This presentation gives some basic information regarding the definition , etiology and pathophysiology of " obstructive sleep apnea" which is a serious sleep disorder .Treatment methods are briefly reviewed with special emphasis on the role of the oral surgeon and orthodontist in the management of this medical condition .
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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
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
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
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
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.
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
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
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:
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
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
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
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
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
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
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
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