This document discusses obstructive sleep apnea (OSA). It defines OSA as recurrent episodes of apnea or hypopnea due to upper airway collapse during sleep. It reviews the prevalence of OSA in different populations and risk factors such as obesity, genetics, and upper airway abnormalities. The pathogenesis of OSA involves reduced airway size and increased collapsibility, as well as neural, muscle and fluid shift factors. Clinical symptoms, diagnostic tools like polysomnography, and treatment options including positive airway pressure and oral appliances are described in detail.

1. ABDULLAH MD. HASAN
2nd YEAR PGT
DEPTT. OF MEDICINE

2. WHAT IS OSA..?
Sleep disorder characterized by recurrent
episodes of apnoea / hypopnoea due to
narrowing or collapse of upper respiratory
tract during sleep despite ongoing breathing
efforts .

3. OSA PREVALENCE..
TABLE 1. STUDIES ON THE PREVALENCE OF OBSTRUCTIVE SLEEP APNEA
First Author (Reference) Prevalence
Country N ethnicity Diagnostic
method
Men Women
United States Young (7) 602 White Polysomnography 4.0% 2.0%
Bixler (9) 1,741 White Polysomnography 3.9% 1.2%
Australia Bearpark (10) 485 White MESAM IV* 3.1% –
India Udwadia (15) 250 Indian Polysomnography 7.5% 4.5%
China Ip (12) 258 Chinese Polysomnography 4.1% –
Ip (13) Chinese Polysomnography – 2.1%
Korea Kim (14) 457 Korean Polysomnography 4.5% 2.3%

4. RISK FACTORS FOR OSA..
OSA
OBESITY
GENETIC
UPPER
AIRWAY
ABNORMALIT
IES
ENDOCRINE

5.  OBESITY
 Single most important risk factor
 1 SD increase of BMI assoc. with 3 fold increase risk of of
OSA (Wisconsin sleep cohort)
• GENETICS
• Family aggregation of OSA (Cleveland family study)
• 40 % of genetic polymorphism in OSA is common with
obesity – but 60 % is independent of obesity (S.R.Patel
et al Int. Journ. Of obesity 2008)
• Candidate genes – ApoE4 , Leptin

6.  UPPER AIRWAY ABNORMALITIES
 Congenital syndromes
 Retroposed mandible
 Nasal obstruction
 ENDOCRINE FACTORS
 Hypothyroidism 1 , acromegaly 1 associated with
increased risk .
 Female sex hormones are protective 2
1 . J Clin Endocrinol Metab 95: 483–495, 2010)
2. Young T, Finn L, Austin D, et al: Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort
Study. Am J Respir Crit Care Med 2003; 167:1181-1185

7. PATHOGENESIS OF OSA..
Upper airway
size
Upper airway
collapsibility
Neural
component
Muscle
factors
Fluid shift
PATHOGENE
-SIS OF OSA

8. AIRWAY SIZE...

9. AIRWAY COLLAPSIBILITY...

11.  NEURAL FACTORS
 Decreased motor neural output to upper airway dilators 1
 Decreased airway reflexes
1.Horner RL: Respiratory motor activity: Influence of neuromodulators and implications for sleep disordered
breathing. Can J Physiol Pharmacol 2007; 85:155-165

12.  MUSCLE FACTORS
 Progressive damage of upper airway dilators (Friberg et
al)1
 Increased inflammatory markers in muscle cells .2
 FLUID SHIFT
 Increased fluid shift from lower extremities to upper
part of body during sleep .3
1. Friberg D, Gazelius B, Hokfelt T, et al: Abnormal afferent nerve endings in the soft palatal mucosa of sleep apnoics
and habitual snorers. Regul Pept 1997; 71:29-36.
2.Boyd JH, Petrof BJ, Hamid Q, et al: Upper airway muscle inflammation and denervation changes in obstructive
sleep apnea. Am J Respir Crit Care Med 2004; 170:541-546.
3.Redolfi S, Yumino D, Ruttanaumpawan P, et al: Relationship between overnight rostral fluid shift and obstructive
sleep apnea in nonobese men. Am J Respir Crit Care Med 2009; 179:241-246.

14. NOCTURNAL SYMPTOMS :
Loud disruptive snoring
Apneic episodes
Frequent awakening
Gasping , choking , bruxism
Nocturia
Restless sleep

15.  DAY TIME SYMPTOMS
 Morning headaches
 Excessive daytime somnolence
 Fatigue
 Sleepiness during driving
 Cognitive decline , inattention
 Depression with personality changes

17. Two major mechanisms are important for the
patho-physiologic consequences of OSA:-
 Sleep fragmentation – disturbed continuity with
deprivation of deep sleep
 Repeated cycles of de-oxygenation / re-
oxygenation – Paradigm idea that OSA is an
oxidative stress disorder .1 Elevation of
inflammatory markers and activation of pathways
akin to that in obesity
1 . Lavie et al (Sleep Med Rev 2003; 7:35-51. )

19. OSA AND METABOLIC
SYNDROME...’SYNDROME Z’

20. OSA AND INSULIN RESISTANCE..
 OSA is an independent risk factor for insulin
resistance .1
 High incidence of OSA in type II DM -86 % have at
least mild OSA and upto 30 % have severe OSA . 2
1.Ip MS, Lam B, Ng MM, et al: Obstructive sleep apnea is independently associated with insulin
resistance. Am J Respir Crit Care Med 2002; 165:670-676
2. Foster GD, Sanders MH, Millman R, et al: Obstructive sleep apnea among obese patients with type 2
diabetes. Diabetes Care 2009; 32:1017-1019.

22. OSA AND CARDIOVASCULAR
DISEASES
 HYPERTENSION
 Independent association with hypertension after
adjusting for obesity . 1
 Conversely OSA is common in hypertension . 2
 OSA makes individuals more resistant to anti
hypertensive therapy .
1.The Lancet, Volume 373, Issue 9657, Pages 82 - 93, 3 January 2009
2. DL Cohen, RR Townsend - … Journal of Clinical Hypertension, 2013
3.Logan AG, Tkacova R, Perlikowski SM, et al: Refractory hypertension and sleep apnoea: Effect of
CPAP on blood pressure and baroreflex. Eur Respir J 2003; 21:241-247

23.  CARDIOVASCULAR EVENTS
 Pro-inflammatory and oxidative stress state of OSA
leads is related to accelerated atherosclerosis . 1
 OSA is associated with a variety of stroke risk factors
that may independently contribute to stroke risk. 2
 OSA also associated with AF and heart block . 3
1.Savransky V, Nanayakkara A, Li J, et al: Chronic intermittent hypoxia induces atherosclerosis. Am J Respir Crit
Care Med 2007; 175:1290-1297
2.Obstructive Sleep Apnea as a Risk Factor for Stroke and Death - H. Klar Yaggi et al N Engl J Med 2005;353:2034-
41.
3. Mehra R, Benjamin EJ, Shahar E, et al: Association of nocturnal arrhythmias with sleep-disordered breathing:
The Sleep Heart Health Study. Am J Respir Crit Care Med 2006; 173:910-916.

26.  Patient comes to clinical horizon with
 Nocturnal symptoms related by the partner
 Day time symptoms which affects quality of life
 The other spectrum of patients in whom OSA might
be considered
 Hypertension esp. resistant hypertension 1
 Metabolic syndrome
 Poorly controlled DM
 AMI / CVA
1.Ruttanaumpawan et al: Association between refractory hypertension and
obstructive sleep apnea. J Hypertens 2009; 27:1439-1445

27. SCREENING FOR OSA..
 A few peer reviewed questionnaires have
been devised for initial screening
 The Epworth sleepiness score
 The Berlin questionnaire
 Multivariable apnoea prediction index
(MAP index)
 Mallampati score for airway assessment

31. [Study Name/ID pre-filled] Site Name: ________________________
Initials of Completer: ____ ____ ____ Subject ID: ________________________
Date Form Completed: ___ ___ / ___ ___ / 2 0 ___ ___ Visit Type: ______________________
m m d d y y y y
MAP SLEEP SYMPTOM-FREQUENCY QUESTIONAIRE
During the last month, on how many nights or days per week have you had or been told you had
the following (please check only one box per question):
(0)
Never
(1)
Rarely
(less than
once a
week)
(2)
Sometimes
(1-2 times
per week)
(3)
Frequently
(3-4 times
per week)
(4)
Always
(5-7
times per
week)
(.)
Do
not
know
1. Loud snoring      
2. Your legs feel jumpy or jerk      
3. Difficulty falling asleep      
4. Frequent wakenings      
5. Snorting or gasping      
6. Falling asleep when at work      
7. Frequent tossing, turning, or
thrashing
     
8. Your breathing stops or you
choke or struggle for breath
     
9. Excessive sleepiness      
10. Morning headaches      
11. Falling asleep while driving      
12. Feeling paralyzed, unable to
move for short periods when
falling asleep or awakening
     
13. Find yourself in a vivid
dreamlike state when falling
asleep or awakening even
though you know you are awake
     

32. MALLAMPATI SCALE..

33.  The Epworth sleepiness score most apt for assessing
daytime sleepiness – a score ≥ 11 merits further
definitive evaluation
 A high risk categorization in the Berlin Questionnaire
was validated by a positive diagnosis with 86%
sensitivity and 76% specificity
 Mallampati scale – predictive value varied with grade

34. ANCILLARY EVALUATION..
 Vitals
 Height , weight , BMI
 Abdominal fat assessment
 Neck girth
 Airway and otolaryngology assessment
 Cephalo-metric radiography
 Metabolic parameters
 Endocrine assessment
 ECG , ECHO-cardiography

36. OVERNIGHT POLYSOMNOGRAPHY
 Full Overnight Polysomnography remains the gold
standard for diagnosis and assessment of OSA
 Parameters :-
 EEG
 EOG
 EMG – chin and anterior tibialis
 Nasal airflow – pressure transducer > nasal thermistor
 Abdominal and chest wall motion sensor
 O2 Saturation

37. POLYSOMNOGRAPHY SETUP

38. ASSESSMENT OF THE
PARAMETERS..
 Recording sleep
 Monitored with EEG+EMG+EOG
 EEG – 4 leads placed as per 10-20 System
 EOG – placed at lateral canthi
 EMG – chin electromyogram
 Airflow assessment
 Sensitive nasal pressure transducers with cannula are
preferred over nasal thermistors

39.  Respiratory effort
 Assessed by respiratory inductance plethsmography or
strain gauge technique using piezoelectric crystals .
 Oesophageal manometry can be used as a proxy for
pleural pressure
 Oximetry

40. OTHER SETUPS..
 Split – night studies
 2-3 hours of diagnostic monitoring
 Time for CPAP titration is reduced
 Unattended sleep studies
 Are of 3 types (AASM)
 Type 2 - EOG + EEG + respiratory monitoring
 Type 3 – 2 airflow and/or respiratory effort channel with O2
sat
 Type 4 – continuous single or dual bioparameters

41. RESULT OF POLYSOMNOGRAPHY
 Identification of Apnoea/Hypopnoea event
 Identifying Central vs Obstructive apnoea
 Grading of OSA objectively using the Apnoea
Hypopnoea Index (AHI)

42. IDENTIFICATION OF EVENT
 Apnoea – cessation of breathing lasting 10 seconds or
longer
 Hypopnoea – AASM devices 2 scoring systems
 1 . Nasal presure excursions ≥ 30% of baseline + ≥4% O2
desat. + 90% of event duration meets amplitude criteria
for hyponoea
 2 . Nasal presure excursions ≥ 50% of baseline + ≥3% O2
desat. or arousal + 90% of event duration meets
amplitude criteria for hyponoea

43. PSG TRACING OF OSA..

44. PSG TRACING OF CSA..

45. CONSENSUS DEFINITION OF
SEVERITY
 This uses the AHI index
 Normal: <5 episodes/hr
 Mild sleep apnea: ≥5 and <15 episodes/hr
 Moderate sleep apnea: ≥15 and <30 episodes/hr
 Severe sleep apnea: ≥30 episodes/hr
VIDE - AMERICAN ACADEMY OF SLEEP MEDICINE

46. ..EVALUATING HYPERSOMNOLENCE

47. DIFFERENTIALS TO CONSIDER..

49. RATIONALE FOR TREATMENT..
 OSA is a disease with profound health implications .
 Treatment is warranted in view of :-
 Improve quality of life
 Overcome deleterious consequences of OSA

50. MODALITIES FOR TREATMENT
DEFINITIVE MANAGEMENT
• Positive Airway Pressure setups
• CPAP
• Bi-PAP
• Auto CPAP/Bi-PAP
• Adaptive servo-ventilation (ASV)
• Oral appliances
• Surgery

52. MECHANISM OF POSITIVE
PRESSURE DEVICES..
 They increase intra-luminal pressure above the critical
closing pressure thus maintaining airway patency by
acting as a pneumatic splint
 The PAP devices have 4 components
 Airway access
 Positive airway pressure device
 Expiratory dead space venting systems
 Adjunctive setup (O2 , humidification)

54. WHOM TO TREAT..?
 Decision for treatment is rationalised using the AHI Index
(AASM) and follows ATS guidelines . 1
 Severe (AHI ≥30) symptomatic OSA – treatment indicated
unanimously .
 Lower degrees of OSA severity (as per AHI) – treatment
warranted according to symptoms .
 Mild to moderate severity without symptoms – no
consensus universally for treatment .
1 OFFICIAL ATS STATEMENT ADOPTED BY THE ATS BOARD OF DIRECTORS, MARCH 1 994.

55. INSTITUTING CPAP THERAPY..
 Appropriate level of CPAP titrated after overnight 6 hr PSG
 Titrated pressure end point depends on many other factors
 Sleep posture
 Sleep stage
 Sedative drug use
 Other aspects –
 Patient education
 Ergonomic design of mask / other devices
 Proper humidification

56. Bi-PAP THERAPY..
 Provides a fixed higher level of pressure during
inspiration than expiration
 Improves patient adherence .1
 Provides ventilatory support in patients
concomitantly having COPD . 2
1 . Reeves-Hoche MK, Hudgel DW, Meck R, et al: Continuous versus bilevel positive airway pressure for obstructive sleep
apnea. Am J Respir Crit Care Med 1995; 151:443-449.
2. Resta O, Guido P, Picca V, et al: Prescription of nCPAP and nBIPAP in obstructive sleep apnoea syndrome:
Italian experience in 105 subjects. A prospective two centre study. Respir Med 1998; 92:820-827.

57. ‘SMART’ PAP DEVICES
 Auto PAP/Bi-PAP devices have the facility to respond
varying patient parameters depending on the
individual device algorithm .
 Allow delivery of lowest possible positive pressure .
 Suitable in patients unable to tolerate high fixed
pressures in conventional CPAP/Bi-PAP devices .
 Improved patient adherence though have not been
demonstrated comprehensively .

58. ADAPTIVE SERVO VENTILATION
 Dynamic pressure support during hypoventilation
with EPAP during hyperventilatory phases
 Stabilizes abnormal breathing patterns .

59. CPAP OUTCOMES..
 Definite reduction of daytime sleepiness – effect more
pronounced for severe to moderate OSA .1,2
 CPAP>Dental devices in improving AHI and O2 sat.3
 1 . Mason , nadel : textbook of respiratory medicine
 2 , 3 . National Institute for Health and Clinical Excellence, 2008.

60.  Blood pressure – modest reduction in nocturnal and
diurnal BP .1
 Insulin resistance – no improvement in glycaemic control
as evidenced by Hba1C levels could be demonstrated .2
 Metabolic syndrome – OSA leads to objective improvement
of parameters of the Metabolic syndrome . 3 , 4
1 . Heinrich F. Becker, MD et al Circulation. 2003;107:68-73
2 .Sophie D West et al Thorax 2007;62:969–974. doi: 10.1136/thx.2006.074351
3 . Surendra K. Sharma, M.D., et al ; N Engl J Med 2011;365:2277-86.
4. CM Hoyos et al Thorax doi:10.1136/thoraxjnl-2012-203074 ; BMJ

61. DRAWBACKS OF CPAP..
 Poor adherence
 Dry mouth, rhinitis, congestion
 Epistaxis
 Mask discomfort
 Claustrophobia
 Aerophagia
 Chest & back pain
 Meningitis
 Pneumocephalus

62. CPAP ADHERENCE..
• Adherence only 40-60% .
 Adherence increased by
 Proper humidification
 Pressure ramp
 Nasal steroids
 Chin straps / full face mask
 Bi-PAP / ‘smart’ PAP devices
 Supportive , cognitive –behavioral , motivational
enhancement therapy have been successful. 1
1.Terri E. Weaver et al : Indian J Med Res 131, February 2010, pp 245-258

63. ORAL APPLIANCES..
 INDICATIONS – AASM guidelines for oral applinces
 Treatment for snoring or mild- moderate OSA (AHI 15-30) 1
 For severe OSA intolerant to CPAP therapy
 In failed Uvulopharyngoplasty ( Millman et al ; chest 1998)
 IMPACT – a recent Cochrane survey (NIH UK) throws the
following findings
 CPAP > oral appliances in reducing AHI , improving O2 sat
 Oral appliances > Placebo in improving AHI , relieving EDS
1. Ferguson KA, Cartwright R, Rogers R, et al: Oral appliances for snoring and obstructive sleep apnea: A
review. Sleep 2006; 29:244-262

64. ORAL DEVICES USED..
 Oral appliances used are
 Mostly mandibular advancement devices
 Some are tongue retaining devices

66.  INDICATIONS
 Failed CPAP mostly in terms of patient compliance
 Specific anatomic anomaly
 Hypertrophied uvula / soft palate
 Macro glossia
 Constricted oro-pharynx
 Adenoids
 Obstructive tonsils
 DNS
 Enlarged turbinates , Polyps
 Skeletal abnormalies

67. OPTIONS..
 RADIOFREQUENCY VOLUMETRIC TISSUE
REDUCTION OF PALATE
 Tissue of soft palate / tongue / nares ablated by special
needle electrodes using Nd-YAG Laser (456 kHz) .
 Indicated usually for snoring rather than OSA .
 Modest to no improvement of AHI .

68.  LASER ASSISTED UVULOPALATOPLASTY
 CO2 Laser used to vapourise portions of uvula and soft
palate .
 Indicated more for snoring
 AASM didn’t recommend it for OSA
 Moderate to severe post-op pain

69.  UVULOPALATOPHARYNGOPLASTY
 Conventional but more invasive surgery
 Severe OSA with failed CPAP therapy
 Velopharynx enlarged by removal of uvula , tonsillar
pillars and portion of soft palate
 Best results for those with nasopharyngeal obstruction

70.  MANDIBULAR OSTEOTOMY WITH
GENIOGLOSSUS ADVANCEMENT
 Indicated for hypopharyngeal obstruction
 Developed by Powell and colleagues as Stanford step
approach to OSA
 Response rates improved after adding hyoid myotomy
and suspension

71.  MAXILLO-MANDIBULAR ADVANCEMENT
OSTEOTOMY
 Hypopharyngeal obstruction refractory to CPAP or other
conservative upper airway surgery
 Maxillary osteotomy with rigid plate fixation with
bilateral sagittal split mandibular ostetomy
 Offers curative chance in OSA

73. BEHAVIORAL METHODS
 Weight loss
 Avoid alcohol and sedatives
 Avoid sleep deprivation
 Good sleep hygiene
 Avoid supine sleep position
 Stop smoking

74. 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.
 1 % change in weight is associated with 3 % change in
AHI.

75. PHARMACOLOGIC TREATMENT
 Anti-depressant – paroxetine, fluoxetine, protriptiline
 Respiratory stimulant – acetazolamide,
medroxyprogesterone, theophylline, doxapram
 CNS stimulant – caffeine, modafinil, nicotine &
cannabinoids
 Hormones

76. REFLECTING...
 OSA is a sinister ailment with prevalence rates
ranging from 2-7.5% .
 OSA is commonly associated with metabolic
syndrome .
 Treatment is uninanimously indicated only for
severe OSA – treatment for milder forms of OSA
varies according to symptomatology .

77.  No indication of prophylactic treatment in view of
CVS and metabolic abnormalities .
 CPAP remains the sheet anchor of treatment-
however compliance remains poor .
 Surgery is indicated for refractory OSA and
specific indications .
 The impact of supportive treatment remains
largely unsubstantiated .

78. THANK YOU..