obstructive sleep apnea

Dr Debashees nanda M.S (E.N.T)

M.K.C.G Medical collegeBerhampur

What is sleep?A state of (1) sustained immobility in a (2)

characteristic posture accompanied by (3) reduced responsivity to external stimuli;

The Biological Rhythms of Sleep

About every 90 or 100 minutes we pass through 5 stages of sleep.

Throughout the five stages, our brain waves continually fluctuate, thus defining each distinctive stage.

The Circadian RhythmOur biological clock that is genetically

programmed to regulate physiological responses within a 24 – 25 hour period.

Refers to circa=approximately and dias=day.

Please don’t fall asleep during the power point!!

Light Sleep -Stage 1Body movement decreasesSpontaneous Waking may occur (when you

feel like you are falling out of bed)

Intermediate Sleep - Stage 2Officially asleepYour brain waves slow down with some

bursts of brain activity called ‘Sleep Spindles’ half of your sleep in this stage. Helps refresh body

Sleep Talking can occur during this and all future sleep stages.Sleep Talking can occur during this and all future sleep stages.

Deep Sleep – Stage 3 -4 Deep sleep sets in – hard to wake upbrain waves become large and slowYour breathing becomes rhythmic, and your

muscles remain relaxed. Most Restorative stage (reparative hormones

released)30-40 min first and shorter later

Deep Sleep – Stage 3 -4

Towards the end of stage 4, children may wet beds, adults may sleep walk, etc…

Interestingly, even though you are in deep sleep, your brain will still process the meaning of certain stimuli!!

REM Sleep - Rapid Eye Movement

Nearly an hour after you fall asleep, you begin to descend back through the stages of sleep.

During sleep you go stages 1,2,3,4,3,2 then…

You then enter what is known as REM Sleep!

REM –This stage only lasts about 10 minutes. (20 – 30 minutes later in night)

REM Sleep - Rapid Eye Movement

heart rate risesbreathing becomes rapidevery 30 seconds or so, your eyes rapidly

move around.

motor cortex is still active, but your brainstem blocks any messages.

This leaves your muscles so relaxed that you are essentially paralyzed.

Thus, you are not easily awakened.

How Much Sleep Do I Need?Infants

20 hours 50% REM

Children/Adolescents10 hours

25-30% REMBed Later, Up Later

Adults8 hours

20% or less REMElderly

6 hoursBed Later, Up Earlier

(3) Areas of the brain involved in sleep(i) Hypothalamus

Studied the brains of those who had died from the virus encephalitis lethargica

- Victims who had difficulty sleeping: Damage to anterior region

- Victims who had difficulty staying awake Damage to posterior region

Constantin von Economo

Confirmed in lesion studies with animals (Saper et al., 2001)

(ii) Reticular System

(3) Areas of the brain involved in sleep

- Bremer (1936)

Cerveau isole transection = slow-wave sleep pattern

Encephale isole transection = Normal sleep-wake cycle

Thus, “wakefulness” area = somewhere in-between the two

- Mouzzi & Morgan (1949)

Stimulation of the reticular formation of sleeping cats woke them up.

(2) Theories of Sleep - AnalysisEffects of sleep deprivation - Humans

- REM sleep deprivation

- Preventing REM sleep makes the body want it more. (Webb & Agnew, 1967)

- Deprivation of REM sleep causes a transient rebound. (Brunner et al 1990)

- No cognitive or emotional effects however.

(2) Theories of Sleep - AnalysisEffects of sleep deprivation - Animals

- After several days, experimental rats died

- But, post-mortem revealed swollen adrenal glands, gastric ulcers and internal bleeding

- Result a consequence of stress and physical damage??

Measurement of Sleep

Three principle measures of sleep:

(i) Electro-encephalogram (Head)(ii) Electro-oculogram (Eye)(iii) Electro-myogram (Neck)

20 percent of adult population have some form of sleep disorder.

TYPESRespiratory- •Obstructive sleep apnea/hypopnea•Central sleep apnea/hypopnea•Cheyne stokes breathing•Sleep hypoventilation

Non Respiratory-• Narcolepsy• Periodic limb movement disorder• Idiopathic hypersomnia

WHAT IS OSA?

OSA IS :

Common

Dangerous

Easily recognized

Treatable

www.sleepdoctor.com

WHAT IS OSA?Episodes of complete or partial collapse of airway are translated to # of apnea and hypopnea events (AHI).

Apnea = cessation of airflow > 10 secondsHypopnea = Decreased airflow > 10 seconds associated

with: Arousal Oxyhemoglobin desaturation

WHY DOES THIS MATTER?Excessive daytime somnolenceImpaired cognitive performancePoor quality of lifeIncreased risk of MVAAdverse cardiovascular outcomesPulmonary hypertension(?DM/metabolic syndrome)

Pathophysiology of OSAAirway size:

Pathophysiology of OSASites of

Obstruction:Obstruction

tends to propagate

Pathophysiology of OSASites of Obstruction:

Pathophysiology of OSATests to determine site of obstruction:

Muller’s Maneuver -After a forced expiration, an attempt at inspiration

is made with closed mouth and nose, whereby the negative pressure in the chest and lungs is made very subatmospheric; the reverse of Valsalva maneuver.

Sleep endoscopyFluoroscopyManometryCephalometricsDynamic CT scanning and MRI scanning

EPIDEMIOLOGYDisease prevalence = 2 – 4 % of US adult

populationHigher in population subsets

1980’s = morbidity associated with OSA became more widely appreciated

Majority of cases still undiagnosed Concern = increase knowledge = recognize risk factors = identify affected individuals

RISK FACTORSObesityAgeSexRaceCraniofacial anatomySmoking and alcohol consumption

ObesityStrongest risk factorAlters upper airway mechanics during sleep

1. Increased parapharyngeal fat deposition: neck circumference: > 17” males

> 16” females With subsequent: smaller upper airway

increase the collapsibility of the pharyngeal airway

obesity2. Changes in neural compensatory mechanisms that maintain airway patency:

diminished protective reflexes which otherwise

would increase upper airway dilator muscle activity to maintain airway patency

obesity

3. waist circumference Fat deposition around the abdomen

produces reduced lung volumes (functional

residual capacity) which can lead to loss of caudal

traction on the upper airway low lung volumes are associated with diminished oxygen stores

AGE

Anatomic susceptibilityPreferential deposition of fat in the parapharyngeal areaChanges in the body structures around the

pharynxDeterioration of protective reflex mechanisms

Risk Factor: Age

0

5

10

15

20

25

30

35

30-39 Yrs 40-49 Yrs 50-60 Yrs

Female

Male

% with AHI > 5

Adapted from Young T et al. N Engl J Med 1993;328. 2006 American Academy of Sleep medicine

GENDER MALE GENDERIncreased neck and waist circumference? Women not reporting the classic symptoms? Healthcare providers have lower index of

suspicion for considering OSA in women than men.

CRANIOFACIAL ANATOMYMandibular body lengthRetrognathiaTonsilar hypertrophyEnlarged tongue or soft palateInferiorly positioned hyoid boneMaxillary and mandibular retro positionDecreased posterior airway space

SMOKING

0

1

2

3

4

5

Adjusted Odds Ratio for Sleep Apnea (AHI > 15) in Former & Current Smokers vs Nonsmokers

Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.

Former Current Smokers Smokers

(Adjusted for age, race, sex, BMI)

Odds Ratio

2006 American Academy of Sleep Medicine

Other risk factorsAlcohol consumptionSedatives (benzodiazepines)

reduce nerve output to compensatory dilator

muscles increase OSA severity in patients with

preexisting syndrome.

DIAGNOSISCombined assessment of clinical features and

objective sleep study data.The gold standard: overnight

polysomnogramThe Polysomnogram (PSG):

Provides detailed information on sleep state and

respiratory and gas exchange abnormalities.

PSGSimultaneous recordings of multiple

physiological signals during sleep.Electroencephalogram (EEG)Electrooculogram (EOG)Electromyogram (EMG)Electrocardiogram (ECG)Oronasal airflowChest wall effortSnore microphoneOxyhemoglobin saturation

PSGRecurrent episodes of complete or partial collapse of the upper airway are recorded as apnea or hypopnea events.

Apnea = complete cessation of airflow for at least 10 seconds

Hypopnea = 25 – 50% reduction in oronasal airflow associated with desaturation or an arousal from sleep.

Study should be atleast for 6 hours.Healthy individuals

May experience apneas and hypopneas at sleep onset or during REM sleep. But these last less than ten seconds and do not recur.

PSGSleep apnea severity index:

AHI = apnea-hypopnea index = # of apneas and hypopneas / hour of

sleep

Mild: 5 – 15 events/hour of sleepModerate: 15 – 30 event/hour of sleepSevere: > 30 events/hour of sleep

EEG

10 sec

Arousal

Airflow

Effort(Pes)

SaO2

Effort(Abdomen)

Effort(Rib Cage)


10 sec

ArousalEEG

Airflow

Effort(Pes)

SaO2

Effort(Abdomen)

Effort(Rib Cage)


DIAGNOSIS: CLINICAL FEATURESNocturnal symptoms 1. Snoring – reflects the critical narrowing - population survey: habitual snorers 25% of men, 15% of

women - prevalence increases with age (60%, 40%) - the most frequent symptom of OSA - absence makes OSA unlikely

(only 6% of patients with OSA did not report)

Clinical features(nocturnal symptoms continued)2. Witnessed apneas3. Nocturnal choking or gasping

- report of waking at night with a choking sensation; passes within a few seconds4. Insomnia

- sleep maintenance insomnia- (few have difficulty initiating sleep)

Clinical featuresDaytime symptoms 1. Excessive daytime sleepiness - severity can be assessed

subjectively = questionnaires (Epworth Sleepiness Scale)

objectively MSLT = Multiple Sleep Latency Test MWT = Maintenance of wakefulness

Test Osler Test

Clinical features(daytime symptoms) 2. fatigue 3. memory impairment 4. personality changes 5. morning headaches or nausea 6. depression

DIAGNOSISAmerican Academy of Sleep Medicine criterias: A. Excessive daytime sleepiness that is not better explained by other factors B. Two or more of the following that are not

better explained by other factors: choking during sleep; recurrent awakenings; unrefreshing sleep; daytime fatigue; impaired

concentration. C. AHI (five or more obstructed breathing events per hour during sleep).

www.dentonsleepdisorderlab.com

CARDIOVASCULAR RISKStressors arise from

HypoxemiaReoxygenationChanges in intrathoracic pressureCNS arousals

Stimulation of sympathetic nervous systemAcute peripheral vasoconstriction elev BPpersist even in waking hours elev BP

Mean arterial pressure during wakefulness and sleep in subjects enrolled in Wisconsin Sleep Cohort Study. Subjects with polysomnographically demonstrated sleep apnea had higher blood pressures than either snorers without apnea or non-snoring individuals.

Cardiovascular RiskHTN

Most studies suggest that OSA contributes to systemic HTN

Treatment of OSA may improve systemic HTN.Cardiac arrhythmias - bradycardia (increase vagal tone with hypoxemia) - asystole - atrial fibrillation - ectopic ventricular beats

(bigeminy, trigeminy)

PULMONARY HYPERTENSIONHypoxia results in pulmonary

vasoconstrictionAutoregulatory mechanism in order to

eliminate V/Q mismatch in time may cause vasculature

remodeling result in PH (PAP > 25mmg Hg)

OSA and medical co morbidityConflicting data, but possible association of

OSA with:

CVA Heart Failure DM

Other Comorbidities: MVA

00.050.1

0.150.2

0.250.3

0.350.4

0.45

No Apnea Sleep Apnea All Drivers

Accident / driver / 5 yrs

Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.2006 American Academy of Sleep Medicine

• Objective = consequences discussed• Modality

TREATMENTTREATMENT

BEHAVIORAL METHODSWeight lossAvoid alcohol and sedativesAvoid sleep deprivationAvoid supine sleep positionStop smoking

WEIGHT LOSS

Remains a highly effective method10 – 15 % reduction in weight can lead to an

approximately 50 % reduction in sleep apnea severity in moderately obese male patients.

MEDICAL Rx

Positive Pressure Therapy * CPAP * Bi-PAP -pressurized air delivered at two

alternating levels. The inspiratory positive airway pressure is higher and supports a breath as it is taken in. Conversely, the expiratory positive airway pressure is a lower pressure that allows you to breathe out. These pressures are preset and alternate just like your breathing pattern.

CPAPHas been shown to objectively:

Decrease blood pressureDecrease day time sleepiness

Problems:Mask discomfortPatient acceptanceClaustrophobiaaerophagia

Nonsurgical ManagementOral appliance

Mandibular advancement device

Tongue retaining device

SURGICAL METHODSReconstruct upper airway

Uvulopalatopharyngoplasty (UPPP)Laser-assisted uvulopalatopharyngoplasty

(LAUP)Radiofrequency tissue volume reductionGenioglossal advancementNasal reconstructionTonsillectomy

Bypass upper airwayTracheostomy

Surgical ManagementAlgorithms

Friedman et al developed a staging system for type of operation:

Surgical ManagementAlgorithms:

Friedman et al:

Surgical Management Tracheostomy

Primary treatment modality Once placed, uncommon to decannulate

Thatcher GW. Maisel RH. The long-term evaluation of tracheostomy in the management of severe obstructive sleep apnea. [Journal Article] Laryngoscope. 113(2):201-4, 2003 Feb.

Surgical ManagementNasal Surgery

Limited efficacy when used aloneVerse et al 2002 showed 15.8% success rate

when used alone in patients with OSA and day-time nasal congestion with snoring (RDI<20 and 50% reduction)

Adenoidectomy

Surgical ManagementUvulopalatopharyngoplasty

Surgical ManagementUvulopalatopharyngoplasty

The most commonly performed surgery for OSA

Severity of disease is poor outcome predictor

Levin and Becker (1994) up to 80% initial success decreased to 46% success rate at 12 months

Friedman et al showed a success rate of 80% at 6 months in carefully selected patients

Friedman M, Ibrahim H, Bass L. Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg 2002; 127: 13–21.

Surgical ManagementUP3

ComplicationsMinor

Transient VPI Hemorrhage<

1%Major

NP stenosis VPI

Surgical ManagementCahali, 2003

proposed the Lateral Pharyngoplasty for patients with significant lateral narrowing:

Cahali MB. Lateral pharyngoplasty: a new treatment for obstructive sleep apnea hypopnea syndrome. Laryngoscope. 113(11):1961-8, 2003 Nov.

Surgical ManagementLateral Pharyngoplasty

Surgical ManagementLaser Assisted

UvulopalatoplastyHigh initial success

rate for snoringRates decrease, as

for UP3 at twelve months

Performed awake

Surgical ManagementRadiofrequency

Ablation – Fischer et al 2003

Radiofrequency device is inserted into various parts of palate, tonsils and tongue base at various thermal energies

Surgical ManagementTongue Base Procedures

Lingual Tonsillectomy may be useful in patients with hypertrophy, but

usually in conjunction with other procedures

Surgical ManagementTongue Base

Procedures Lingualplasty

Chabolle, et al success rate of 77% (RDI<20, 50% reduction) in 22 patients in conjunction with UPPP

Complication rate of 25% - bleeding, altered taste, odynophagia, edema

Can be combined with epiglottectomy

Surgical ManagementMandibular

ProceduresGenioglossus

Advancement Rarely performed

alone Increases rate of

efficacy of other procedures

Transient incisor paresthesia

Surgical ManagementLingual

Suspension:

Surgical Management Lingual

Suspension:

Surgical ManagementHyoid Myotomy and

SuspensionAdvances hyoid bone

anteriorly and inferiorly

Advances epiglottis and base of tongue.

Surgical ManagementMaxillary-Mandibular Advancement

Severe diseaseFailure with more conservative measuresMidface, palate, and mandible advanced

anteriorlyLimited by ability to stabilize the

segments and aesthetic facial changes

Surgical ManagementMaxillary-

Mandibular AdvancementPerformed in

conjunction with oral surgeons

PRIMARY CARE MANAGEMENT Recognize the prevalenceIdentify affected patients based on risk

factors and symptomsCounsel on behavioral changesRefer to specialistMonitor symptoms and compliance during Rx

Otherwise snore and this will happen to you….

Or sleep alone….

www.corbett.com.au

obstructive sleep apnea

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