Obstructive sleep apnoea - clinical approach to a patient/ AASM guidelines

1. OBSTRUCTIVE SLEEP APNOEA clinical approach Dr. W A P S R Weerarathna Registrar in Medicine WD 10/02-THJ

2. Objectives… Obstructive respiratory events OSA-introduction/clinical definition Pathogenicity At risk individuals for OSA Associations Screening & assessment of OSA Complications/Clinical features EDS & SDB ESS OSA diagnostic criteria OSA evaluation & diagnostic work-up OSA management strategies Summary References

3. What is OSA????

4. Obstructive respiratory events Apnea is defined by the American Academy of Sleep Medicine (AASM) as the cessation of airflow for at least 10 seconds. Hypopnea is defined as a recognizable transient reduction (but not complete cessation) of breathing for 10 seconds or longer, a decrease of greater than 50% in the amplitude of a validated measure of breathing, or a reduction in amplitude of less than 50% associated with oxygen desaturation of 4% or more.

5. Respiratory effort–related arousal (RERA) is an event characterized by increasing respiratory effort for 10 seconds or longer leading to an arousal from sleep but one that does not fulfil the criteria for a hypopnea or apnea . 

6. Obstructive events are characterized by continued thoracoabdominal effort in the setting of partial or complete airflow cessation, Central events by lack of thoracoabdominal effort in this setting. Mixed events have both obstructive and central features. They generally begin without thoracoabdominal effort and end with several thoracoabdominal efforts in breathing.

7. OSA-Introduction OSA is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. It is the most common type of sleep-disordered breathing (SDB) and C haracterized by recurrent episodes of upper airway (UA) collapse during sleep

8. A common disorder affecting at least 2% to 4% of the adult population and is increasingly recognized by the public. obstructive sleep apnea should be considered as a continuum of disease, i.e., a spectrum of abnormalities from snoring to obesity-hypoventilation syndrome D ue to repetitive collapse of the upper airway: sleep fragmentation, hypoxemia, hypercapnia , marked swings in intrathoracic pressure increased sympathetic activity

9. OSA-clinical definition  The occurrence of daytime sleepiness, loud snoring, witnessed breathing interruptions, or awakenings due to gasping or choking in the presence of at least 5 obstructive respiratory events (apneas, hypopneas or respiratory effort related arousals) per hour of sleep. The presence of 15 or more obstructive respiratory events per hour of sleep in the absence of sleep related symptoms is also sufficient for the diagnosis of OSA due to the greater association of this severity of obstruction with important consequences such as increased cardiovascular disease risk.

10. OSA- Patogenicity OSA is caused by soft tissue collapse in the pharynx Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure. If transmural pressure decreases, the cross-sectional area of the pharynx decreases. If this pressure passes a critical point, pharyngeal closing pressure is reached. Exceeding pharyngeal critical pressure ( Pcrit ) causes tissues collapsing inward. The airway is obstructed.

11. OSA-at risk Patients at High Risk for OSA Who Should Be Evaluated for OSA Symptoms- Obesity (BMI > 35) Congestive heart failure Atrial fibrillation Treatment refractory hypertension Type 2 diabetes Nocturnal dysrhythmias Stroke Pulmonary hypertension High-risk driving populations Preoperative for bariatric surgery

12. OSA-associations Hypothyroidism ( macroglossia ,increased soft tissue mass , myopathy ) Neurologic syndromes (  postpolio syndrome, muscular dystrophies, and autonomic failure syndromes such as Shy- Drager syndrome) Stroke Acromegaly ( macroglossia and increased soft tissue mass) Environmental exposures (smoke, environmental irritants or allergens, and alcohol and hypnotic-sedative medications)

13. OSA-screen/routine evaluation Questions about OSA that Should Be Included in Routine Health Maintenance Evaluations Is the patient obese? Is the patient retrognathic ? Does the patient complain of daytime sleepiness? Does the patient snore? Does the patient have hypertension?

14. OSA-detailed assessment OSA Symptoms that Should Be Evaluated during a Comprehensive Sleep Evaluation Witnessed apneas Snoring Gasping/choking at night Excessive sleepiness not explained by other factors Nonrefreshing sleep Total sleep amount Sleep fragmentation/maintenance insomnia Nocturia Morning headaches Decreased concentration Memory loss Decreased libido/irritability

15. OSA-complications H ypertension, S troke, myocardial infarction, C or pulmonale , D ecreased daytime alertness, and Motor vehicle accidents,

16. OSA-Clinical exam I ncreased neck circumference ( > 17 inches in men, > 16 inches in women), Body mass index (BMI) ≥ 30 kg/m 2 , A Modified Mallampati score of 3 or 4, The presence of retrognathia , Lateral peritonsillar narrowing, M acroglossia , T onsillar hypertrophy, Elongated/enlarged uvula, H igh arched/narrow hard palate, Nasal abnormalities (polyps, deviation, valve abnormalities, turbinate hypertrophy)

17. Following the history and physical examination, patients can be stratified according to their OSA disease risk. H igh risk should have the diagnosis confirmed and severity determined with objective testing As part of the initial sleep evaluation, and prior to objective testing, patients should receive education regarding possible diagnoses, diagnostic steps, and the procedure involved in any testing

18. EDS- excessive day time sleepiness One of the most common and difficult symptoms Reduces quality of life, impairs daytime performance, and causes neurocognitive deficits ( eg , memory deficits). Assessed using the Epworth Sleepiness Scale (ESS) . This questionnaire is used to help determine how frequently the patient is likely to doze off in 8 frequently encountered situations

19. ESS-Epworth Sleepiness S cale

20. ESS score of 12 is associated with a greater propensity to fall asleep on the Multiple Sleep Latency Test (MSLT)  ESS is useful for evaluating responses to treatment; the ESS score should decrease with effective treatment.

21. OSA-CVD risk Vagal stimulation causes bradycardia Bradycardia and hypoxia provoke serious cardiac rhythm disturbances i.e. premature beats asystole , ventricular tachycardia , cardiac arrest.

22. SDB- indicies   Apnea-hypopnea index (AHI) The AHI is defined as the average number of episodes of apnea and hypopnea per hour. Respiratory disturbance index (RDI) Defined as the average number of respiratory disturbances (obstructive apneas , hypopneas , and respiratory event–related arousals [RERAs]) per hour.

23. OSA-diagnostic criteria Individuals must fulfill criterion A or B, plus criterion C to be diagnosed with OSAS: A . Excessive daytime sleepiness that is not explained by other factors B . Two or more of the following that are not explained by other factors: -Choking or gasping during sleep -Recurrent awakenings from sleep - Unrefreshing sleep -Daytime fatigue - Impaired concentration

24. C. Overnight monitoring demonstrates 5 to 10 or more obstructed breathing events per hour during sleep or greater than 30 events per 6 hours of sleep. These events may include any combination of obstructive apnea, hypopnea , or respiratory effort–related arousals.

25. OSA-evaluation-objective testing An overnight sleep study,or polysomnography (PSG): In-laboratory measurement of sleep architecture and electroencephalographic (EEG) arousals, eye movements, chin movements, airflow, respiratory effort, oximetry , electrocardiographic (ECG) tracings, body position, snoring, and leg movements  ect …

26. Routine laboratory tests usually are not helpful in obstructive sleep apnea (OSA) unless a specific indication is present. Routine radiographic imaging of the UA is not performed.

27. PSG- procedure

28. PSG-AASM guide lines Sleep stages are recorded via an EEG, electrooculogram , and chin electromyogram (EMG). Heart rhythm is monitored with a single-lead ECG. Leg movements are recorded via an anterior tibialis EMG. Breathing is monitored, including airflow at the nose and mouth (using both a thermal sensors and a nasal pressure transducer), effort (using inductance plethysmography ), and oxygen saturation. The breathing pattern is analyzed for the presence of apneas and hypopneas

29. PSG-OSA- cessation of airflow for at least 10 seconds with persistent respiratory effort

30. CSA- cessation of airflow for at least 10 seconds with no respiratory effort 

31. AHI- Apnoea H ypopnoea Index D erived from the total number of apneas and hypopneas divided by the total sleep time. Most sleep centres use a cut-off of 5-10 episodes per hour as normal. 5-15 episodes per hour for mild 15-30 episodes per hour for moderate > 30 episodes per hour for severe.

32. PM-Home testing for OSA 3 levels of portable monitors(PM) are (a) level 2, a portable monitor with the same parameters as a full attended PSG (includes EEG) (b) level 3, with at least 4 channels, including flow, effort, oximetry and heart rate (c) level 4, with fewer than 4 channels, often oximetry with flow or oximetry alone.  level 3 monitors are best used to confirm the diagnosis of OSA

33. MLST-Multiple Sleep Latency Test  Objective measurement of excessive daytime sleepiness (EDS)  consists of 4-5 naps of 20-minute duration every 2 hours during the day. The latency to sleep onset for each nap is averaged to determine the daytime sleep latency. Normal daytime sleep latency is greater than 10-15 minutes. OSAHS is generally associated with latencies of less than 10 minutes.

34. OSA-Treatment options Mild apnoea have a wider variety of options, Moderate-to-severe apnoea should be treated with nasal continuous positive airway pressure (CPAP ) or BiPAP Alternative theraphies - Behavioral Oral appliances(OA) Surgical therapy for UA Adjunctive

35. Behavioral/conservative management  Weight loss-  10% reduction in weight leads to a 26% reduction in the respiratory disturbance index (RDI) Avoidance of alcohol for 4-6 hours prior to bedtime Sleeping on one’s side rather than on the stomach or back!

36. Components of Patient Education Programs Findings of study, severity of disease Pathophysiology of OSA Explanation of natural course of disease and associated disorders Risk factor identification, explanation of exacerbating factors, and risk factor modification , Genetic counseling when indicated Treatment options What to expect from treatment Outline the patient's role in treatment, address their concerns, and set goals Consequences of untreated disease Drowsy driving/sleepiness counseling Patient quality assessment and other feedback regarding evaluation

37. CPAP therapy The most effective treatment for OSA Increases the calibre of the airway in the retropalatal and retroglossal regions It increases the lateral dimensions of the UA and thins the lateral pharyngeal walls Maintain UA patency during sleep & preventing the soft tissues from collapsing.

38. CPAP for OSA

39. CPAP-criteria in OSA  All patients with an apnea-hypopnea index (AHI) greater than 15 regardless of symptomatology . For patients with an AHI of 5-14.9, CPAP is indicated if the patient has one of the following: Excessive daytime sleepiness ( EDS) H ypertension Cardiovascular disease.

40. CPAP-complications Sensation of suffocation or claustrophobia Difficulty exhaling Inability to sleep Musculoskeletal chest discomfort Aerophagia Sinus discomfort. Pneumothorax and/or pneumomediastinum (extremely rare) Pneumoencephalos (isolated case report) Tympanic membrane rupture (rare). Mask-related problems include skin abrasions, rash, and conjunctivitis Nasal problems can include rhinorrhea , nasal congestion, epistaxis , and nasal and/or oral dryness.

41. OSA-surgery Nasal surgery ( septoplasty , sinus surgery, and others) Tonsillectomy ± adenoidectomy Uvulopalatopharyngoplasty (UPPP) Laser assisted uvulopalatoplasty (LAUP) Radiofrequency volumetric tissue reduction Linguaplasty Genioglossus and hyoid advancement (GAHM) Sliding genioplasty Maxillo-mandibular advancement osteotomy Tracheostomy

42. OSA-medical therapy Modafinil is approved by the US Food and Drug Administration (FDA) for use in patients who have residual daytime sleepiness despite optimal use of CPAP. SSRI’s such as paroxetine and fluoxetine have been shown to increase genioglossal muscle activity and decrease REM sleep (apneas are more common in REM), although this has not translated to a reduction in AHI in apnea patients

43. General OSA Outcomes Assessment Resolution of sleepiness OSA specific quality of life measures Patient and spousal satisfaction Adherence to therapy Avoidance of factors worsening disease Obtaining an adequate amount of sleep Practicing proper sleep hygiene Weight loss for overweight/obese patients

44. OSA & associated syndromes Syndrome Z : syndrome X(metabolic syndrome) + OSA. Overlap syndrome : chronic obstructive pulmonary disease +OSA

45. Summary Obstructive sleep apnea (OSA) is a common chronic disorder that often requires lifelong care. Available practice parameters provide evidence-based recommendations for addressing aspects of care. There are various options in managing OSA with suitable patient criteria.

46. References Clinical guide lines for the evaluation, management & long-term care In OSA in adults-Adult OSA task force of the American Academy of Sleep Medicine (AASM)

47. THANK YOU…..