Dr R.

Muventhiran Institut Perubatan Respiratori Kuala Lumpur

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Is part of a group characterized by disordered respiration during sleep known as sleep related breathing disorders:
Obstructive Sleep Apneas Central Sleep Apnea and Periodic Breathing SRBD

Sleep related hypoventilation and hypoxemic syndromes

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

WAKE Airway edema Decreased lung volumes Adipose soft tissue deposition CO2/ O2 Compromised craniofacial

Sleep onset 1.! UA musc tone 2.! Lung volume 3.! Central resp drive VENTILATORY CONTROL INSTABILITY Importance of controller/plant gain Decreased central respiratory and UA muscle drive UA opening

SLEEP UA closure/apnea CO2/ O2

DEFICIENT UA ANATOMY Compensated by high pharyngeal activity

Hypoxic and hypercapnic responsiveness Increased central respiratory and UA muscle drive If level of reaches arousal threshold Arousal 1.! UA musc tone 2.! Lung volume

Hyperventilation/ ventilatory overshoot

Hypoxic and hypercapnic responsiveness

! Obesity (BMI> 30) !AF

!Congestive heart Failure !Refractory HPT !Type 2 DM !CVA !Nocturnal arrhythmias !Pulmonary hypertension

!High-risk driving population

!Pre-operative for bariatric surgery

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None of the questionnaires are sensitive or specific to substitute for objective assessment by a sleep study

Berlin Questionnare STOP BANG questionnaire

To predict whether pt high risk or low risk for having OSA Screening tool for preoperative evaluation to detect OSA

! identified high risk based on AHI>5 ! sensitivity:0.86 ! specificity : 0.77 Sensitivity : 84% ( AHI>5), 92% (AHI>15) and 100% (AHI>30)

OSA PHYSICAL EXAMINATION INCREASED 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)

INTERNATIONAL CLASSIFICATION OF SLEEP DISORDERS, 2ND 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 breathing interuptions during sleep !PSG shows the following !i) scoreable respiratory events (A+H+RERA) /hr > 5/hr ! ii) Evidence of respiratory effort during all or a portion of each respiratory event !PSG shows the following ! i) scoreable respiartory events ( A+H+RERA)/hr >15/hr ! ii) Evidence of respiratory effort during all or a portion of each respiratory event ! The disorder is not better explained by another current sleep disorder, medical or neurologic disorder, medication use or substance use disorder DIAGNOSTIC CRITERIA= A+B+D OR C+D

Gold standard: In laboratory polysomnogram A 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 AHI MILD MODERATE SEVERE Treat Treat Treat No significant co-morbidities Observation or conservative treatment Treat Treat ASYMPTOMATIC Significant comorbidities ? Treat* Treat Treat

Conservative treatment: weight loss ,side sleep position,treat nasal congestion ,avoid alcohol For asymptomatic pts with mild OSA and significant medical co-morbidities, treatment decisions should be individualised based on patients motivation to undergo treatment

AMERICAN ACADEMY OF SLEEP MEDICINE PRACTICE PARAMETER RECOMMENDATION FOR MEDICAL TREATMENT OF OSA WEIGHT ! successful dietary weight loss may improve the AHI in REDUCTION obese OSA pts (guidelines) ! dietary weight loss should be combined with primary treatment of OSA (Option) ! Bariatric surgery may be adjunctive in treatment of OSA in obese pts (Option) POSITIONAL ! Positional therapy ,consisting of a method that keeps the THERAPIES patient in a non-supine position, is an effective secondary therapy or can be supplement to primary therapies for OSA in pts who have a low AHI in the non-supine versus the supine OXYGEN SUPPLEMEN TATION NASAL CORTICOST EROIDS ! Oxygen supplementation is not recommended as a primary treatment for OSA ( Option) ! Topical nasal cortiocsteroids may improve the AHI in pts with OSA and concurrent rhinitis and ,thus may be useful adjunct to primary therapies for OSA ( Guideline)

TREATMENT ALTERNATIVES FOR OSA (ADULTS) SNORING Primary !Treat nasal congestion ! Lateral positioning ! Avoid alcohol MILD If symptomatic and keen: ! PAP

Secondary

! if medical tx does not improve congestion! OA or surgery ( but snoring improvement is variable) ! LAUP ! Radio-frequency palatoplasty ! UPPP !Pillar procedure- may reduce snoring but not AHI ! Weight loss

If symp but not keen for PAP ! OA or ! Upper airway surgery Depends on pt preference and financial

Adjunctive

! weight loss ! lateral positioning

LAUP laser assisted uvulopalatplasty

TREATMENT ALTERNATIVES FOR OSA (ADULTS) MODERATE Primary Secondary Treatment of choice: PAP !If not acceptable !OA (50% effective*) !Upper airway surgery( 30% effective*) * Defined as tx AHI<10/ hr SEVERE PAP !If not acceptable !MMA 30% - AHI<10/hr !OA

Adjunctive Weight loss If pursuing bariatric surgery still PAP has to be given Lateral positioning

Weight loss If pursuing bariatric surgery still PAP has to be given Lateral positioning

MMA : Maxillary Mandibular Avancement

TYPE 1: ATTENDED PSG Measures (channels) Minimum of seven channels including ECG, EEG, EOG, chin EMG, airflow, respiratory effort, oxygen saturation Documented or objectively measured EMG or motion sensor desirable but optional Possible

TYPE 2: UNATTENDED PSG Minimum of seven channels including EEG, EOG, chin EMG, heart rate or ECG, airflow, respiratory effort, oxygen saturation Possible Optional No

Body position Leg movement Personnel interventions

TYPE 3: MODIFIED PORTABLE SLEEP APNEA TESTING Measures (channels) Minimum of four, including ventilation (at least two channels of respiratory movement or respiratory movement and airflow), heart rate or ECG, and oxygen saturation Possible Optional No

TYPE 4: CONTINUOUS SINGLE OR DUAL BIOPARAMETER RECORDING Minimum of one oxygen saturation, flow, or chest movement

Body position Leg movement Personnel interventions

No No No

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 treatments for sleep apnea (oral appliances, surgery, weight loss). Unattended PM in patients home is permitted when all guidelines are followed.

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Portable Monitoring Task Force of AASM recommended home studies only after a comprehensive sleep evaluation by a clinician certified in sleep medicine and then supervised and interpreted by person with same level of speciality training

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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 confirmatory laboratory testing and encourage treatment of pts with false positive results

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One published cost-utility model showed that PSG generated higher utility than a portable cardiorespiratory monitory and the magnitude of the PSG easily justified the added initial expense Chervin et al . Ann Intern Med 1999

Pt presents to CSS for evaluation of suspected OSA

Does pt have high pretest probability of moderate or severe OSA Yes Symptoms or signs of comorbid medical disorders No Symptoms or signs of comorbid sleep disorders No Sleep study (PM or in lab) Yes

No

Evaluate for other sleep disorders, consider in-lab PSG

No In-lab PSG OSA diagnosed ? No OSA diagnosed ? Yes Treatment Yes

Yes

PM

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Initially was hoped to reduce the average overnight pressure level ! resulting in improved adherence
Subjects Results There were no differences in hours of nightly use, despite a mean decrease in overnight pressure of 2 cm H20 ! Mostly men with moderate to severe OSAH ! CPAP-nave ! No other SRBD or comorbidities

Ayas et al Meta-analysis of Sleep 2007 randomized trials comparing ACPAP with fixed pressure CPAP

Smith et al

Recent metaanalysis of 30 studies

Found a statistically significant difference of machine usage of 12 mins WHICH IS NOT CLINICALLY SIGNIFICANT

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However individual may tolerate APAP>CPAP Based on currently available evidence, the AASM suggests the long term use of autotitrating CPAP in self-adjusting role to treat OSAH as an option only

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Medical Treatment for OSA 1.! End Expiratory Pressure(EPAP) devices 2.! Oral Pressure Therapy
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Non-medical treatment options for OSA Hypoglossal Nerve Stimulation

NONE of these options are more or as efficacious as PAP therapy

FDA cleared in 2008 for treatment of mild, moderate and severe OSA Mechanism of ! consists of a small valve attached externally to each nostril action with 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 pressurize and stabilize the upper airway during the critical endexpiratory period, when the airway has been found to be most narrow in the breaths prior to an apnea. ! Whereas CPAP provides positive pressure during both inspiration and expiration, EPAP only creates pressure during expiration.

Indications

! Patients (mild, moderate or severe) who have rejected or are non-compliant with prescribed CPAP ! Newly diagnosed mild/moderate OSA patients without significant co-morbidities ! CPAP compliant patients looking for alternatives for travel ! Severe breathing disorder (including respiratory muscle weakness, 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 the ear drum ! 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

Contraindications

Limitations

Evidence Summary

! Mean AHI reduction in about 50% ! Berry et al Sleep 2011: ! Works in a subset of patients with OSA but no obvious way to select them ! The effectiveness of nasal EPAP is dependent on achieving sustained expiratory pressure and appears only to be possible in about 50% of patients

! novel treatment for sleep apnea that includes a polymer mouthpiece, tubing, and small console. Mechanism of action ! 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 otherwise cause. ! The tongue is stabilized, the size of the airway increases, and breathing improves.

Advantages

! no bulky mask or restraining headgear without a risk of pressure 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 and claustrophobia ! required that you be able to breathe through your nose without mouth breathing to use it safely. ! If you have underlying lung disease, loose teeth, or advanced periodontal (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 ! Swelling of the soft palate ! Tongue tenderness

Limitations

Side effects

The oral pressure therapy system consists of a bedside console containing a pump, a soft polymer mouthpiece, and a flexible tube connecting the mouthpiece to the console.

With the mouthpiece in place, gentle oral vacuum creates a pressure gradient intended to move the soft palate against the tongue to relieve airway obstruction during sleep.

Evidence

ATLAST study*: ! multicenter, prospective, clinical trial was conducted to determine the safety and effectiveness of the Winx System for the 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 ! DOES NOT WORK FOR EVERYONE ! If it did not work on first night ,it will not work

Summary

*Colrain et al J Sleep Research 2012

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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 breathing should be expected in many patients. Long-term data is not available for either one of these interventions.

Summary

! 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 Mechanisms of action ! implantable HGNS therapy system! electrical signals are generated by an implanted neurostimulator and delivered to the ipsilateral HGN via an implanted cuff electrode! stimulates the hypoglossal nerve during sleep opens the upper airway ! delivering stimulation immediately prior to and during the inspiratory phase of respiration ! Expensive ! Invasive

Limitations

Evidence

Prospective single arm interventional trial:* ! AHI (43!19) ! ESS ( statistical improvement) ! Favorable safety, efficacy and compliance STAR trial multicenter,(randomized, prospective trial) to demonstrate long-term safety and efficacy ! Improvement in AHI,ODI,ESS ! An alternative option

Summary

*Eastwood et al Sleep 2011

Pts with systolic heart failure and OSA : a)! significantly heavier b)! snore habitually c)! Have a higher systemic arterial blood pressure Other than these symptoms, the rest of symptoms of OSA and heart failure tend to overlap
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In pts with systolic heart failure, OSA is associated with: 1.! Increased sympathetic activity 2.! Reduced left ventricular ejection fraction !! Which may be reversed if OSA is treated with CPAP
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In patients with established CAD, OSA is an independent prognostic factor for recurrent cardiovascular disorders and survival In systolic heart failure, 2 observational studies ! suggests that OSA contributes to mortality and that CPAP therapy improves survival

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Kaneko et al NEJM 2003, Mansfield et al Am J Respir Crit Care Med 2004, Egea et al Sleep Medicine 2008 Mooe et alAm J Respir Crit Care Med 2001, Peker et al Am J Respir Crit Care Med 2000, Hender et al Sleep Med Clin 2007. Hanly et al Chest 1989, Lanfranchi et al Circulation 1999

Risk factors for OSA in patients with heart failure similar to patients without heart failure !! indications for a PSG are the same as in patients without heart failure !! In addition; factors that increases suspicion for OSA in heart failure patients: 1.! Nocturnal angina 2.! Who remain in NYHA Class III and IV or with progressive systolic or diastolic failure despite optimal medical therapy 3.! Patients on cardioverter or defibrilator
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In the presence of cardiovascular disease, every attempt should be made to treat OSA with PAP devices

Optimization of cardiopulmonary function

! To eliminate or improve periodic breathing ! To decrease right atrial and central venous pressure ! reducing upper airway congestion/edema! may result in increasing upper airway size ! Increases lung volumes( FRC) which may improve increase upper airway size as lung volumes increase ! Should be advised*

Weight loss

Javaheri et al Int J Cardiol 2006

Avoidance of

Alcohol Benzodiazepines

! The use increases likelihood of UA occlusion by promoting relaxation of muscles of the UA

Phosphodiesterase-5 ! Its use may worsen OSA inhibitors ! In a randomized double blind placebo controlled study*: 50 mg of sildenafil significantly increased OSA index and desaturation in a group of patients with OSA

*Roizenblatt et al. Arch Intern Med 2006

PAP devices Evidence

! Treatment of choice ! Adherence to CPAP is a critical factor 4 randomized trials of CPAP therapy in pts with systolic heart failure In 3 of these studies ; LVEF increased significantly when compared to control by 10%, 5% and 2% In the 4 th study: CPAP adherence was poor The increase in LVEF is important because it is a predictor of survival in pts with systolic heart failure For subjects with HF who can not tolerate positive airway pressure devices- as an alternative Nocturnal O2 improvement in both hypoxemia and periodic breathing

Supplemental nasal oxygen

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

Upper airway procedures Oral appliance

No data in patients with heart failure Limited data available in heart failure * "! in patients with stable CHF who are experiencing problems with SDB, MAD intervention appears to reduce a)! the severity of SDB b)! sleep apnoea-related symptoms We speculate the efficacy of these devices in heart failure similar to that in general population Post application repeat sleep study recommended

*Eskafi et al Swedish Dent J Suppl 2004

Epidemiology: !! The prevalence of the disorder among women aged 30-39 years old is estimated to be 5-6%1
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The prevalence of OSA in pregnant women is not known because no large population-based epidemiological studies have been performed

1. Young et al N Engl J Med 1993, 2. Olivarez et al Am J Obstet Gynecol 2010

Night-time features of SDB include snoring, dyspnea, breathing pauses and sudden awakening with a choking sensation !! Snoring and shortness of breath are common during pregnancy usually at 2nd trimester !! The prevalence of snoring during the third trimester ranging from 10.4 to 46% !! SDB more common in 3rd trimester as pregnancy progresses !! Pregnant women with apnea symptoms have a higher likelihood of i.! gestational hypertensive disorders ii.! gestational diabetes iii.! unplanned Caesarian sections
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Guilleminault et al Sleep Medicine 2000,Franklin et al Chest 2000, Bourjeily et al Eur Resp J 2010

Physiological changes that potentiate the development of SDB in pregnancy: ! 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

Physiological changes that prevent the development of SDB in pregnancy: ! High circulating progesterone i.! can protect upper airway from obstruction ii.! Increase upper airway dilator muscle activity and its responsiveness to chemical stimuli( CO2 during sleep) iii.! Right-shifted oxyhemoglobin dissociation curve and increase in heart rate , stroke volume and cardiac output with reduction in peripheral vascular resistance! improve delivery of oxygen to placenta and fetal tissues iv.! As pregnancy progresses less time spent in supine position during sleep

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

Case reports and studies of pregnant women with OSA indicate that those with i.! Obesity ii.! Large neck circumference iii.! Abnormal oropharyngeal anatomy iv.! Small oropharynx are at risk of developing OSA during pregnancy or developing a more severe case of OSA if already diagnosed
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Women with i.! chronic or gestational hypertension ii.! pre-eclampsia iii.! gestational diabetes or iv.! history of infants with IUGR should be evaluated for SDB especially if they have predisposing factors such as obesity
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Maasilta et al Chest 2001, Poyares et al Sleep Medicine 2007

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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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Sleepiness in pregnant women is not specific for SDB This may be explained by physiological changes in pregnancy such as gestational weight gain that may result in symptoms that mimic the symptoms of sleep-related breathing disorders

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Small retrospective and prospective cohort studies have reported an association between OSA and and the development of pre-eclampsia or gestational HPT In these studies, presence of OSA or OSA symptoms was associated with a twofold increase in pre-eclampsia1 A small retrospective study ( n=57) found that women with OSA had a higher rate of preeclampsia than normal weight women (19% vs 7%, p= 0.02)2

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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 recurrent hypoxia and re-oxygenation cycles ! increased systemic inflammation , oxidative stress, endothelial dysfunction and increased oxidative vascular injury1 The same pathophysiological mechanisms have been implicated in the development of preeclampsia and may represent a common pathway to disease Case reports and small cohorts studies to determine whether maternal OSA increases fetal growth restriction or stillbirth# most observational data suggests it does not2

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1Somers

2011

et al Circulation 2008, 2Bourjeily et al Clin Chest Med

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Recent data from a large Taiwanese study1 add strength to the association between maternal OSAS and poor fetal outcome OSA could exacerbate partial sleep deprivation of later pregnancy! increase maternal irritability and perhaps greater risk of post-partum depression and impaired mother-infant interactions

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1Macones

et al Am J Obstet Gynaecol 2012

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In general there is no consensus about screening and treating SDB in pregnancy The main aim is to eliminate maternal hypoxemia( saturations< 90%) and clinical symptoms and to obtain an RDI of < 5/hr This treatment plan is not evidence based

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 factors These 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* ! Can be considered as i.! Combination therapy with CPAP ii.! In pts who are unable to use CPAP (Pien et al Sleep 2004: although its effectiveness not proven in pregnant population) ! Can be an option but production and fitting sessions can take a long time *Guilleminault et al Sleep Medicine 2007

Oxygen therapy

Oral appliance

Pregestational OSA

! Should be evaluated by sleep physician, particularly if the pt is : i.! Untreated or ii.! Has not been evaluated for past 6 mths ! Can be evaluated for: i.! The need for repeat PSG ii.! Initiation of therapy iii.! 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 with titration can be used ! Pts BP and urine protein should also be monitored ( risk of developing pregnancy related HPT) ! Suggest early testing for diabetes and repeat glucose tolerance test at 24 to 28 weeks of gestation (high risk for pre-existing and future diabetes or insulin resistance)1
1Bourjeily

et al Clin Chest Med 2011

Women suspected of OSA

! Pts with symptoms( excessive daytime sleepiness, witnessed apnea, unexplained hypoxemia) or who are suspected of OSA should be referred sleep medicine specialist for evaluation ! We suggest treatment for all women with mild, moderate or severe OSA ! Followed up by sleep medicine specialist ! For reassessment of OSA severity and overall management and treatment strategy

Post-partum follow up

Greatest intra-partum risk for women with OSA is anesthesia !! Pts with OSA have increased risk of I.! Post-operative hypoxemia II.! Hypercapnia III.! Sudden death
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In managing OSA patients in labour and delivery , early placement of regional anesthesia may:1 i.! Prevent the need for general anesthesia if emergency cesarean delivery may be necessary ii.! Obviate the need for parenteral opioids for labor pain
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1Bolden

et al J clin Anest 2009

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Pts who have been using CPAP or oral appliances before delivery for OSA should be instructed to bring their devices during delivery Should have their oxygenation continuously monitored during labor

1Bolden

et al J clin Anest 2009

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Perioperative hypoxemia should be evaluated for potential etiologies including life-threatening conditions Pts with OSA should be monitored until patient can maintain their baseline oxygen saturations while at rest Management of sleep apnea related hypoxemia treatment of underlying sleep apnea by pts prior determined OSA treatment( CPAP or oral appliance) In absence of an established treatment of OSA , supplemental oxygen could be considered to to avoid hypoxemia associated with respiratory events
1Bolden

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et al J clin Anest 2009

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Pts should be positioned in semi-upright or lateral position Analgesic strategy that minimizes need for systemic opioids should be used If opioids need to be used, single doses rather than standing orders are preferred Dose required to induce hypoxemia in patients with OSA is approximately half the dose required to induce hypoxemia in those without OSA

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1Bolden

et al J clin Anest 2009

Pregnant women with new or recurrent symptoms pt EDS or sleep disturbances Examine clinically and pregnancy history: 1.! Loud snoring, EDS, witnessed apnea esp in women with excessive weight gain 2.! Chronic HPT, gestational HPT or preeclampsia in esp prepregnancy obsesity and large neck size 3.! Gestational diabetes and previous unexplained IUGR assoc. with snoring and obesity 4.! Worsening/recurrence of symptoms in pts with pre-existing OSA Treatment: ACPAP or recalibration of CPAP in pre-existing OSA or other modality eg BiPAP In prepregnancy obesity and SDB : main goal ! to eliminate maternal hypoxemia, RDI> 5 and symptoms

Assess & treat SDB as early to prolong gestation, delay preeclampsia onset and reduce IUGR severity Overnight PSG to determine objective snoring , oxyhemoglobin desturations, flow limitation events(FLE) and RDI

If one exists: 1.! RDI 5-30/hr with few/no SaO2 <90% and clinical symptoms 2.! RDI>30/hr 3.! Recurrent SaO2<90% 4.! Chronic HPT and objective evidence of snoring and FLE 5.! Gestational HPT/pre-eclampsia and objective evidence of snoring and FLE 6.! Indication of insufficient treatment of perexisting OSA