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: 483495, 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...
10. 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
11. 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.
13. DAY TIME SYMPTOMS Morning headaches Excessive daytime
somnolence Fatigue Sleepiness during driving Cognitive decline ,
inattention Depression with personality changes
14. 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. )
15. OSA AND METABOLIC SYNDROME...SYNDROME Z
16. 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.
17. 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
18. 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.
19. 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
20. 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
21. [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
22. MALLAMPATI SCALE..
23. 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
25. 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
26. POLYSOMNOGRAPHY SETUP
27. 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
28. 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
29. 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
30. RESULT OF POLYSOMNOGRAPHY Identification of
Apnoea/Hypopnoea event Identifying Central vs Obstructive apnoea
Grading of OSA objectively using the Apnoea Hypopnoea Index
(AHI)
31. 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
32. PSG TRACING OF OSA..
33. PSG TRACING OF CSA..
34. CONSENSUS DEFINITION OF SEVERITY This uses the AHI index
Normal: 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
50. ORAL DEVICES USED.. Oral appliances used are Mostly
mandibular advancement devices Some are tongue retaining
devices
51. 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
52. 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
.
53. LASER ASSISTED UVULOPALATOPLASTY CO2 Laser used to
vapourise portions of uvula and soft palate . Indicated more for
snoring AASM didnt recommend it for OSA Moderate to severe post-op
pain
54. 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
55. 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
56. 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
57. BEHAVIORAL METHODS Weight loss Avoid alcohol and sedatives
Avoid sleep deprivation Good sleep hygiene Avoid supine sleep
position Stop smoking
58. 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.
60. 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 .
61. 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 .
