OSA Updates

8/13/2019 OSA Updates

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Dr R. MuventhiranInstitut Perubatan RespiratoriKuala Lumpur


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! Is part of a group characterized by disorderedrespiration during sleep known as sleep relatedbreathing disorders:

Sleep relatedhypoventilation and

hypoxemic syndrome s

ObstructiveSleep Apneas

SRBD

Central SleepApnea and

PeriodicBreathing


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! OSAHS represents one end of a spectrum withnormal quiet regular breathing at one end,moving through worsening levels of snoring,to increased upper airways resistance, and tohypopnoeas and apnoeas at the other end


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WAKE

DEFICIENT UAANATOMY

SLEEP

Adiposesoft tissuedeposition

Compensatedby high

pharyngealactivity

CompromisedcraniofacialAirway

edema

Decreasedlung

volumes

Sleep onset1. UA musc tone2. Lung volume3. Central resp

drive

UA closure/apnea

CO2/ O2

Increased centralrespiratory and UA

muscle drive

Hypoxic and

hypercapnicresponsivenessImportance of

controller/plantgain

VENTILATORYCONTROL

INSTABILITY

If level of reachesarousal threshold

Arousal

1.

UA musc tone2. Lung volume

Decreased centralrespiratory and UA

muscle drive

UAopening

Hyperventilation/ventilatory overshoot

CO2/ O2

Hypoxic and hypercapnicresponsiveness


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Obesity (BMI> 30) Congestive heart Failure AF

Refractory HPT Type 2 DM Nocturnal arrhythmias

CVA Pulmonary hypertension

High-risk driving population Pre-operative for bariatric surgery


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! None of the questionnaires are sensitive or specific tosubstitute for objective assessment by a sleep study

BerlinQuestionnare

To predict whetherpt high risk or lowrisk for having OSA

identified high risk based on AHI>5 sensitivity:0.86 specificity : 0.77

STOP BANGquestionnaire

Screening tool forpreoperativeevaluation to detectOSA

Sensitivity : 84% ( AHI>5), 92%(AHI>15) and 100% (AHI>30)


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OSA PHYSICAL EXAMINATIONINCREASED BMI

PRESENCE OF NASAL OBSTRUCTION

INCREASED MALLAMPATI OR MODIFIED MALLAMPATI SCORE

HIGH ARCHED PALATE (NARROW AIRWAY)

RETROGNATHIA

INCREASED NECK CIRCUMFERENCE ( MEN>17 INC, WOMEN>16 INC)

EVIDENCE OF RIGHT HEART FAILURE ( JVD,PEDAL EDEMA)


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INTERNATIONAL CLASSIFICATION OF SLEEP DISORDERS, 2 ND EDITION , CRITERIA FOR OSA

A At least one of the following i) Complaints of unintentional sleep episodes during

wakefulness ,daytime sleepiness , un-refreshing sleep,fatigue or insomnia Ii) awakenings with breath holding, gasping or choking Iii) bed partner reports loud snoring and/or breathinginteruptions during sleep

B PSG shows the following i) scoreable respiratory events (A+H+RERA) /hr > 5/hr ii) Evidence of respiratory effort during all or a portion ofeach respiratory event

C PSG shows the following i) scoreable respiartory events ( A+H+RERA)/hr >15/hr

ii) Evidence of respiratory effort during all or a portion ofeach respiratory event

D The disorder is not better explained by another currentsleep disorder, medical or neurologic disorder, medicationuse or substance use disorder

DIAGNOSTIC CRITERIA= A+B+D OR C+D


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! Gold standard: In laboratory polysomnogramA standard PSG typically consists of! EEG! segmental (+/-) tibialis electromyogram! electro-oculogram! respiratory airflow (usually measured by oronasal

flow monitors)! thoraco-abdominal movement! oxygen saturation tracings (oximetry).! Electrocardiogram (ECG) and body position are also

frequently monitored, as is snoring


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CONSIDERATION WHOM TOTREAT?

SYMPTOMATIC ASYMPTOMATIC ASYMPTOMATIC

AHI No significantco-morbidities

Significant co-morbidities

MILD Treat Observation or

conservativetreatment

? Treat*

MODERATE Treat Treat Treat

SEVERE Treat Treat Treat

Conservative treatment: weight loss ,side sleep position,treat nasal

congestion ,avoid alcoholFor asymptomatic pts with mild OSA and significant medical co-morbidities,treatment decisions should be individualised based on patients motivationto undergo treatment


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AMERICAN ACADEMY OF SLEEP MEDICINE PRACTICE PARAMETERRECOMMENDATION FOR MEDICAL TREATMENT OF OSA

WEIGHTREDUCTION

successful dietary weight loss may improve the AHI inobese OSA pts (guidelines)

dietary weight loss should be combined with primarytreatment of OSA (Option)

Bariatric surgery may be adjunctive in treatment of OSA inobese pts (Option)

POSITIONALTHERAPIES

Positional therapy ,consisting of a method that keeps thepatient in a non-supine position, is an effective secondarytherapy or can be supplement to primary therapies for OSAin pts who have a low AHI in the non-supine versus thesupine

OXYGENSUPPLEMENTATION

Oxygen supplementation is not recommended as a primarytreatment for OSA ( Option)

NASALCORTICOSTEROIDS

Topical nasal cortiocsteroids may improve the AHI in ptswith OSA and concurrent rhinitis and ,thus may be usefuladjunct to primary therapies for OSA ( Guideline)


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TREATMENT ALTERNATIVES FOR OSA ADULTS)

SNORING MILD

Primary Treat nasal congestion

Lateral positioning Avoid alcohol

If symptomatic and keen:

PAP

Secondary if medical tx does notimprove congestion ! OA orsurgery ( but snoringimprovement is variable) LAUP Radio-frequencypalatoplasty UPPP Pillar procedure- may reduce

snoring but not AHI

If symp but not keen for PAP OA or Upper airway surgeryDepends on pt preference andfinancial

Adjunctive Weight loss weight loss lateral positioning

LAUP laser assisted uvulopalatplasty


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TREATMENT ALTERNATIVES FOR OSA ADULTS)

MODERATE SEVERE

Primary Treatment of choice:

PAP

PAP

Secondary If not acceptable OA (50% effective*) Upper airwaysurgery( 30% effective*)* Defined as tx AHI


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TYPE 1: ATTENDED PSG TYPE 2: UNATTENDED PSG

Measures(channels)

Minimum of sevenchannels including ECG,EEG, EOG, chin EMG,airflow, respiratoryeffort, oxygensaturation

Minimum of sevenchannels including EEG,EOG, chin EMG, heart rateor ECG, airflow, respiratoryeffort, oxygen saturation

Body position Documented orobjectively measured

Possible

Leg movement EMG or motion sensordesirable but optional

Optional

Personnelinterventions

Possible No


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TYPE 3: MODIFIEDPORTABLE SLEEP APNEATESTING

TYPE 4: CONTINUOUSSINGLE OR DUALBIOPARAMETERRECORDING

Measures

(channels)

Minimum of four, including

ventilation (at least twochannels of respiratorymovement or respiratorymovement and airflow),heart rate or ECG, andoxygen saturation

Minimum of one

oxygen saturation,flow, or chestmovement

Body position Possible No

Leg movement Optional No

Personnelinterventions

No No


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Indications for Use of Unattended Portable Monitoring

PM must be combined with a comprehensive sleep evaluation.

Patient has a high pretest probability of moderate to severe OSA.

No co-morbid medical conditions that may degrade PM accuracy Severe pulmonary disease. Neuromuscular disease. Congestive heart failure.

No clinical suspicion of other sleep disorders CSA. Narcolepsy. PLMD. Parasomnias. Circadian rhythm sleep disorders.

Not for screening asymptomatic populations.Patients who cannot have PSG due to immobility, safety, or critical illness.

Unattended PM may be used to monitor response to non-PAP treatmentsfor sleep apnea (oral appliances, surgery, weight loss).

Unattended PM in patients home is permitted when all guidelines arefollowed.


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! Portable Monitoring Task Force of AASMrecommended home studies only after acomprehensive sleep evaluation by a cliniciancertified in sleep medicine and then supervised and

interpreted by person with same level of specialitytraining


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! Cost effectiveness analysis have been scarce! PM usually less costly than Laboratory PSG but in some

situations PM can increase cost , delay confirmatorylaboratory testing and encourage treatment of pts with falsepositive results

! One published cost-utility model showed that PSG generatedhigher utility than a portable cardiorespiratory monitory andthe magnitude of the PSG easily justified the added initialexpense

Chervin et al . Ann Intern Med 1999


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Pt presents to CSS forevaluation of suspected

OSA

Does pt have high pretestprobability of moderate or

severe OSA

Symptoms or signs ofcomorbid medical

disorders

Symptoms or signs ofcomorbid sleep disorders

In-labPSG

TreatmentOSAdiagnosed?PMSleep study (PM or in lab)

Evaluate for other sleepdisorders, consider in-lab

PSG

OSA diagnosed ?

No

Yes

No

No

No

No

Yes

Yes

Yes

Yes


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! Initially was hoped to reduce the average overnightpressure level ! resulting in improved adherence

Subjects Results

Ayas et alSleep 2007

Meta-analysis ofrandomized trials

comparing ACPAPwith fixed pressureCPAP

Mostly men withmoderate to

severe OSAH CPAP-nave No other SRBD

or comorbidities

There were nodifferences in

hours of nightlyuse, despite amean decreasein overnightpressure of 2 cmH20

Smith et al Recent meta-analysis of 30studies

Found a statistically significantdifference of machine usage of 12mins WHICH IS NOT CLINICALLYSIGNIFICANT


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! However individual may tolerate APAP>CPAP

! Based on currently available evidence, the AASMsuggests the long term use of autotitrating CPAP inself-adjusting role to treat OSAH as an opt o only


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! Medical Treatment for OSA1. End Expiratory Pressure(EPAP) devices2. Oral Pressure Therapy

! Non-medical treatment options for OSA1. Hypoglossal Nerve Stimulation

NONE of these options are more or as efficacious asPAP therapy


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FDA cleared in 2008 for treatment of mild, moderate andsevere OSA

Mechanism ofaction

consists of a small valve attached externally to each nostrilwith hypoallergenic adhesive.

valve acts as a one-way resistor, nearly permitting

unobstructed inspiration. During expiration, airflow is directed through small air

channels, increasing resistance. This creates EPAP which is maintained until the start of the

next inspiration. As a result, the device helps pressurizeand stabilize the upper airway during the critical end-expiratory period, when the airway has been found to bemost narrow in the breaths prior to an apnea.

Whereas CPAP provides positive pressure during bothinspiration and expiration, EPAP only creates pressureduring expiration.


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Indications Patients (mild, moderate or severe) who have rejected orare non-compliant with prescribed CPAP

Newly diagnosed mild/moderate OSA patients withoutsignificant co-morbidities

CPAP compliant patients looking for alternatives for travel

Contra-indications

Severe breathing disorder (including respiratory muscleweakness, bullous lung disease, bypassed upper airway,pneumothorax, pneumomediastinum, etc)

Severe heart disease (including heart failure) Pathologically low blood pressure An acute upper respiratory (including nasal, sinus or

middle ear) inflammation or infection or perforation of theear drum

Limitations No long term studies Only short term studies No comparison with other forms of alternative therapy

such as oral appliances May cost probably more than CPAP


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Evidence Mean AHI reduction in about 50% Berry et al Sleep 2011:

Summary Works in a subset of patients with OSA but no obvious wayto select them

The effectiveness of nasal EPAP is dependent on achieving

sustained expiratory pressure and appears only to bepossible in about 50% of patients


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novel treatment for sleep apnea that includes a polymer mouthpiece, tubing,and small console.

Mechanism ofaction

a gentle vacuum that pulls the soft palate and tongue forward Sleep apnea occurs when the upper airway collapses during

sleep ! due to the soft tissues at the back of the mouth and

throat falling back and closing off the passageway for air. macroglossia, may predispose for this occurrence. In addition, excessive tissue at the back of the mouth,

including enlarged tonsils, may also contribute. By bringing these tissues forward with suction, the Winx

system can relieve the obstruction that they may otherwisecause.

The tongue is stabilized, the size of the airway increases, andbreathing improves.


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Advantages no bulky mask or restraining headgear without a risk ofpressure sores or skin rashes.

mouthpiece is small and fitted to maximize comfort. The console is quiet and portable no pressurized air with the associated problems of nasal

congestion, leaks, and dryness. preferred to overcome issues related to intimacy andclaustrophobia

Limitations required that you be able to breathe through your nosewithout mouth breathing to use it safely.

If you have underlying lung disease, loose teeth, or advancedperiodontal (gum) disease, you should not use Winx.

One unattractive drawback is that is also sucks saliva (or spit)into a canister that must be emptied in the morning.

Does not work in pts with soft palate surgery

Side effects Swelling of the soft palate Tongue tenderness


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The oral pressure therapy system consistsof a bedside console containing a pump, asoft polymer mouthpiece, and a flexibletube connecting the mouthpiece to theconsole.

With the mouthpiece in place, gentleoral vacuum creates a pressuregradient intended to move the softpalate against the tongue to relieveairway obstruction during sleep.


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Evidence ATLAST study*: multicenter, prospective, clinical trial was conducted to

determine the safety and effectiveness of the Winx System forthe treatment of OSA

63 pts ( CPAP nave, CPAP rejecters, CPAP users)

Responders :achieved median AHI reduction from 26.2 to 5.7. Median objectively recorded usage per night was 6.0 hours. 76% of participants responded they would use the Winx

System to treat their OSA. Significant reduction of AHI for moderate and severe OSA

Summary DOES NOT WORK FOR EVERYONE If it did not work on first night ,it will not work

*Colrain et al J Sleep Research 2012


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! Summary! Newer interventions such as nasal EPAP and oral negative

pressure devices may offer alternatives for some patients.! These devices tend to work better in patients with less severe

disease, and significant residual sleep disordered breathingshould be expected in many patients.

! Long-term data is not available for either one of theseinterventions.


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Initially introduced about 15 years ago Due to some technical problems ! no further studies were conducted over

the last 10 yrs Major limitation of previous techniques: induces arousal Not as effacacious as CPAP

Mechanismsof action

implantable HGNS therapy system ! electrical signals aregenerated by an implanted neurostimulator and deliveredto the ipsilateral HGN via an implanted cuff electrode ! stimulates the hypoglossal nerve during sleep opens theupper airway

delivering stimulation immediately prior to and during theinspiratory phase of respiration

Limitations Expensive Invasive


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Evidence Prospective single arm interventional trial:* AHI (43 ! 19) ESS ( statistical improvement) Favorable safety, efficacy and complianceSTAR trial multicenter,(randomized, prospective trial) to

demonstrate long-term safety and efficacy Improvement in AHI,ODI,ESS

Summary An alternative option

*Eastwood et al Sleep 2011


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! Pts with systolic heart failure and OSA :a) significantly heavierb) snore habituallyc) Have a higher systemic arterial blood pressureOther than these symptoms, the rest of symptoms of OSA andheart failure tend to overlap


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! In pts with systolic heart failure, OSA is associated with:1. Increased sympathetic activity2. Reduced left ventricular ejection fraction! Which may be reversed if OSA is treated with CPAP

! In patients with established CAD, OSA is an independentprognostic factor for recurrent cardiovascular disorders andsurvival

! In systolic heart failure, 2 observational studies ! suggests that

OSA contributes to mortality and that CPAP therapy improvessurvival

Kaneko et al NEJM 2003, Mansfield et al Am J Respir Crit Care Med 2004, Egea etal Sleep Medicine 2008Mooe et alAm J Respir Crit Care Med 2001, Peker et al Am J Respir Crit Care Med2000, Hender et al Sleep Med Clin 2007.Hanly et al Chest 1989, Lanfranchi et al Circulation 1999


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! Risk factors for OSA in patients with heart failure similar topatients without heart failure

! indications for a PSG are the same as in patients without heartfailure

! In addition; factors that increases suspicion for OSA in heartfailure patients:

1. Nocturnal angina2. Who remain in NYHA Class III and IV or with progressive

systolic or diastolic failure despite optimal medical therapy3. Patients on cardioverter or defibrilator


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! In the presence of cardiovascular disease, every attemptshould be made to treat OSA with PAP devices

Optimization of

cardiopulmonaryfunction

To eliminate or improve periodic breathing To decrease right atrial and central venous pressure

! reducing upper airway congestion/edema ! mayresult in increasing upper airway size

Increases lung volumes( FRC) which may improveincrease upper airway size as lung volumes increase

Weight loss Should be advised*

Javaheri et al Int J Cardiol 2006


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Avoidance of Alcohol The use increases likelihood of UAocclusion by promoting relaxation ofmuscles of the UABenzodiazepines

Phosphodiesterase-5inhibitors

Its use may worsen OSA In a randomized double blind

placebo controlled study*: 50 mg ofsildenafil significantly increased OSAindex and desaturation in a group ofpatients with OSA

*Roizenblatt et al. Arch Intern Med 2006


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PAP devices Treatment of choice Adherence to CPAP is a critical factor

Evidence 4 randomized trials of CPAP therapy in pts with systolicheart failureIn 3 of these studies ; LVEF increased significantly whencompared to control by 10%, 5% and 2%In the 4 th study: CPAP adherence was poorThe increase in LVEF is important because it is a predictorof survival in pts with systolic heart failure

Supplemental

nasal oxygen

For subjects with HF who can not tolerate positive airway

pressure devices- as an alternativeNocturnal O2 improvement in both hypoxemia andperiodic breathing

Kaneko et al NEJM 2003, Mansfield et al Am J Respir Crit Care Med 2004,Egea et al Sleep Medicine 2008, Smith et al Eur Heart J 2007


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Upper airwayprocedures

No data in patients with heart failure

Oral appliance Limited data available in heart failure *" in patients with stable CHF who are experiencing

problems with SDB, MAD intervention appears to reducea) the severity of SDBb) sleep apnoea-related symptomsWe speculate the efficacy of these devices in heart failuresimilar to that in general populationPost application repeat sleep study recommended

*Eskafi et al Swedish Dent J Suppl 2004


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! Night-time features of SDB include snoring, dyspnea,breathing pauses and sudden awakening with a chokingsensation

! Snoring and shortness of breath are common duringpregnancy usually at 2nd trimester

! The prevalence of snoring during the third trimester rangingfrom 10.4 to 46%

! SDB more common in 3 rd trimester as pregnancy progresses! Pregnant women with apnea symptoms have a higher

likelihood ofi. gestational hypertensive disordersii. gestational diabetesiii. unplanned Caesarian sections

Guilleminault et al Sleep Medicine 2000,Franklin et al Chest 2000, Bourjeily etal Eur Resp J 2010


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Physiological changes that potentiate the development of SDB inpregnancy: Reduction in upper airway size( dt weight gain, increased

fluid volume, nasal congestion) Decreased functional residual capacity and residual volume Increasing minute ventilation Supine position and sleep fragmentation

Trakada et al Eur J Obstet Gynaecol Reprod Biol 2003,Izci-Balserak et al Int J Sleep Wakefulness 2008


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Physiological changes that prevent the development of SDB inpregnancy: High circulating progesteronei. can protect upper airway from obstructionii. Increase upper airway dilator muscle activity and its

responsiveness to chemical stimuli( CO 2 during sleep)iii. Right-shifted oxyhemoglobin dissociation curve and

increase in heart rate , stroke volume and cardiac outputwith reduction in peripheral vascular resistance ! improvedelivery of oxygen to placenta and fetal tissues

iv. As pregnancy progresses less time spent in supine positionduring sleep

Izci-Balserak et al Int J Sleep Wakefulness 2008,Blyton et al Sleep 2004


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! Diagnosis:! Gold standard for diagnostic tests for OSA is the in laboratory

overnight PSG! Limited channel sleep studies have not been validated for use

in pregnant women at this point of time

! The use of a questionnaire for screening OSA would be

helpful! However, the available tools for screening OSA function

poorly in pregnant women

! The Berlin questionnaire:! In primary care : positive predictive value of 0.89! Cohort of pregnant women: sensitivity 35%, specificity 65% 1

1. Netzer et al Ann Intern Med 1999


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! Small retrospective and prospective cohort studies havereported an association between OSA and and thedevelopment of pre-eclampsia or gestational HPT

! In these studies, presence of OSA or OSA symptoms was

associated with a twofold increase in pre-eclampsia 1

! A small retrospective study ( n=57) found that women withOSA had a higher rate of preeclampsia than normal weightwomen (19% vs 7%, p = 0.02) 2

1Bourjeily et al Clin Chest Med 2011, 2 Louis et al Am J Obstet Gynecol 2011


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! Mechanistic studies demonstrate that OSA-related recurrenthypoxia and re-oxygenation cycles ! increased systemicinflammation , oxidative stress, endothelial dysfunction andincreased oxidative vascular injury 1

! The same pathophysiological mechanisms have beenimplicated in the development of preeclampsia and mayrepresent a common pathway to disease

! Case reports and small cohorts studies to determine whethermaternal OSA increases fetal growth restriction or stillbirth # most observational data suggests it does not 2

1Somers et al Circulation 2008, 2Bourjeily et al Clin Chest Med2011


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CPAP In pregnant women: Safe, well-tolerated, with good compliance

Abolish inspiratory flow limitations Reduce mean arterial pressure between wake and sleep by 3

mmHg Reduce severe attacks of dyspnea Improve cardiac output, total peripheral resistance during sleep

and nocturnal oxygenation Improve maternal and fetal outcomes in with pre-eclampsia risk

factorsThese are from case studies or limited studies$ In SDB diagnosed before or at the onset of pregnancy, CPAP MAY

need to be recalibrated around 24 weeks*

Oxygentherapy

Can be considered asi. Combination therapy with CPAPii. In pts who are unable to use CPAP(Pien et al Sleep 2004: although its effectiveness not proven inpregnant population)

Oralappliance

Can be an option but production and fitting sessions can take along time

*Guilleminault et al Sleep Medicine 2007


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PregestationalOSA

Should be evaluated by sleep physician, particularly if the ptis :

i. Untreated orii. Has not been evaluated for past 6 mths Can be evaluated for:i. The need for repeat PSGii. Initiation of therapyiii. Reassessment of treatment to ensure it is optimized CPAP is the most effective treatment If unable to tolerate CPAP, even in some moderate-to-severe

cases, a dental appliance for mandibular advancement withtitration can be used

Pts BP and urine protein should also be monitored ( risk ofdeveloping pregnancy related HPT) Suggest early testing for diabetes and repeat glucose

tolerance test at 24 to 28 weeks of gestation (high risk forpre-existing and future diabetes or insulin resistance) 1

1Bourjeily et al Clin Chest Med 2011


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Womensuspected ofOSA

Pts with symptoms( excessive daytime sleepiness, witnessedapnea, unexplained hypoxemia) or who are suspected ofOSA should be referred sleep medicine specialist forevaluation

We suggest treatment for all women with mild, moderate orsevere OSA

Post-partumfollow up

Followed up by sleep medicine specialist For reassessment of OSA severity and overall management

and treatment strategy


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! Greatest intra-partum risk for women with OSA is anesthesia! Pts with OSA have increased risk ofI. Post-operative hypoxemiaII. HypercapniaIII. Sudden death

! In managing OSA patients in labour and delivery , earlyplacement of regional anesthesia may: 1

i. Prevent the need for general anesthesia if emergencycesarean delivery may be necessary

ii. Obviate the need for parenteral opioids for labor pain

1Bolden et al J clin Anest 2009


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! Perioperative hypoxemia should be evaluated for potentialetiologies including life-threatening conditions

! Pts with OSA should be monitored until patient can maintaintheir baseline oxygen saturations while at rest

! Management of sleep apnea related hypoxemia treatment ofunderlying sleep apnea by pts prior determined OSAtreatment( CPAP or oral appliance)

! In absence of an established treatment of OSA , supplementaloxygen could be considered to to avoid hypoxemiaassociated with respiratory events



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! Pts should be positioned in semi-upright or lateral position

! Analgesic strategy that minimizes need for systemic opioidsshould be used

! If opioids need to be used, single doses rather than standingorders are preferred

! Dose required to induce hypoxemia in patients with OSA isapproximately half the dose required to induce hypoxemia inthose without OSA



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OSA Updates