Brief discussion about etiology of obstructive sleep apnea

1. OSA
ETIOLOGY &
SYMPTOMPS
by
DR.FAIZAN ALI

2. OSA
 Anatomic disorder bcoz of etiology lies
in anatomic area e.g upper airway
obstruction,retrognathia,tonsillar
hypertrophy,macroglossia etc
 State dependant condition

3. OSA
 can be defined as a cessation of
breathing during sleep because of a
mechanical obstruction such as a retro
positioning of the tongue in the airway,
a large amount of tissue in the upper
airway, or even a partially collapsed
trachea.
(Semin Orthod 2009;15:63-69.)

4. History
 Obstructive sleep apnea (OSA) was first
described by Charles Dickens in 1837.
 He coined the term “Pickwickian syndrome”
but described a similar presentation of a
typical OSA patient; obese, somnolent, and
with an excessive appetite.
 It was only in 1956 that Sidney Burwell
carefully documented a case of an OSA patient,
rationalized the signs and symptoms, and made
a distinction between this disease and other
illnesses.

5. OSA
Common respiratory sleep
disorder characterized by
1. snoring
2. episodes of breathing
cessation or absence of
respiratory airflow (10
seconds) during sleep.

6. Characterized by
recurrent interruptions of breathing during sleep
due to temporary obstruction of the airway by lax,
excessively bulky, or malformed pharyngeal tissues
(soft palate, uvula, and sometimes tonsils), with
resultant hypoxemia and chronic lethargy.
(Epstein LJ, Kristo D, Strollo PJ, Friedman N, Malhotra A, Patil SP, Ramar K, Rogers R, Schwab RJ,
Weaver EM, WeinsteinMD. Clinical guideline for the evaluation, management and long-term care of
obstructive sleep apnea in adults. Adult obstructive sleep apnea task force of the American Academy of
Sleep Medicine. J Clin Sleep Med. 2009; 5:263-76)
OSA

7.  Upper airway has
three major
functions:
1. ventilation,
2. swallowing
3. speech.
 For ventilation, the
upper airway must
remain patent, but
for the other
functions, it must
narrow or close.
 In addition,
ventilation must be
maintained when the
nose is occluded or,
alternatively, when

11.  The apnea event is
considered when the
air flow is interrupted
during sleep for a
period of 10 s or
more.
 Hypopnea is a
reduction of at least
50% of the breathing
capacity combined
with a saturation
decrease of the
oxyhemoglobin in at
least 3%.

13. Narrowing
of air way
Vibration of tissues of
posterior airway
SNORING

15. Air flow
obstruction
Hypoxemia
&
Hypercapnia
Sleep Arousal
Sleep
architecture
EDS

16. This disease affects
an average
4% of adult males
2% of adult
females increasing as
of the fifth decade of
life .
The prevalence of the disease
has been found to be
8% in men
2% of women in the United States
(Semin Orthod 2009;15:94-98.)

17.  About 80 percent to 90 percent of adults
with OSA remain undiagnosed.
 OSA occurs in about two percent of children
and is most common at preschool ages
 OSA with resulting daytime sleepiness
occurs in at least four percent of men and
two percent of women
 About 24 percent of men and nine percent
of women have the breathing symptoms of
OSA with or without daytime sleepiness

18. Risk factors according to
American academy of sleep
medicine
 People who are overweight (Body Mass
Index of 25 to 29.9) and obese (Body Mass
Index of 30 and above)
 Men and women with large neck sizes: 17
inches or more for men, 16 inches or more
for women
 Middle-aged and older men, and post-
menopausal women
 Ethnic minorities
 People with abnormalities of the bony and
soft tissue structure of the head and neck

19. Risk factors according to
American academy of sleep
medicine
 Adults and children with Down
Syndrome
 Children with large tonsils and
adenoids
 Anyone who has a family member with
OSA
 People with endocrine disorders such as
Acromegaly and Hypothyroidism
 Smokers
 Those suffering from nocturnal nasal
congestion due to abnormal
morphology, rhinitis or both.

20. Positive risk factor
 Neck circumference(Indicate upper body
obesity) greater than43.2 cm
 Nasal septal deviation,
 Internal or external valve collapse
 Turbinate hypertrophy,
 Nasal polyps,
 chronic sinusitis
 Macro glossia
 Retro positioning of mandible
 Enlargement of upper airway soft tissue
structures
 Inferior positioned hyoid bone

22. Obesity
Increase in size of
soft tissue structures
in upper airway
Dec. functional
size of upper
airway
Predispose toOSA

23. Classification of OSA
 Fujita et al simply categorized the
upper airway obstruction as
 Retro palatal
 Retro glossal.
 The retro palatal level involves the soft
palate, uvula, and palatine tonsils.
 The retroglossal level involves the
tongue base and supraglottic
structures.

24. Fujita et
 Type I obstruction is the presence of
restriction only at the retro palatal
level.
 Type II obstruction is the presence of
restriction only at the retroglossal
level.
 Type III is the presence of both
obstructions at both levels

25. Moore classification of OSA
Considered the airway obstruction as a
spectrum of disease, starting from
primary snoring as the mildest form,to
upper airway resistance syndrome
(UARS) and then to the different
degrees of OSA;
 mild, moderate, and severe.

27. Index use for OSA
 AHI (A common measurement of sleep
apnea is the apnea-hypopnea index
(AHI). This is an average that
represents the combined number of
apneas and hypopneas that occur per
hour of sleep.)
 RDI(respiratory distress index)
 Apnea index,
 Oxygen desaturation index (ODI)

28. Scales use to measure OSA
 Mallampati Scale
 Friedman Score
 The Epworth sleepiness score,

29. Sleep nasoendoscopy
Identifies the level of and the degree of
obstruction when the patient is asleep.
Obstructions are classified as
palatal, multilevel, or tonguebased with a
grading system:
Grade 1—palatal snoring;
Grade 2—palatal level obstruction;
Grade3—multisegmental involvement with
intermittent oro- and hypopharyngeal
collapse;
Grade4—sustained multilevel collapse
Grade5—tongue base obstruction.

31. Symptoms
1. Loud irregular snoring.
2. Snorts, gasps, and other unusual breathing
sounds during sleep.
3. Long pauses in breathing during sleep

32. Excessive daytime sleepiness
Hall mark of this disease
causes
impaired cognition
increased accident rates
multiple medical and dental disorder

33. 5. Fatigue
6. Obesity
7. Changes in cognitive functions such
as alertness, memory, personality, or
behavior
8. Impotence
9. Morning
headaches19

34. Consequences
Cardiovascular.
1. Systemic hypertension
2. Coronary heart disease
3. Cardiac arrhythmias
4. Sudden nocturnal death
5. Other (stroke, pulmonary hypertension)
Social/behavioral.
1. Drowsy driving/accidents
2. Decreased work performance
3. Poor quality of life19
4. Increased mortality20-22

35. Dentofacial features
 Narrow
upper airway
dental arches
 Hypoplastic maxilla
 Retrognathic mandible
 Increased ant.facial height
 Increased craniocervical angulation
than normal

36.  Post.buccal cross bite
 Vertical maxillary excess