoms of decreased attention, cognition, and poor
memory. Hyperactivity and inattention are a common
presenting complaint of obstructive sleep apnea, especially in children [5].
In addition to asking about sleepiness, it is essential
to investigate other common clinical symptoms of
6.2 History Taking
obstructive sleep apnea. The presence, frequency, and
intensity of snoring are key features in patients with
Because many patients presenting for evaluation of
obstructive sleep apnea report excessive daytime sleepiness, it is important to further investigate the presence
and severity of excessive daytime sleepiness. Subjective
scales, such as the Epworth Sleepiness Scale (See
. Fig.6.1), can quickly attempt to measure the level of
sleepiness during the day as reported by the patient. This
can be further assessed (many times more effectively) by
directly inquiring about different circumstances where
sleepiness occurs or affects them. Providers can ask
patients if they feel sleepiness affects activities such as
driving, work, school, or social activities. Many times,
the patient may underestimate the severity or even presence of excessive daytime sleepiness. This can be due to
the chronic nature of the symptoms, as it may be difcult for the patient to know what normal alertness during the day is supposed to be if symptoms have persisted
for years. Sleepiness also affects the ability of the brain
to self-assess performance, hence leading to inaccurate
judgments by the patient on their ability to stay alert. It
can be helpful to ask any family members, friends, or
coworkers about the patient’s level of sleepiness, as they
may have a different and more accurate perspective.
Inquiring about when and how often daytime sleepiness
occurs can also be helpful in the evaluation, especially
because there are numerous causes for a presenting complaint of excessive daytime sleepiness that also need to
be considered in the differential diagnosis (See
.
Table6.1). Insufcient sleep (getting less than 7hours
per a day on average) is the most common cause of
excessive daytime sleepiness in the United States.
It can also be helpful to ask if the patient’s sleepiness
is more consistent with fatigue or decreased energy, as
obstructive sleep apnea. Snoring may not be apparent to
the patient, and it is important to ask a bed partner or
collateral source about the presence of snoring or noisy
breathing. Patients may report that their bed partner or
someone sharing a room with them notices apneas or
pauses in their breathing during sleep. Other symptoms
that can be attributed to obstructive sleep apnea include
nighttime awakenings, night sweats, nocturia, acid
reux, and morning headaches. These symptoms are
noted more commonly in patients with sleep apnea, but
are nonspecic and can be related to numerous other etiologies. Finally, many patients with obstructive sleep
apnea may present with insomnia or disrupted sleep.
It is important to consider evaluation for other
causes of hypersomnia, especially because patients with
obstructive sleep apnea may also have other contributing sleep disorders also responsible for poor sleep quality (See Table6.1). Evaluation for insufcient sleep by
asking about bedtime, wake times, and sleep schedules is
essential. Adults require at least seven hours of sleep for
optimal health, and insufcient sleep is the most common causes of sleepiness [6]. Restless legs syndrome can
be a cause of excessive daytime sleepiness by causing
nighttime sleep disruption. This diagnosis can be evaluated by asking the patient about extremity discomfort or
an urge to move their legs that is worse at night. The
symptoms improve with movement and cause disruption of their sleep. Though rare, screening for narcoleptic symptoms such as cataplexy, sleep-related
hallucinations, and sleep paralysis can be helpful in the
appropriate clinical scenario. Cataplexy is brief episodes
of transient muscle weakness triggered by emotion, typically positive emotion such as laughter. Sleep paralysis

Clinical Evaluation oftheObstructive Sleep Apnea Patient
71
6
. Fig. 6.1 Epworth
sleepiness scale (From: Johns
MW.A new method for
measuring daytime
sleepiness: the Epworth
sleepiness scale. Sleep
1991;14(6):5400–545)
Epworth Sleepiness scale
Using the following scale, circle the most appropriate number for each situation.
0=would doze, less than once a month
1=slight chance of dozing
2=moderate chance of dozing
3=high chance of dozing
Situation Chance of Dozing
Sitting and reading 0 1 2 3
Watching TV 0 1 2 3
Sitting inactive in a public place (theatre, in a meeting) 0 1 2 3
As a passenger in a car for an hour without a break 0 1 2 3
Lying down to rest in an afternoon 0 1 2 3
Sitting and talking to someone 0 1 2 3
Sitting quietly after a lunch without alcohol 0 1 2 3
In a car, while stopped for a few minutes in traffic 0 1 2 3
8 numbers you have circled TOTAL = ______________________
From: Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness
scale. Sleep 1991;14(6):5400-545.
. Table 6.1 Important causes of excessive daytime
sleepiness to consider
Insufcient sleep
Obstructive sleep apnea
Central sleep apnea
Narcolepsy
Idiopathic hypersomnia
Circadian rhythm disorders
Restless legs syndrome
Medications
Drugs of abuse
Traumatic brain injury
Neurodegenerative disorders (e.g., dementia, Parkinson’s disease)
is a transient feeling of being awake but not being able
to move, usually occurring while falling or waking up
from sleep. Cataplexy is rarely seen outside a diagnosis
of narcolepsy, but both sleep paralysis and sleep-related
hallucinations can be seen in a variety of sleep disorders,
including sleep apnea and sleep deprivation.
Certain medical diagnoses place patients at higher
risk for obstructive sleep apnea. These include pulmonary conditions such as chronic obstructive pulmonary
disease and asthma as well as neurological conditions
such as stroke or neuromuscular disorders. Patients with
craniofacial disorders or midface hypoplasia, such as
patients with cleft palate or Down’s syndrome are at
higher risk of sleep-disordered breathing. Patients with
cardiac diseases such as heart failure and cardiac
arrhythmias (atrial brillation) have very high rates of
both central and obstructive sleep apnea [7]. It will also
be important to ask about any previous upper airway

72
R. K. Malhotra and R. Zeballos-Chavez
surgeries that the patient may have undergone for a previous diagnosis of sleep apnea or airway difculties.
Patients may try to mask their symptoms of sleepiness by using caffeine or tobacco. While completing the
social history, the provider should ask about any use of
caffeine, tobacco, or other recreational drugs which can
cause sleepiness during the day or insomnia at night. A
history of smoking also puts the patient at risk for sleep
apnea.
It is important to learn more about the patient’s
employment, as certain occupations come with specic regulations in regards to sleepiness and a diagno-
6
sis of obstructive sleep apnea. This typically includes
occupations such as pilots or drivers with commercial
driver’s licenses. Federal agencies have regulations in
regards to adherence to therapy or possibly time off
of work during evaluation for sleep apnea if there is
perceived risk that the symptoms may put the worker
or society at risk. It may also be helpful to ask if any
family members have a history of obstructive sleep
apnea (or symptoms suspicious for sleep apnea), as
obstructive sleep apnea can run in families, especially
if related to craniofacial or upper airway anatomical
abnormalities.
6.3 Physical Examination
The clinical history as described above is critical in the
evaluation of possible obstructive sleep apnea. There
are key features on the physical examination that are
also very helpful in the clinical evaluation. One of the
most helpful objective measure is an elevated body mass
index (BMI) or a nding of obesity. The higher the BMI,
the higher the risk for obstructive sleep apnea (due to
increase of fatty tissue in oropharyngeal structures
including tongue). It is also important to measure the
neck circumference as an increased neck circumference>17 inches in men and >16 inches in women are
also considered risk factors and should be included in
the initial clinical evaluation [8]. An elevated blood pressure (or a history of hypertension), abnormal respiratory signs, or low oxygen saturations can be associated
with sleep-disordered breathing.
A detailed upper airway and craniofacial examination will be helpful in looking for characteristics that can
predispose the patient to a narrow airway. The clinician
should document the presence and size of tonsillar tissue as well as a gauge of how crowded the airway is
upon visual inspection. One common method is the
Mallampati classication which grades the airway from
1(least crowded) to 4(most crowded). The Mallampati
classication or score was initially utilized by clinicians
in determining ease of intubation but was later found to
correlate with risk of obstructive sleep apnea. The score
is obtained by asking the patient while sitting to open
their mouth and fully protrude their tongue (no phonation) and examining the airway. Mallampati 1 classication is when you can see the soft palate, hard palate,
uvula, and tonsillar pillars. A Mallampati 2 classication is when you can view the other three structures, but
not the tonsillar pillars. In a Mallampati class 3, only the
soft and hard palate, and base of the uvula is visualized.
In a Mallampati class 4, only the hard palate is noted,
suggesting a crowded airway putting the patient at highest risk for sleep apnea [9].
More detailed visualization of the upper airway can
be performed by nasal endoscopy, though this is not
routinely performed at most sleep centers unless surgical
intervention is being considered. Craniofacial
abnormalities such as retrognathia, micrognathia, macroglossia, scalloping of the tongue, or signicant overjet
also place the patient at high risk for obstructive sleep
apnea. Physical examination of nasopharynx should
include evaluation for nasal obstruction from nasal turbinate hypertrophy, septal deviation, nasal polyps, or
other obstructing lesions.
Due to the common occurrence of cardiac disease
and sleep apnea, and detailed cardiovascular examination listening for murmurs, abnormal heartbeats, or
signs of heart failure (lower extremity edema or elevated
jugular venous distention) should be performed. An
abnormal pulmonary exam may also suggest heart failure (rales or crackles) or other pulmonary disorders
(wheezing) putting the patient at risk for obstructive
sleep apnea or other sleep-disordered breathing such as
sleep-related hypoventilation or hypoxemia. Evaluating
the distal extremities for any clubbing or cyanosis is also
helpful to determine if there is any underlying cardiovascular or pulmonary disease.
A detailed neurological examination, especially
focusing on cranial nerve and motor function, can assist
in the evaluation of obstructive sleep apnea. If patients
have signicant motor weakness or signs of a central
nervous system injury, this puts them at risk for not only
obstructive sleep apnea, but also more complicated
sleep-disordered breathing such as sleep-related hypoventilation or central sleep apnea which may require more
complex evaluation and treatment.
6.4 Conclusion
Though objective testing is necessary to conrm a diagnosis of obstructive sleep apnea, the history and physical examination is key to a comprehensive evaluation of
the patient with suspected sleep apnea. The history and
physical not only helps guide which testing is necessary
as the next step, but also evaluates for other possible
causes for the patients presenting sleep symptoms.

Clinical Evaluation oftheObstructive Sleep Apnea Patient
73
6
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Sleep Medicine; 2014.
2. Young TB. Epidemiology of daytime sleepiness: denitions,
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16):12.
3. Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R,
Ramar K, Harrod CG.Clinical practice guideline for diagnostic
testing for adult obstructive sleep apnea: an American Academy
of sleep medicine clinical practice guideline. J Clin Sleep Med.
2017;13(3):479–504.
4. Chervin RD.Sleepiness, fatigue, tiredness, and lack of energy in
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5. Chervin RD, Archbold KH, Dillon JE, Panahi P, Pituch KJ, Dahl
RE, Guilleminault C.Inattention, hyperactivity, and symptoms
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6. Watson NF, Badr MS, Belenky G, Bliwise DL, Buxton OM,
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7. Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R,
Kirchner HL, etal. Association of nocturnal arrhythmias with
sleep-disordered breathing: the sleep heart health study. Am J
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8. Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A,
Patil SP, Ramar K, Rogers R, Schwab RJ, Weaver EM, Weinstein
MD.Clinical guideline for the evaluation, management and longterm care of obstructive sleep apnea in adults. J Clin Sleep Med.
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9. Nuckton TJ, Glidden DV, Browner WS, Claman DM.Physical
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Further Reading
Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R,
Ramar K, Harrod CG.Clinical practice guideline for diagnostic
testing for adult obstructive sleep apnea: an American Academy
of sleep medicine clinical practice guideline. J Clin Sleep Med.
2017;13(3):479–504.

Diagnostic Testing
forObstructive Sleep Apnea
MeghnaP.Mansukhani, BhanuPrakashKolla, andKannanRamar
Contents
7.1 Background – 76
7.2 Diagnosis ofOSA – 76
7.2.1 History andExamination – 76
7.2.2 Screening Tools – 76
7.2.3 Diagnostic Tests – 77
7.2.4 Types ofSleep Studies – 77
7.2.5 Denition ofOSA – 77
7.2.6 Scoring ofRespiratory Events – 77
7.2.7 Clinical Guidelines – 78
75
7
7.3 Home Sleep Apnea Test (HSAT) – 78
7.3.1 Advantages – 78
7.3.2 Disadvantages – 78
7.3.3 Patient Selection – 78
7.3.4 Data Obtained – 79
7.3.5 Conduct andInterpretation ofTest – 79
7.3.6 Accuracy ofResults – 79
7.3.7 Discussion ofResults – 80
7.3.8 Recommended Follow-Up – 80
7.3.9 Clinical Outcomes – 80
7.3.10 Cost-Eectiveness – 80
7.3.11 Summary ofHSAT – 80
7.4 Polysomnography (PSG) – 80
7.4.1 Patient Selection – 80
7.4.2 Number andDuration ofTests – 81
7.4.3 Conduct andInterpretation oftheStudy – 81
7.4.4 Follow-Up – 81
7.4.5 Discussion ofResults – 81
7.4.6 Repeat Testing intheLong Term – 81
7.4.7 Summary ofPSG – 82
7.5 Conclusions – 82
Further Reading – 82
© 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_7
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