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Obstructive Sleep Apnea
‫االنسدادي‬ ‫الليلي‬ ‫المؤقت‬ ‫النفس‬ ‫انقطاع‬ ‫أو‬ ‫ٌهر‬‫ب‬‫ال‬
Dr. Marwan Mouakeh
Consultant Orthodontist, Scientific Adviser of Al-Hokail
Polyclinic Academy - Khobar , KSA
• Good sleep hygiene is critical for one’s overall
physical and mental health.
• Normally it should take about 10 - 15 minutes to
fall asleep after going to bed.
• If you are asleep in less than 5 minutes, that could
be a sign of excessive sleepiness .
Introduction
•There are 2 forms of sleep: REM sleep and non-REM sleep.
REM stands for rapid eye movement and is associated with
dreaming. It accounts for 25% of normal sleep, coming in
longer periods toward morning. The rest of our sleep time is
spent in NREM, which consists of four stages from light sleep
(stage 1) to deep sleep (stage 4).
The Sleep Cycle
• Repeated episodes of partial or complete
upper airway obstruction during sleep .
 A Sleep disorder characterized by recurrent
episodes of narrowing or collapse of pharyngeal
airway during sleep despite ongoing breathing
efforts.
What Is Obstructive Sleep Apnea (OSA) ?
• 1st description of the disorder in the
medical literature was in 1965 .
Gastaut H, Tassinari CA, Duron B. Polygraphic study of diurnal and nocturnal
(hypnic and respiratory) episodal manifestations of Pickwick syndrome [in
French]. Rev Neurol (Paris) 1965; 112:568–579
 Obstructive sleep apnea (OSA) is a public health
problem and a potentially life-threatening condition .
What Is Obstructive Sleep Apnea (OSA) ?
Patent Vs Collapsed Airway
Cardinal Symptoms of OSA
 Snoring
 Sleepiness
 Sleep Apnea Episodes
 Terminology
– Apnea = Cessation of airflow > 10 seconds
– Hypopnea = Decreased airflow > 10 seconds
( transient reduction of breathing )
Terminology
 AHI (Apnea - Hypopnea Index)
– apnea + hypopnea / hour of sleep
 RDI (Respiratory Disturbance Index)
– apnea + hypopnea + arousal / hour of sleep
Apnea Hypopnea
↓ in airflow > 80% ↓ in airflow 50 % - 30%
↓ O2 sat ↓ O2 sat > 4%
> 10 sec ≥ 10 sec
Ending in arousal Ending w/ arousal
•Defining Severity of OSA
 Length of time in apnea event
 % ↓ O2 Desaturation
 Apnea- Hypopnea Index (AHI):
– Mild 5-15 events / hour
– Moderate 15-30 events / hour
– Severe > 30 events / hour
•Defining Severity of OSA
• Clinical features of Obstructive Sleep Apnea:
Excessive daytime sleepiness
Morning headache
Cardiopulmonary dysfunction
– hypertension
– cardiac arrhythmias
– heart failure
Impaired memory and concentration
Reduced intellectual ability
Disturbed personality and mood .
•The dominant symptoms of OSA are excessive sleepiness,
impaired concentration and snoring.
•Incidence of OSA
 Approximately 40% of adults over 40 years old
snore (about 100 million Americans) .
 Middle age (30 – 60 yo) American
– 4% of men and 2% of women (18 million)
 Geriatrics
– 24 - 42% have RDI > 5
 Two thirds are obese
•Incidence of OSA
 National Commission on Sleep Disorders Research (1993)
– 95% of pts w/ OSA may be undiagnosed
 More prevalent than asthma
 Equally prevalent as diabetes
Pathophysiology of OSA
Sleeping
Decreased pharyngeal
muscles tonicity
Upper Airway
collapse
Apnea
Hypoxia
Hypercapnia
Respiratory efforts
Increase in tonicity
Clearance of upper
airways
Micro reveille
Hyperventilation:
correction of O2 & CO2
Mechanisms of OSA
Pathophysiology of OSA
 Tissue laxity and redundant mucosa
 Anatomic abnormalities
 Decreased muscle tone with REM sleep
 Airway collapse
 Desaturation ( O2 )
 Arousal with restoration of airway
 Sleep Fragmentation leading to
Hypersomnolence
 Etiology of OSA
 Multifactorial :
- Anatomic factors
- Neuromuscular factors
– Anatomic factors resulting in narrowing of pharynx :
•Skeletal anatomy (micrognathia, retrognathia)
•Soft tissue (macroglossia, tonsillar hypertrophy,
fatty infiltration of pharyngeal tissue assoc w/
obesity)
 Etiology of OSA
 Skeletal anatomy ( micrognathia, retrognathia)
 Etiology of OSA
•Skeletal anatomy
•Inferiorly positioned hyoid
bone .
• Constricted osseous
airways .
 Etiology of OSA
•Tonsillar hypertrophy
•Enlarged Adenoids
•Skeletal Abnormalities
 Etiology of OSA
•Long soft palate
•Skeletal Abnormalities
 Etiology of OSA
•Macroglossia
•Skeletal Abnormalities
 Etiology of OSA
– Neuromuscular factors
•Decreased activity of pharyngeal dilator muscles
•Increased compliance of pharyngeal airway
•Active inhibition of muscle activity during REM
sleep
•Alcohol, sedatives, and muscle relaxants
 Etiology of OSA
 Complications
• Desaturation ( O2 )with compensatory
polycythemia
• Hypercapnia ( CO2)with pulmonary
hypertension
• Systemic hypertension
• Arrhythmias
•Risk Factors
 Obesity, body mass index > 28 kg/m2
 Increased age
 Male sex
 Hypertension
 Hypothyroidism / Acromegaly
 Use of sedatives/narcotics/alcohol
 Smoking
 Obesity
 Strongest risk factor for OSA
– Present in > 60% of patients referred for
a diagnostic sleep evaluation
– Wisconsin Sleep Cohort Study
• A one standard deviation difference in BMI was
associated with a 4-fold increase in disease
prevalence
Risk Factors
• Obesity
 Alters upper airway mechanics during sleep
1. Increased parapharyngeal fat deposition:
neck circumference: > 17” males
> 16” females
With subsequent:
 smaller upper airway
 increase the collapsibility of the pharyngeal
airway
• Obesity
2. Changes in neural compensatory
mechanisms that maintain airway
patency:
 diminished protective reflexes
which otherwise would increase upper
airway dilator muscle activity to
maintain airway patency
Risk Factor: Age
Adapted from Young T et al. N Engl J Med 1993;328.
Risk Factor: Smoking
Adapted from Wetter DW et al. Arch Intern Med 1994:154
©1994 American Medical Association.
Diagnosis
Of
Obstructive Sleep Apnea
 Diagnosis
 History
 Physical examination
 Radiographs
 Polysomnography
History
 Snoring
 Restless sleep
 Morning Headache
 Insomnia
History
 Excessive daytime sleepiness
 Personality changes
 Insomnia
 Symptoms
• Loud snoring
• Excessive daytime sleepiness
• Choking/gasping during sleep
• Unrefreshing sleep
• Daytime fatigue
• Impaired concentration
Symptoms and Signs of OSA
•Diagnosis: Clinical Features
 Nocturnal symptoms
1. Snoring :
– reflects the critical narrowing
- population survey: habitual snorers
25% of men, 15% of women
•Diagnosis: Clinical Features
 Nocturnal symptoms
1. Snoring :
- prevalence increases with age (60%, 40%)
- the most frequent symptom of OSA
- absence makes OSA unlikely
(only 6% of patients with OSA did not report)
 Nocturnal Symptoms
2. Witnessed Apneas
3. Nocturnal Choking or Gasping
4- Restless Sleep
5. Insomnia
•Diagnosis: Clinical Features
• Clinical features
 Daytime symptoms
1. Excessive daytime sleepiness
- severity can be assessed
 subjectively = questionnaires
(Epworth Sleepiness Scale)
 objectively
MSLT = Multiple Sleep Latency Test
The most common symptom of OSA is
excessive daytime sleepiness, which can be
assessed using the Epworth Sleepiness Scale.
•Epworth Sleepiness Scale
0 = would never doze
1 = slight chance of dozing
2 = moderate chance of dozing
3 = high chance of dozing
•A score of more than 10 suggests clinically
significant daytime sleepiness, although a lower
score does not exclude it.
•Clinical features
 (Daytime symptoms)
2. Fatigue
3. Memory impairment
4. Personality changes
5. Morning headaches or nausea
6. Depression
 Signs of OSA
•Obesity (particularly upper body)
•Mandibular/maxillary hypoplasia
(receding chin)
• Crowding of the oropharynx
•Large tonsils or tongue
•Nasal and nasopharyngeal
obstruction
 Evaluation
 Thyroid function tests
 Arterial blood gas
 Complete blood count
 ECG
 Echocardiography
 Radiological studies
 Polysomnography
•Radiography
 Cephalometrics
 Computed tomography
 Magnetic resonance imaging
 Evaluation
• Cephalometrics
Airway evaluation
Adenoids
Tongue
•Computed tomography
 Volumetric reconstruction
- Disadvantages :
– Cost
– Weight limitations
– Ionizing radiation
 Evaluation
•Magnetic Resonance Imaging
 Excellent soft tissue anatomy
 Multiple planes
 No ionizing radiation
- Disadvantages :
– Cost
– Weight limitations
– Noisy
– Claustrophobia
 Evaluation
Polysomnography
 Simultaneous recordings of multiple physiological
signals during sleep.
 Electroencephalogram
(EEG)
 Electrooculogram (EOG)
 Electromyogram (EMG)
 Electrocardiogram (ECG)
 Oronasal airflow
 Chest wall effort
 Snore microphone
 Oxyhemoglobin saturation
 The gold standard: Overnight Polysomnogram
 Evaluation
Obstructive sleep apnea. Note the absence of flow (red arrow)
despite paradoxical respiratory effort (green arrow ).
Polysomnogram
Apnea Patterns
There are 3 characteristic patterns of apnea.
An obstructive apnea is defined by the absence of airflow despite
persistent ventilatory efforts,.
A central apnea, in contrast, is the absence of airflow due to the lack
of ventilatory effort.
A mixed apnea includes both central and obstructive components,
usually with an initial central component followed by the obstructive
component.
• Diagnosis of OSA
 American Academy of Sleep Medicine criterias:
A. Excessive daytime sleepiness that is not better
explained by other factors
B. Two or more of the following that are not better
explained by other factors:
choking during sleep; recurrent awakenings;
unrefreshing sleep; daytime fatigue; impaired
concentration.
C. AHI (five or more obstructed breathing
events per hour during sleep).
Medical Consequences
 The narrowing and closure of the airway
during sleep causes fragmented sleep and
patho-physiologic conditions:
– Neurobehavioral Derangement
– Cardiopulmonary Derangement
Medical Consequences
Neurobehavioral Derangement
 Excessive daytime sleepiness
 Depression
 Impotence
 Personality change, Irritability
 Learning and memory difficulties
 Morning headache
 Lack of energy
 Loss of employment, Uninsurability, Marital
Discord
 Traffic accident, 7x higher
The accident incidence was seven-fold greater in patients with
sleep apnea than in matched controls without the disorder
• MVA ( motor-vehicles accidents )
Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.
 Hypertension
– Occur in 50% OSA patients
– About 30% of HTN have OSA
– Repetitive hypoxia and hypercapnia at night may contribute
to inc in sympathetic tone resulting in HTN
Medical Consequences
Cardiopulmonary Derangement
 RV hypertrophy and failure
– Resulting from pulmonary HTN due to hypoxemia
 Cardiac arrythmias
– Most common being nocturnal bradycardia, which occurs
during apneic episode followed by tachycardia at resolution
of apnea
 MI, angina
Medical Consequences
Cardiopulmonary Derangement
Treatment of OSA
 Indication for Treatment
 AHI 15 or more (moderate-severe)
 AHI 5-14 (mild) and with documented
symptoms of :
– Excessive daytime sleepiness, or
– Impaired cognition, mood disorders or insomnia, or
– Documented hypertension, ischemic heart disease
or history of stroke .
 Treatment of OSA
Behavioral Modifications
Nonsurgical modalities
Surgical modalities
 Behavioral Modifications
– Weight reduction
– Avoid CNS depressants (alcohol, sedatives)
– Sleep on side w/ tennis ball on back
– Stop smoking
– External nasal dilators/steroid spray
 Treatment of OSA
 Weight Reduction
– Exercise
– Diet
– Bariatric Surgery
 Treatment of OSA
•Weight Loss
 Remains a highly effective method
 10 – 15 % reduction in weight can lead to
an approximately 50 % reduction in sleep
apnea severity in moderately obese male
patients.
Stop / Reduce Smoking
 Treatment of OSA
• Sleep Position Training
 Avoid sleeping in the supine position
 Treatment of OSA
• Sleep Position Training
Use of a tennis ball sewn into the back of a night shirt as
a means of training the patient to avoid the supine
position and sleep in the lateral recumbent position.
 Treatment of OSA
•Pharmacotherapy
 Protriptyline – decreases REM sleep
 Thyroxine or Medroxyprogestrone : in
Hypothyroidism patients
 Progestrone : in postmenopausal women
 Decongestants : nasal congestion , pharyngeal
odema .
 Antibiotics
Non-Surgical Treatment:
•Non-Surgical Treatment
CPAP
Continuous Positive Airway Pressure
• CPAP
•Sullivan introduced CPAP in 1981
Non-Surgical Treatment
• Continuous Positive Airway Pressure
Act as a pneumatic splint to maintain patency of the pharyngeal
airway by preventing collapse of the pharyngeal tissues .
Non-Surgical Treatment
• Nasal & Facial Masks
Non-Surgical Treatment
NASAL
NASAL
PILLOWS
NASAL
FULL FACE NASAL PILLOWS
CPAP &
humidification
 CPAP
 Titrate the airway pressure needed to overcome
airway obstruction
 Average CPAP setting is about 5-15 cm H2O
 May be delivered via a nasal
or face mask
 Effective in > 90%
Non-Surgical Treatment
• CPAP
 Has been shown to objectively:
– Decrease MVA
– Decrease blood pressure
– Decrease day time sleepiness
 Problems:
– Mask discomfort
– Patient acceptance
– Claustrophobia
Non-Surgical Treatment
Polysomnogram : Before CPAP
Polysomnogram : After CPAP
•Non-Surgical Treatment - CPAP
 Physical issues :
– Facial skin abrasions/discomfort
– Air leaks leading to drying of eye
– Difficulty with expiration
– Nasal dryness and congestion
– Sore throat
– Loud noise
 Tongue retaining devices
– Keep tongue in forward position by creating negative
pressure in a plastic bulb, fit between the lips
 Mandibular advancing devices
– Cause forward/downward movement of mandible when
attached to dental arches
 Soft palate lifter
– Effective only for treatment of snoring
•Non-Surgical Treatment:
Oral Devices
• Tongue Retaining Devices ( TRD)
• TRDs use suction pressure to maintain the tongue
in a protruded position during sleep .
Mandibular Advancement Devices
Mandibular Advancement Devices
•The aim of all of these devices is to improve the patency of the
upper airway during sleep by increasing its dimensions and
reducing its collapsibility .
• Mandibular Advancement Devices
 Advance Base of the
tongue to ↑ airway
 Advance and raise hyoid
bone, tightening the
pharyngeal musculature
which reduces airway
collapsibility.
 Stretch the masseter
muscles which
stimulates the
genioglossus muscle
• Oral Devices
• Activator, Herbst, Twin
block …
• Tongue Retaining
appliances
 Reposition and stabilize
the mandible & tongue
(sometimes soft palate)
 Increase size of airway in
lateral dimension
 Mandibular Advancement Devices
• Fabrication of Mandibular Protruding Appliance
•Good Impressions of upper & lower dental arches
• Assessment of the amount of maximum mandibular
protrusion
• Recording the Protruded position of the mandible
• Progressive mandibular
protrusion to ensure treatment
efficiency .
• Start by 50-60% of the
maximum active protrusion .
•
•Titration
• Recording the Protruded position of the mandible
•Positive relationships between
amount of mandibular protrusion
and :
- Increased airways patency
- Decreased airways resistance
- Decreased episodes of OSA
•Titration
• Oral appliances
 Most effective in non-obese patients with
retro or micrognathia
 Better for mild to moderate cases
 51% achieve normal sleep, 61% improved
RDI < 20
 Consider TMJ dysfunction and occlusal
changes
• Oral Devices : Contra-indications
•Insufficient tooth support
•Periodontal problems
•Poor oral hygiene ( multiple caries )
•Temporomandibular disorders
• Mandibular protrusion < 5 mm
• Bruxism ??
- Articular
- Dental ???
Oral appliance treatment for obstructive sleep
apnea in a partly edentulous patient
Oral appliance treatment for obstructive sleep
apnea in a partly edentulous patient
• Oral Devices : Contra-indications
•Class III malocclusion
•Severe malocclusion
- Orthodontic
Dental Appliance Treatment for Obstructive Sleep Apnea
DOI 10.1378/chest.06-2038 Chest 2007;132;693-699
Andrew S. L. Chan, Richard W. W. Lee and Peter A. Cistulli
Nightly use of an MPD for 2 years
by OSA patients and snorers was
found to increase their airway
passages because of an increase in
pharyngeal area, which to a large
extent was caused by a reduction
in velum area.
Franson et al . Am J Orthod Dentofacial
Orthop 2002;122:371-9)
Influence of mandibular protruding device on
airway passages and dentofacial characteristics
in obstructive sleep apnea and snoring
• American Sleep Disorders Association
Standards of Practice Committee
– Primary snoring
– Pts w/ mild OSA who do not respond to general
treatment
– Pts w/ moderate to severe OSA who cannot
tolerate nasal CPAP and who refuse or are not
candidate for surgical treatment .
• Non-Surgical Treatment:
Oral Devices
 Summary of the Key Adverse Effects of Oral Appliances
Short-term adverse effects
Excessive salivation
Mouth dryness
Tooth pain
Gum irritation
Headaches
Temporomandibular joint discomfort.
•Long-term adverse effects
Reduction in overjet
Increase in facial height
Increase in degree of mouth opening
Changes in inclination of incisors
Increase in mandibular plane angle
 Surgical Methods- Soft tissues
 Reconstruct upper airway
Uvulopalatopharyngoplasty (UPPP)
Laser-assisted uvulopalatopharyngoplasty
(LAUP)
Genioglossal advancement
Nasal reconstruction
 Adenotonsillectomy :
preferred treatment in children
 Partial Glossectomy
 Bypass upper airway
Tracheostomy
•Uvulopalatopharyngoplasty (UPPP)
•Fujita (1981)
•Most common procedure
•1st line tx for retropalatal collapse
•10-50% success
 OSA : Surgical Treatment
•Uvulopalatopharyngoplasty (UPPP)
Devised to surgically excise the tonsils
(if present) and portions of the soft
palate, and reorientate the tonsillar
pillars in order to enlarge the
oropharyngeal space .
 OSA : Surgical Treatment
•Tongue reduction
 Lingual tonsillectomy
 Laser midline glossectomy
 Lingual plasty
 Radiofrequency volumetric tissue
reduction
 OSA : Surgical Treatment
•Partial Glossectomy
 An enlarged tongue (macroglossia)
may call for tongue reduction surgery
extending from the midline of the
posterior tongue down to the free
margin of the epiglottis.
 Since speech and swallowing may be
significantly compromised by this
procedure, it is limited to few cases
where there is true macroglossia
present.
 OSA : Surgical Treatment
 Adenotonsillectomy - preferred treatment in
children .
 Tracheostomy - cure for OSAS
– used for failure of more conservative treatment
– life threatening cardiopulmonary complications
– alternative techniques to lessen complications
 Surgical Methods - Soft tissues
 Surgical Methods - Maxillofacial elements
 Mandibular advancement
 Maxillomandibular advancement ± advancement
genioplasty
 Geniotubercle advancement ± hyoid suspension
 Advancement genioplasty .
 Geniotubercle advancement
For advancing the tongue forwards
without changing lower facial
aesthetics or the dental occlusion .
 The advancement of the central
block of bone below the mandibular
incisor effectively advances the
attachment of the genioglossus and
geniohyoid muscles which brings
forward both the tongue and hyoid
bone.
 OSA : Surgical Treatment
– Advances hyoid bone
anteriorly and inferiorly.
– Advances epiglottis and base
of tongue .
– Performed in conjunction
with other procedures .
– Dysphagia may result .
 Hyoid Myotomy and Suspension
 OSA : Surgical Treatment
 Adult female patient
 OSA
Severe skeletal open bite
•Surgical-Orthodontic Treatment
Assessment and Management of Obstructive
Sleep Apnea in Adults
Otherwise snore
and this will
happen to you….
Or sleep alone….

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Obstructive sleep apnea

  • 1. Obstructive Sleep Apnea ‫االنسدادي‬ ‫الليلي‬ ‫المؤقت‬ ‫النفس‬ ‫انقطاع‬ ‫أو‬ ‫ٌهر‬‫ب‬‫ال‬ Dr. Marwan Mouakeh Consultant Orthodontist, Scientific Adviser of Al-Hokail Polyclinic Academy - Khobar , KSA
  • 2. • Good sleep hygiene is critical for one’s overall physical and mental health. • Normally it should take about 10 - 15 minutes to fall asleep after going to bed. • If you are asleep in less than 5 minutes, that could be a sign of excessive sleepiness . Introduction
  • 3. •There are 2 forms of sleep: REM sleep and non-REM sleep. REM stands for rapid eye movement and is associated with dreaming. It accounts for 25% of normal sleep, coming in longer periods toward morning. The rest of our sleep time is spent in NREM, which consists of four stages from light sleep (stage 1) to deep sleep (stage 4). The Sleep Cycle
  • 4. • Repeated episodes of partial or complete upper airway obstruction during sleep .  A Sleep disorder characterized by recurrent episodes of narrowing or collapse of pharyngeal airway during sleep despite ongoing breathing efforts. What Is Obstructive Sleep Apnea (OSA) ?
  • 5. • 1st description of the disorder in the medical literature was in 1965 . Gastaut H, Tassinari CA, Duron B. Polygraphic study of diurnal and nocturnal (hypnic and respiratory) episodal manifestations of Pickwick syndrome [in French]. Rev Neurol (Paris) 1965; 112:568–579  Obstructive sleep apnea (OSA) is a public health problem and a potentially life-threatening condition . What Is Obstructive Sleep Apnea (OSA) ?
  • 6. Patent Vs Collapsed Airway Cardinal Symptoms of OSA  Snoring  Sleepiness  Sleep Apnea Episodes
  • 7.  Terminology – Apnea = Cessation of airflow > 10 seconds – Hypopnea = Decreased airflow > 10 seconds ( transient reduction of breathing )
  • 8. Terminology  AHI (Apnea - Hypopnea Index) – apnea + hypopnea / hour of sleep  RDI (Respiratory Disturbance Index) – apnea + hypopnea + arousal / hour of sleep Apnea Hypopnea ↓ in airflow > 80% ↓ in airflow 50 % - 30% ↓ O2 sat ↓ O2 sat > 4% > 10 sec ≥ 10 sec Ending in arousal Ending w/ arousal
  • 9. •Defining Severity of OSA  Length of time in apnea event  % ↓ O2 Desaturation  Apnea- Hypopnea Index (AHI): – Mild 5-15 events / hour – Moderate 15-30 events / hour – Severe > 30 events / hour
  • 11. • Clinical features of Obstructive Sleep Apnea: Excessive daytime sleepiness Morning headache Cardiopulmonary dysfunction – hypertension – cardiac arrhythmias – heart failure Impaired memory and concentration Reduced intellectual ability Disturbed personality and mood . •The dominant symptoms of OSA are excessive sleepiness, impaired concentration and snoring.
  • 12. •Incidence of OSA  Approximately 40% of adults over 40 years old snore (about 100 million Americans) .  Middle age (30 – 60 yo) American – 4% of men and 2% of women (18 million)  Geriatrics – 24 - 42% have RDI > 5  Two thirds are obese
  • 13. •Incidence of OSA  National Commission on Sleep Disorders Research (1993) – 95% of pts w/ OSA may be undiagnosed  More prevalent than asthma  Equally prevalent as diabetes
  • 15. Sleeping Decreased pharyngeal muscles tonicity Upper Airway collapse Apnea Hypoxia Hypercapnia Respiratory efforts Increase in tonicity Clearance of upper airways Micro reveille Hyperventilation: correction of O2 & CO2 Mechanisms of OSA
  • 16. Pathophysiology of OSA  Tissue laxity and redundant mucosa  Anatomic abnormalities  Decreased muscle tone with REM sleep  Airway collapse  Desaturation ( O2 )  Arousal with restoration of airway  Sleep Fragmentation leading to Hypersomnolence
  • 17.  Etiology of OSA  Multifactorial : - Anatomic factors - Neuromuscular factors
  • 18. – Anatomic factors resulting in narrowing of pharynx : •Skeletal anatomy (micrognathia, retrognathia) •Soft tissue (macroglossia, tonsillar hypertrophy, fatty infiltration of pharyngeal tissue assoc w/ obesity)  Etiology of OSA
  • 19.  Skeletal anatomy ( micrognathia, retrognathia)  Etiology of OSA
  • 20. •Skeletal anatomy •Inferiorly positioned hyoid bone . • Constricted osseous airways .  Etiology of OSA
  • 22. •Long soft palate •Skeletal Abnormalities  Etiology of OSA
  • 24. – Neuromuscular factors •Decreased activity of pharyngeal dilator muscles •Increased compliance of pharyngeal airway •Active inhibition of muscle activity during REM sleep •Alcohol, sedatives, and muscle relaxants  Etiology of OSA
  • 25.  Complications • Desaturation ( O2 )with compensatory polycythemia • Hypercapnia ( CO2)with pulmonary hypertension • Systemic hypertension • Arrhythmias
  • 26. •Risk Factors  Obesity, body mass index > 28 kg/m2  Increased age  Male sex  Hypertension  Hypothyroidism / Acromegaly  Use of sedatives/narcotics/alcohol  Smoking
  • 27.  Obesity  Strongest risk factor for OSA – Present in > 60% of patients referred for a diagnostic sleep evaluation – Wisconsin Sleep Cohort Study • A one standard deviation difference in BMI was associated with a 4-fold increase in disease prevalence Risk Factors
  • 28. • Obesity  Alters upper airway mechanics during sleep 1. Increased parapharyngeal fat deposition: neck circumference: > 17” males > 16” females With subsequent:  smaller upper airway  increase the collapsibility of the pharyngeal airway
  • 29. • Obesity 2. Changes in neural compensatory mechanisms that maintain airway patency:  diminished protective reflexes which otherwise would increase upper airway dilator muscle activity to maintain airway patency
  • 30. Risk Factor: Age Adapted from Young T et al. N Engl J Med 1993;328.
  • 31. Risk Factor: Smoking Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.
  • 33.  Diagnosis  History  Physical examination  Radiographs  Polysomnography
  • 34. History  Snoring  Restless sleep  Morning Headache  Insomnia
  • 35. History  Excessive daytime sleepiness  Personality changes  Insomnia
  • 36.  Symptoms • Loud snoring • Excessive daytime sleepiness • Choking/gasping during sleep • Unrefreshing sleep • Daytime fatigue • Impaired concentration Symptoms and Signs of OSA
  • 37. •Diagnosis: Clinical Features  Nocturnal symptoms 1. Snoring : – reflects the critical narrowing - population survey: habitual snorers 25% of men, 15% of women
  • 38. •Diagnosis: Clinical Features  Nocturnal symptoms 1. Snoring : - prevalence increases with age (60%, 40%) - the most frequent symptom of OSA - absence makes OSA unlikely (only 6% of patients with OSA did not report)
  • 39.  Nocturnal Symptoms 2. Witnessed Apneas 3. Nocturnal Choking or Gasping 4- Restless Sleep 5. Insomnia •Diagnosis: Clinical Features
  • 40. • Clinical features  Daytime symptoms 1. Excessive daytime sleepiness - severity can be assessed  subjectively = questionnaires (Epworth Sleepiness Scale)  objectively MSLT = Multiple Sleep Latency Test
  • 41. The most common symptom of OSA is excessive daytime sleepiness, which can be assessed using the Epworth Sleepiness Scale.
  • 42. •Epworth Sleepiness Scale 0 = would never doze 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing •A score of more than 10 suggests clinically significant daytime sleepiness, although a lower score does not exclude it.
  • 43. •Clinical features  (Daytime symptoms) 2. Fatigue 3. Memory impairment 4. Personality changes 5. Morning headaches or nausea 6. Depression
  • 44.  Signs of OSA •Obesity (particularly upper body) •Mandibular/maxillary hypoplasia (receding chin) • Crowding of the oropharynx •Large tonsils or tongue •Nasal and nasopharyngeal obstruction
  • 45.  Evaluation  Thyroid function tests  Arterial blood gas  Complete blood count  ECG  Echocardiography  Radiological studies  Polysomnography
  • 46. •Radiography  Cephalometrics  Computed tomography  Magnetic resonance imaging  Evaluation
  • 48. •Computed tomography  Volumetric reconstruction - Disadvantages : – Cost – Weight limitations – Ionizing radiation  Evaluation
  • 49. •Magnetic Resonance Imaging  Excellent soft tissue anatomy  Multiple planes  No ionizing radiation - Disadvantages : – Cost – Weight limitations – Noisy – Claustrophobia  Evaluation
  • 50. Polysomnography  Simultaneous recordings of multiple physiological signals during sleep.
  • 51.  Electroencephalogram (EEG)  Electrooculogram (EOG)  Electromyogram (EMG)  Electrocardiogram (ECG)  Oronasal airflow  Chest wall effort  Snore microphone  Oxyhemoglobin saturation  The gold standard: Overnight Polysomnogram  Evaluation
  • 52. Obstructive sleep apnea. Note the absence of flow (red arrow) despite paradoxical respiratory effort (green arrow ). Polysomnogram
  • 53. Apnea Patterns There are 3 characteristic patterns of apnea. An obstructive apnea is defined by the absence of airflow despite persistent ventilatory efforts,. A central apnea, in contrast, is the absence of airflow due to the lack of ventilatory effort. A mixed apnea includes both central and obstructive components, usually with an initial central component followed by the obstructive component.
  • 54. • Diagnosis of OSA  American Academy of Sleep Medicine criterias: A. Excessive daytime sleepiness that is not better explained by other factors B. Two or more of the following that are not better explained by other factors: choking during sleep; recurrent awakenings; unrefreshing sleep; daytime fatigue; impaired concentration. C. AHI (five or more obstructed breathing events per hour during sleep).
  • 55. Medical Consequences  The narrowing and closure of the airway during sleep causes fragmented sleep and patho-physiologic conditions: – Neurobehavioral Derangement – Cardiopulmonary Derangement
  • 56. Medical Consequences Neurobehavioral Derangement  Excessive daytime sleepiness  Depression  Impotence  Personality change, Irritability  Learning and memory difficulties  Morning headache  Lack of energy  Loss of employment, Uninsurability, Marital Discord  Traffic accident, 7x higher
  • 57. The accident incidence was seven-fold greater in patients with sleep apnea than in matched controls without the disorder • MVA ( motor-vehicles accidents ) Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.
  • 58.  Hypertension – Occur in 50% OSA patients – About 30% of HTN have OSA – Repetitive hypoxia and hypercapnia at night may contribute to inc in sympathetic tone resulting in HTN Medical Consequences Cardiopulmonary Derangement
  • 59.  RV hypertrophy and failure – Resulting from pulmonary HTN due to hypoxemia  Cardiac arrythmias – Most common being nocturnal bradycardia, which occurs during apneic episode followed by tachycardia at resolution of apnea  MI, angina Medical Consequences Cardiopulmonary Derangement
  • 61.  Indication for Treatment  AHI 15 or more (moderate-severe)  AHI 5-14 (mild) and with documented symptoms of : – Excessive daytime sleepiness, or – Impaired cognition, mood disorders or insomnia, or – Documented hypertension, ischemic heart disease or history of stroke .
  • 62.  Treatment of OSA Behavioral Modifications Nonsurgical modalities Surgical modalities
  • 63.  Behavioral Modifications – Weight reduction – Avoid CNS depressants (alcohol, sedatives) – Sleep on side w/ tennis ball on back – Stop smoking – External nasal dilators/steroid spray  Treatment of OSA
  • 64.  Weight Reduction – Exercise – Diet – Bariatric Surgery  Treatment of OSA
  • 65. •Weight Loss  Remains a highly effective method  10 – 15 % reduction in weight can lead to an approximately 50 % reduction in sleep apnea severity in moderately obese male patients. Stop / Reduce Smoking  Treatment of OSA
  • 66. • Sleep Position Training  Avoid sleeping in the supine position  Treatment of OSA
  • 67. • Sleep Position Training Use of a tennis ball sewn into the back of a night shirt as a means of training the patient to avoid the supine position and sleep in the lateral recumbent position.  Treatment of OSA
  • 68. •Pharmacotherapy  Protriptyline – decreases REM sleep  Thyroxine or Medroxyprogestrone : in Hypothyroidism patients  Progestrone : in postmenopausal women  Decongestants : nasal congestion , pharyngeal odema .  Antibiotics Non-Surgical Treatment:
  • 70. • CPAP •Sullivan introduced CPAP in 1981 Non-Surgical Treatment
  • 71. • Continuous Positive Airway Pressure Act as a pneumatic splint to maintain patency of the pharyngeal airway by preventing collapse of the pharyngeal tissues . Non-Surgical Treatment
  • 72. • Nasal & Facial Masks Non-Surgical Treatment
  • 73. NASAL NASAL PILLOWS NASAL FULL FACE NASAL PILLOWS CPAP & humidification
  • 74.  CPAP  Titrate the airway pressure needed to overcome airway obstruction  Average CPAP setting is about 5-15 cm H2O  May be delivered via a nasal or face mask  Effective in > 90% Non-Surgical Treatment
  • 75. • CPAP  Has been shown to objectively: – Decrease MVA – Decrease blood pressure – Decrease day time sleepiness  Problems: – Mask discomfort – Patient acceptance – Claustrophobia Non-Surgical Treatment
  • 78. •Non-Surgical Treatment - CPAP  Physical issues : – Facial skin abrasions/discomfort – Air leaks leading to drying of eye – Difficulty with expiration – Nasal dryness and congestion – Sore throat – Loud noise
  • 79.  Tongue retaining devices – Keep tongue in forward position by creating negative pressure in a plastic bulb, fit between the lips  Mandibular advancing devices – Cause forward/downward movement of mandible when attached to dental arches  Soft palate lifter – Effective only for treatment of snoring •Non-Surgical Treatment: Oral Devices
  • 80. • Tongue Retaining Devices ( TRD) • TRDs use suction pressure to maintain the tongue in a protruded position during sleep .
  • 82. Mandibular Advancement Devices •The aim of all of these devices is to improve the patency of the upper airway during sleep by increasing its dimensions and reducing its collapsibility .
  • 83. • Mandibular Advancement Devices  Advance Base of the tongue to ↑ airway  Advance and raise hyoid bone, tightening the pharyngeal musculature which reduces airway collapsibility.  Stretch the masseter muscles which stimulates the genioglossus muscle
  • 84. • Oral Devices • Activator, Herbst, Twin block … • Tongue Retaining appliances
  • 85.  Reposition and stabilize the mandible & tongue (sometimes soft palate)  Increase size of airway in lateral dimension  Mandibular Advancement Devices
  • 86. • Fabrication of Mandibular Protruding Appliance •Good Impressions of upper & lower dental arches
  • 87. • Assessment of the amount of maximum mandibular protrusion
  • 88. • Recording the Protruded position of the mandible • Progressive mandibular protrusion to ensure treatment efficiency . • Start by 50-60% of the maximum active protrusion . • •Titration
  • 89. • Recording the Protruded position of the mandible •Positive relationships between amount of mandibular protrusion and : - Increased airways patency - Decreased airways resistance - Decreased episodes of OSA •Titration
  • 90. • Oral appliances  Most effective in non-obese patients with retro or micrognathia  Better for mild to moderate cases  51% achieve normal sleep, 61% improved RDI < 20  Consider TMJ dysfunction and occlusal changes
  • 91. • Oral Devices : Contra-indications •Insufficient tooth support •Periodontal problems •Poor oral hygiene ( multiple caries ) •Temporomandibular disorders • Mandibular protrusion < 5 mm • Bruxism ?? - Articular - Dental ???
  • 92.
  • 93. Oral appliance treatment for obstructive sleep apnea in a partly edentulous patient
  • 94. Oral appliance treatment for obstructive sleep apnea in a partly edentulous patient
  • 95. • Oral Devices : Contra-indications •Class III malocclusion •Severe malocclusion - Orthodontic
  • 96. Dental Appliance Treatment for Obstructive Sleep Apnea DOI 10.1378/chest.06-2038 Chest 2007;132;693-699 Andrew S. L. Chan, Richard W. W. Lee and Peter A. Cistulli
  • 97. Nightly use of an MPD for 2 years by OSA patients and snorers was found to increase their airway passages because of an increase in pharyngeal area, which to a large extent was caused by a reduction in velum area. Franson et al . Am J Orthod Dentofacial Orthop 2002;122:371-9) Influence of mandibular protruding device on airway passages and dentofacial characteristics in obstructive sleep apnea and snoring
  • 98. • American Sleep Disorders Association Standards of Practice Committee – Primary snoring – Pts w/ mild OSA who do not respond to general treatment – Pts w/ moderate to severe OSA who cannot tolerate nasal CPAP and who refuse or are not candidate for surgical treatment . • Non-Surgical Treatment: Oral Devices
  • 99.  Summary of the Key Adverse Effects of Oral Appliances Short-term adverse effects Excessive salivation Mouth dryness Tooth pain Gum irritation Headaches Temporomandibular joint discomfort. •Long-term adverse effects Reduction in overjet Increase in facial height Increase in degree of mouth opening Changes in inclination of incisors Increase in mandibular plane angle
  • 100.  Surgical Methods- Soft tissues  Reconstruct upper airway Uvulopalatopharyngoplasty (UPPP) Laser-assisted uvulopalatopharyngoplasty (LAUP) Genioglossal advancement Nasal reconstruction  Adenotonsillectomy : preferred treatment in children  Partial Glossectomy  Bypass upper airway Tracheostomy
  • 101. •Uvulopalatopharyngoplasty (UPPP) •Fujita (1981) •Most common procedure •1st line tx for retropalatal collapse •10-50% success  OSA : Surgical Treatment
  • 102. •Uvulopalatopharyngoplasty (UPPP) Devised to surgically excise the tonsils (if present) and portions of the soft palate, and reorientate the tonsillar pillars in order to enlarge the oropharyngeal space .  OSA : Surgical Treatment
  • 103. •Tongue reduction  Lingual tonsillectomy  Laser midline glossectomy  Lingual plasty  Radiofrequency volumetric tissue reduction  OSA : Surgical Treatment
  • 104. •Partial Glossectomy  An enlarged tongue (macroglossia) may call for tongue reduction surgery extending from the midline of the posterior tongue down to the free margin of the epiglottis.  Since speech and swallowing may be significantly compromised by this procedure, it is limited to few cases where there is true macroglossia present.  OSA : Surgical Treatment
  • 105.  Adenotonsillectomy - preferred treatment in children .  Tracheostomy - cure for OSAS – used for failure of more conservative treatment – life threatening cardiopulmonary complications – alternative techniques to lessen complications  Surgical Methods - Soft tissues
  • 106.  Surgical Methods - Maxillofacial elements  Mandibular advancement  Maxillomandibular advancement ± advancement genioplasty  Geniotubercle advancement ± hyoid suspension  Advancement genioplasty .
  • 107.  Geniotubercle advancement For advancing the tongue forwards without changing lower facial aesthetics or the dental occlusion .  The advancement of the central block of bone below the mandibular incisor effectively advances the attachment of the genioglossus and geniohyoid muscles which brings forward both the tongue and hyoid bone.  OSA : Surgical Treatment
  • 108. – Advances hyoid bone anteriorly and inferiorly. – Advances epiglottis and base of tongue . – Performed in conjunction with other procedures . – Dysphagia may result .  Hyoid Myotomy and Suspension  OSA : Surgical Treatment
  • 109.  Adult female patient  OSA Severe skeletal open bite •Surgical-Orthodontic Treatment
  • 110.
  • 111. Assessment and Management of Obstructive Sleep Apnea in Adults
  • 112. Otherwise snore and this will happen to you…. Or sleep alone….