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Obstructive Sleep Apnea: Obstructive Sleep Apnea:

Obstructive Sleep Apnea: - PowerPoint Presentation

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Obstructive Sleep Apnea: - PPT Presentation

Poor bedfellow Dessislava Ianakieva MD Sleep Medicine Fellow 51717 Objectives Understand the mechanism of sleep apnea Know factors that increase the incidence of sleep apnea in adults ID: 625824

osa sleep obstructive apnea sleep osa apnea obstructive treatment airway pressure cpap hypertension increased children severe events risk patients

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Slide1

Obstructive Sleep Apnea:Poor bedfellow

Dessislava

Ianakieva

, MD

Sleep Medicine Fellow

5/17/17Slide2

Objectives

Understand the mechanism of sleep apnea

Know factors that increase the incidence of sleep apnea in adults

Understand the meaning of “AHI”

Understand the effects of sleep apnea on the cardiovascular system

Learn the basic treatments of sleep apnea.

Understand the risk factors for and symptoms of pediatric sleep apnea.

Understand basic treatments of pediatric sleep apnea.Slide3

Obstructive sleep apnea:

The basicsSlide4

Evaluating sleep disorders:

Polysomnogram

Essentials of Sleep Technology: Pediatrics. Westchester, IL. American Academy of Sleep Medicine, 2006

Tech Observer

Video Camera

SaO

2

Leg EMG (2)

Microphone

EKG

Chin EMG (2)

EEG

EOG

Nasal EtCO

2

Records behavior

Respiratory Effort

Nasal Oral AirflowSlide5

PolysomnogramSlide6

Obstructive Sleep Apnea

Complete or partial upper airway obstruction

Often results in reductions in oxygen saturation

Often terminated by brief arousals from sleep

Duration of each obstruction is at least 10 secondsSlide7

Respiratory Events: Definitions

HypopneaSlide8

Blood oxygen levels reduce to

>

3% of baseline value

Inhale

Exhale

Airway obstructs

Airway opens

Paradoxing

Paradoxing Ends

EKG

Airflow

Thoracic effort

Abd.

effort

SAO2

Effort gradually increases

Obstructive Apnea EventSlide9

VideoSlide10

Hypnogram in OSA

Normal hypnogramSlide11

Obstructive Sleep Apnea in Adults

Estimated prevalence:

9% in women

24% in menSlide12

Physiologic changes in OSA

Intermittent hypoxia

Intermittent hypercapnia

Increased negative intrathoracic pressure swings

Increased arousals from sleep

Sleep fragmentation

Sympathetic nervous system activationMetabolic dysregulation Endothelial dysfunction Systemic inflammation Hypercoagulability Impaired cardiac function Left atrial enlargement Myocardial ischemia Cardiac remodelingArrhythmiaSlide13

Other consequences of untreated OSA

Overall increase in mortality

Excessive daytime sleepiness

Motor vehicle accidents

Mood disorders

Decreased quality of life

OSA: Sudden cardiac death peaks between 12-6 AMCardiovascular events occur in the early hoursSlide14

Sleep Apnea and Sudden Death

Respiratory depressants may block the arousal process

Alcohol

Benzodiazepines

Barbiturates

Opioids

Avoid alcohol within 4 hours of bedtimeSlide15

Symptoms of OSA

Middle Age

Pauses in breathing

Snoring

Nocturia

Frequent nocturnal awakenings

Morning headacheDry mouth Morning GERDExcessive daytime sleepinessImpaired cognitionOlder > 60 yearsExcessive daytime sleepinessNocturiaSlide16

Risk factors for OSA

Male sex

Older age (40-70 years)

Postmenopausal status

BMI >35

Craniofacial and upper airway abnormalities

Resistant hypertensionPCOSSlide17

Diagnosis of OSA

In-lab

polysomnogram

is the gold standard

Home sleep apnea test

- unattended

Apnea Hypopnea Index (AHI)= respiratory events per hour of sleepApnea (90%obstruction of flow) + hypopnea (30% flow limitation)Normal < 5 Mild: 5-15 Moderate:15-30 Severe > 30 Slide18

Screening questionnaire: STOP-BANG

STOP-Bang score ≥ 3

Sensitivity

89% to detect moderate to severe OSA

93% to detect severe OSA

Specificities

30% for moderate to severe29% for severe OSASlide19

Physical Exam Findings

BMI > 35

Central obesity

Midface hypoplasia

Retrognathia

Neck circumference

Women > 16in Men >17 in

High arched palate

Mallampati

MacroglossiaSlide20
Slide21

OSA and cardiovascular disease

Circulation. 2008;118:1080-1111Slide22

OSA and Hypertension

sympathetic nerve activity and catecholamine levels

Repetitive hypoxemia and hypercapnia

chemoreflex-mediated sympathetic activation and vasoconstriction

At the termination of apneas:↑ cardiac output and severe vasoconstrictionBP can rise from 130/60 mm Hg awake to 220/130 mm Hg during apneas Diastolic nocturnal hypertension

Loss of nocturnal dipping of blood pressure.

From Somers VK,

Dyken ME, Clary MP, et al. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995;96:1897-1904.)Slide23

OSA And Incident Hypertension

N

Engl

J Med 2000; 342:1378.

Mild OSA (AHI 5-15):

2 fold increased risk

Moderate to severe OSA (AHI >15):3 fold increased risk Sleep Heart Health Study (6424 patients) Linear relationship between the severity of OSA and the risk of systemic hypertensionSlide24

OSA And Hypertension

71% of patients with resistant hypertension have OSA compared to 38% of patients with controlled hypertension.

Increased risk of hypertension in patients with OSA who were not compliant with CPAP at 12 years of follow up. Slide25

OSA and Diabetes

OSA is an

independent risk factor

for the development of T2DM

15%–30% of patients with OSA have T2DM

severity of OSA correlates to increased T2DM incidence and poor glycemic control Sleep Health Heart StudyMild OSA – Diabetes OR=1.27 ( CI 0.98–1.64)Moderate-to-severe OSA- Diabetes OR=1.46 (95% CI 1.09–1.97)OSA severity was associated with increased insulin resistanceNocturnal hypoxemia independently associated with glucose intoleranceSlide26

Nature and Science of Sleep 2015:7Slide27

Treatment options for OSA in adultsSlide28

Indications for treatment

AHI >5 events per hour of sleep plus one or more clinical or physiologic sequelae attributable to OSA.

AHI ≥15 events per hour of sleep, even in the absence of symptoms

Mission critical work (airline pilots, air traffic controllers, locomotive engineers, DOT drivers) with AHI between 5 and 15 events per hour of sleep, even if there are no clinical or physiological symptoms attributable to OSA.

Treatment options:

Positive airway pressure therapy

Oral appliancesPositional therapyBariatric surgeryAdenotonsillectomy Slide29

Positive airway pressure modalitiesSlide30

Continuous Positive Airway Pressure (CPAP) Best Treatment for Significant OSA

CPAP splints open the airway wherever the obstructionSlide31

Effect of OSA treatment on comorbid conditionsSlide32

A prospective cohort study followed 1651 men for a mean of 10 years following polysomnography.

Treatment with CPAP reduced incidence of fatal and non-fatal cardiovascular events

Lancet. 2005;365(9464):1046.

A prospective cohort study followed 449 patients with mild or moderate OSA (~6 years follow up)

Treatment of OSA (Primarily CPAP) associated with reduction of likelihood of cardiovascular events

Adjusted HR 0.36 (95% CI 0.21-.62)

Am J Respir Crit Care Med. 2007;176(12):1274.CPAP Treatment And Cardiovascular EventsSlide33

CPAP Treatment And Cardiovascular Events

Reduction in AHI from 29 to 3.7 events per hour

No statistically significant effect on cardiovascular events

Significant reduction in snoring and daytime sleepiness

Improvement in health-related quality of life and mood

CAVEAT:

Average CPAP use ~ 3.3 hours per nightExcluded patients with excessive daytime sleepinessSlide34

CPAP treatment and hypertension

CPAP treatment decreases in systolic blood pressure of 2.5 to 3.0 mm Hg

Patients with uncontrolled hypertension are likely to gain the largest benefit (reduction in blood pressure) from CPAP

CPAP improves blood pressure control more than nocturnal oxygen supplementationSlide35

CPAP and Resistant Hypertension

RCT of

of

117 patients assessed the effect of continuous positive airway pressure (CPAP) treatment on 24-h urinary aldosterone excretion in patients with Resistant hypertension (RHT) and moderate/severe OSA.

Decreased aldosterone excess in resistant hypertensive individuals with OSA

Effect was observed with optimal use only (>6hr of use per night)

More pronounced in effect: non-dippers, not on spironolactone, less obese, lowest nocturnal oxygen saturationJ Hypertens. 2017 Apr;35(4):837-844Slide36

Positive Airway Pressure And Heart Failure

Men with severe OSA (AHI >30 ) were 58 % more likely to develop heart failure

Sleep. 2015;38(5):677.

Epub

2015 May 1

A meta-analysis (6 RCT)

CPAP was associated with a 5% improvement in ejection fractionPLoS One. 2013;8(5):e62298Canadian Positive Airway Pressure (CANPAP) trialGreater reduction in AHIImprovements in mean nocturnal O2 satImprovement in left ventricular ejection fractionImprovement in 6 minute walk distanceCanadian Positive Airway Pressure (CANPAP) trialCirculation 2007; 115:3173.Slide37

Positive Airway Pressure Therapy And Atrial Fibrillation

Heart Rhythm. 2013 Mar;10(3):331-7.

CPAP therapy effect on AF:

Reduces the structural and electrical remodeling of the left atrium due to OSA

Decreases serum markers of oxidative stress (cytokines and free radicals)

Rate of recurrent AF after cardioversion

:Untreated OSA- 86%Treated OSA 42%Without OSA 53 %Slide38

Continuous Positive Airway Pressure Therapy In OSA and Glycemic Control

Clinically significant improvement in glycemic control

Amelioration of evening fasting glucose metabolism

Reduction in the dawn phenomenon

Diabetes

Obes Metab, 2016.Slide39

Oral appliance: Mandibular repositioning devises

Advancement to the maximum tolerable distance or 65% of the maximum protrusion

Indicated for mild-moderate OSA

50% reduction in the AHI

Discontinuation rates of14–63% after 4-5 years

Med Oral

Patol Oral Cir Bucal. 2015 Sep 1;20(5):e605-15Slide40

Bariatric surgery and OSA

Higher prevalence of OSA among the morbidly obese:

55% in women and 80% in men

.

2

Remission of OSA (AHI < 5 events/h) at 1 year follow up:

66% RYGB patients vs 40% ILI patients50% reduction in AHI with 10%-15% reduction in body weight Journal of Clinical Sleep Medicine, Vol. 9, No. 5, 201Slide41

Pediatric Obstructive Sleep ApneaSlide42

Snoring in children

10% of children snore

1-5 % have sleep disordered breathing

Snoring > 3 times per week associated with increased risk of OSA

Peak prevalence: 2 and 8 years of age

Chronic nasal congestion

Adenotonsillar hypertrophySlide43

Diagnosis Of Sleep Apnea In Children

Overnight oximetry specific but not sensitive

In-lab

polysomnogram

- gold standard

Pediatric obstructive apnea index

Excluding central apnea and hypopneaMild: 1-5Moderate: 5-10Severe: >10Respiratory events are shorter (2 breaths)Smaller oxygen desaturations Slide44

VideoSlide45

OSA Risk factors in children

Tonsillar and adenoidal hypertrophy

History of prematurity and multiple gestation

Family history of OSA

Craniofacial abnormalities

Neuromuscular disorders

MyelomeningoceleHistory of low birth weightFamily history of OSAUncontrolled epilepsyObesitySlide46

Syndromes associated with OSA

Trisomy 21 (Down Syndrome)

Prader

-Willi

Robin sequence

Treacher

CollinsBeckwith-WiedemannAchondroplasiaSmith MagenisTurner SyndromeStrickler SyndromeFetal Alcohol SyndromeArnold-Chiari malformationSlide47

Snoring

Pauses in breathing

Chocking or gasping

Increased work of breathing

Enuresis

Excessive sweating

Hyperextended neckFrequent awakeningsPoor school performanceAggressive behaviorHyperactivityExcessive daytime sleepiness

Morning headachesFailure to thrive

OSA symptoms in children

Common signs and symptoms

during sleep:Common signs and symptoms during wakefulness:Only 9-13% exhibit daytime sleepinessSlide48

Physical exam findings

Tonsillar hypertrophy

Retrognathia

Obligate mouth breathers

Midface hypoplasia

Dental crowding

MacroglossiaSlide49

Effects Of Untreated Pediatric OSA

Failure to thrive

Increased energy expenditure due to increased work of breathing

Decreased nocturnal growth hormone secretion may be decreased in children with increased upper airway resistance

Improvement in growth hormone secretion after

adenotonsillectomy

Cadiovascular effects in children with POAHI >5 Lower RV ejection fractionIncreased LV diastolic dysfunction Remodeling with larger interventricular septal thickness index on echocardiogramEffects noted were independent of the effect of obesity Slide50

Effects Of Untreated Pediatric OSA

Endothelial dysfunction

Metabolic dysregulation

Impaired glucose tolerance

Hyperlipidemia

NASH

Impairment of neurocognitive developmentPoor school performanceBehavioral problemsSlide51

Grey matter volume reductions superior frontal, prefrontal, superior and lateral parietal cortices that control of cognition and mood Slide52

Adenoidal FaciesSlide53

Mild sleep apnea:

Optimization of nasal passage patency

Nasal steroid

Leukotriene receptor antagonists

Saline rinse

Weight loss

OrthodontiaModerate-severe sleep apnea:Tonsillectomy and AdenoidectomyResidual or severe sleep apnea:CPAP therapyOther surgical interventionsMandibular distractionTreatment of OSA in ChildrenSlide54

Effects of treatment of pediatric sleep apnea

Improvement of:

Behavior

Attention span

Quality of life

Neurocognitive functioning

EnuresisParasomniasRestless sleep Reversal of associated cardiovascular sequelaeImprovement in cardiac functionDecrease in average heart rate and blood pressureImprovement in endothelial function Slide55

Adenotonsillectomy

Success rate of

adenotonsillectomy

is 75%-85%

Poor prognostic factors:

Obesity

Severe OSA pre-surgery with an POAHI of >20/hrCildren aged >7 yearsHigh Mallampati score African-American ethnicityCraniofacial abnormalities (e.g., Pierre Robin syndrome)Chromosomal abnormalities (e.g., trisomy 21)Neuromuscular diseaseSlide56

Risk Factors For Complications Following

Adenotonsillectomy

Evaluate for atlantoaxial instability and

Likely to require adjuvant surgical procedures

Severity and sites of airway obstruction

Likely to require adjuvant surgical procedures

At risk for significant hypoventilation At risk for pulmonary and cardiac dysfunctionIncreased severity of OSA with increased obesity

Increased adenoid and tonsil size Increased risk for respiratory complications Slide57

Surgical treatment did:

Reduce symptoms

Improve behavior and quality of life

Normalization of polysomnographic findings 79% vs. 46%

Adenotonsillectomy

Surgical treatment

did not significantly improve attention or executive function as measured by neuropsychological testingn engl j med 368;25 june 20, 2013The Childhood Adenotonsillectomy Trial (CHAT)Slide58

Mandibular Distraction

Bilateral

corticotomy

of the mandible

Insertion of either internal or external metal distractors

Gradual distraction of the mandible while new bone fills in the gap

Indicated in children with significant micrognathia and severe sleep apneaPaediatr Respir Rev. 2015 June ; 16(3): 189–196.Slide59

CPAP Therapy In Children

Indications:

Residual OSA after

adenotonsillectomy

OSA related to obesity

Craniofacial abnormalities

Neuromuscular disordersOSA without adenotonsillar hypertrophyPreference for non-sugical treatmentMental age of 8Weigh >30 kg Desensitization Regular evaluation for mask fitBOTTOM LINE: Elimination of symptoms, signs, and polysomnographic abnormalities in 90 % Slide60

Questions ???Slide61

References:

Durán-

CantollaJ

et al. Efficacy of mandibular advancement device in the treatment of obstructive sleep apnea syndrome: A randomized controlled crossover clinical trial.

Med Oral

Patol

Oral Cir Bucal. 2015 Sep 1;20(5)Marin JM et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365(9464):1046. Buchner NJ et al. Continuous positive airway pressure treatment of mild to moderate obstructive sleep apnea reduces cardiovascular risk. Am J Respir Crit Care Med. 2007;176(12):1274.Marie-Françoise Vecchierini et al. A custom-made mandibular repositioning device for obstructive sleep apnoea–hypopnoea syndrome: the ORCADES study. Sleep Medicine. Volume 19, March 2016, Pages 131–140McEvoy RD et. Al. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. N Engl J Med. 2016;375(10):919. Epub 2016 Aug 28.Peppard PE, Young T, Palta

M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000; 342:1378.Tomas Konecny et al.Obstructive Sleep Apnea and Hypertension Hypertension. 2014;63:203-209.Marin JM et al. Association between treated and untreated obstructive sleep apnea and risk of hypertension. JAMA. 2012;307(20):2169.

Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.Holmqvist F et al. Impact of obstructive sleep apnea and continuous positive airway pressure therapy on outcomes in patients with atrial fibrillation-Results from the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF). Am Heart J. 2015 May;169(5):647-654.e2. Epub 2015 Feb 7. Hla KM et al. Coronary heart disease incidence in sleep disordered breathing: the Wisconsin Sleep Cohort Study. Sleep. 2015;38(5):677.

Epub 2015 May 1.Mansfield DR et al. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med. 2004;169(3):361. Sun H et al. Impact of continuous positive airway pressure treatment on left ventricular ejection fraction in patients with obstructive sleep apnea: a meta-analysis of randomized controlled trials. PLoS One. 2013;8(5):e62298. Epub 2013 May 1Nieminen P et al. Growth and biochemical markers of growth in children with snoring and obstructive sleep apnea. Pediatrics. 2002;109(4):e55. Chan JY et al. Cardiac remodelling and dysfunction in children with obstructive sleep apnoea: a community based study. Thorax. 2009;64(3):233.Gozal D et al. Obstructive sleep apnea and endothelial function in school-aged nonobese children: effect of adenotonsillectomy. Circulation. 2007 Nov;116(20):2307-14. Epub 2007 Oct 29. Marcus CL et al. A randomized trial of adenotonsillectomy for childhood sleep apnea. N Engl J Med. 2013;368(25):2366. Waters KA et al. Obstructive sleep apnea: the use of nasal CPAP in 80 children. Am J Respir Crit Care Med. 1995;152(2):780. Slide62