Obstructive Sleep Apnea A Serious Epidemic

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Transcript Obstructive Sleep Apnea A Serious Epidemic

Obstructive Sleep Apnea
A Serious Epidemic
M.A.Hamadeh,M.D,FCCP,FAAM
Assoc. Clinical Professor, Med.
University of Illinois School of
Medicine
Director, Sleep Disorders Centers,
Christ Hospital & Medical Center
Sleep Apnea
Sleep Apnea is:
• Common
• Dangerous
• Easily recognized
• Treatable
Types of Sleep Disordered Breathing
• Apnea
– Cessation of airflow > 10 seconds
• Hypopnea
– Decreased airflow 30% from baseline
lasting > 10 seconds associated with >
4% oxyhemoglobin desaturation
Apnea Patterns
Obstructive
Airflow
Respiratory
effort
Mixed
Central
Obstructive Apnea
Central Apnea
Mixed Apnea
Obstructive Hypopnea
Respiratory Effort-related
Arousals
RERA: Respiratory Effortrelated Arousal (Guilleminault, 1993)
A sequence of breaths characterized by
increasing respiratory effort leading to an
arousal from sleep which does not meet
criteria for an apnea or hypopnea. These
events must fulfill both of the following
criteria:
1. Pattern of progressively more negative
esophageal pressure, terminated by a sudden
change in pressure to a less negative level and
an arousal
2. The event lasts 10 seconds or longer.
UARS (Upper Airway Resistance Syndrome):
> 5 RERA’s per hour of sleep
What About “Simple Snoring?”
• Snoring in pregnancy is associated with
•
increased hypertension and growth retardation,
controlling for weight, age, smoking (Franklin, Chest, 2000)
Snoring is associated with cognitive decline (Quesnot,
J Am Geriatric Soc, 1999)
• Snoring medical students are more likely to fail
•
•
exams, controlling for BMI, age, sex (Ficker, Sleep, 1999).
Snoring is a risk factor for cardiovascular disease
in women. (Hu, J Am Coll Cardiol 2000).
Snoring is a risk for type II diabetes (Al-Delaimy, Am J
Epidemiol 2002).
• Snoring women have faster progression of CAD
(Leineweber C. Sleep 2004)
Measures of Sleep Apnea
Frequency
• Apnea Index
– # apneas per hour of sleep
• Apnea / Hypopnea Index (AHI)
– # apneas + hypopneas per hour
of sleep
• Respiratory Disturbance Index
– # apneas + hypopneas + RERAs per hour of sleep
Severity Criteria Based on PSG
From the American Academy of
Sleep Medicine (Sleep, 1999)
• “Mild” sleep apnea is 5-15 events/hr
• “Moderate” sleep apnea is 15-30
events/hr
• “Severe” sleep apnea is over 30
events/hr
• (“Events” includes apneas, hypopneas,
and RERA’s)
One Definition of Obstructive Sleep
Apnea (OSA)
CPAP will be covered for adults with sleepdisordered breathing if:
– AHI (or RDI) > 15
OR
– AHI (or RDI) > 5 with (“mild, symptomatic”)
• Hypertension
• Stroke
• Sleepiness
• Ischemic heart disease
• Insomnia
• Mood disorders
Sleep-Disordered Breathing is a
Spectrum
Prevalence of Sleep Apnea
30-60 year olds
25
20
Percent of
Population
15
Male
Female
10
U.S. Pop
5
0
AHI > 5
Adapted from Young T et al. N Engl J Med 1993;328.
SAS
Asthma
Why Sleep Apnea Isn’t Going Away…..
SDB with Aging
Sleep Apnea vs Sleep Disorders
• Prevalence of common sleep
disorders
– Insomnia: 10-30%
– Sleep Apnea: 5%
– RLS: 10%
– Narcolepsy: 0.05%
• Diagnoses of patients presenting
to sleep centers (Coleman II, 2000)
– Sleep apnea: 67.8
– RLS: 4.9%
– Narcolepsy 3.2%
The Upper Airway
2
1
9
3
6
4
7
5
8
Control of Dilator Muscles
Effects On Pharyngeal Muscle Activity
Awake
Genioglossus EMG
Normal
Subject
Tensor Palatini
EMG
Airflow
Genioglossus EMG
OSA
Patient
Tensor Palatini
EMG
Airflow
NREM
Pathophysiology of Apnea
Wakefulness
Sleep
Pathophysiology of Sleep Apnea
Awake: Small airway + neuromuscular compensation
Sleep Onset
Hyperventilate: connect
hypoxia & hypercapnia
Loss of neuromuscular
compensation
+
Airway opens
Decreased pharyngeal
muscle activity
Pharyngeal muscle
activity restored
Airway collapses
Arousal from sleep
Apnea
Hypoxia &
Hypercapnia
Increased ventilatory
effort
Clinical Consequences
Sleep Apnea
Sleep Fragmentation
Hypoxia/ Hypercapnia
Cardiovascular
Complications
Excessive Daytime
Sleepiness
Morbidity
Mortality
Consequences:
Excessive Daytime Sleepiness
• Increased motor vehicle crashes
• Increased work-related accidents
• Poor job performance
• Depression
• Family discord
• Decreased quality of life
Consequences:
Automobile Accidents
Sassani, et al., Sleep 2004; 27:453
Consequences:
Automobile Accidents
Risk of Traffic Accident: OSA + ETOH
12
10
8
Odds
Ratio
6
4
2
0
NO ETOH
Adapted from Teran-Santos J et al.
N Engl J Med 1999;340.
+ ETOH
ETOH On Day of Accident
Consequences: Cardiovascular
• Systemic hypertension
• Cardiac arrhythmias
• Cardiovascular disease
– Myocardial ischemia
– Congestive heart failure
• Cerebrovascular disease
Consequences: Mortality
Wisconsin Cohort
Busselton, Australia
RDI < 5
RDI 5-15
RDI > 15
Years of follow-up
Young et al. Sleep 2008; 31:1071-1078
Marshall et al. Sleep 2008; 31:1079-1085
Consequences: Hypertension
Shepard JW Jr. Med Clin North Am 1985;69.
Cardiovascular Consequences:
Hypertension
Prospective Study of Association Between OSA and Hypertension
3
2.5
2
Odds
Ratio
Adjusted
for age, sex, BMI,
neck circ., cigs.,
ETOH, baseline Htn
1.5
1
0.5
0
0
0.1 - 4.9
5 - 14.9
Apnea / Hypopnea Index (AHI)
Adapted from Peppard PE et al.
N Engl J Med 2000;342.
> 15
Consequences: Arrhythmias
Consequences: Cardiovascular
Disease
Cross Sectional Study of Association Between OSA and CVD
2.5
2
Odds
Ratio
AHI
0 - 1.3
1.5
1.4 - 4.4
1
4.5 - 11.0
> 11.0
0.5
0
CAD
HF
CVA
Adjusted for age, sex, race, BMI, Htn, cigs., chol.
Adapted from Shahar E et al.
Am J Respir Crit Care Med 2001;163.
OSA and Stroke
4.5
4
3.5
3
2.5
2
1.5
1
0.5
0
*
*
AHI<5
AHI 5-20
AHI>20
Unadjusted
Arzt, et al., AJRCCM 2005; 172:1447.
A/G
Adjusted
A/G/BMI
Adjusted
Sleep Apnea Risk Factors
• Obesity
• Increasing age
• Male gender
• Anatomic abnormalities of upper
airway
Family history
•
• Alcohol or sedative use
• Smoking
• Associated conditions
Risk Factor: Obesity
>4% Arterial saturation dipa h-1
80
70
60
50
40
30
20
10
0
70
80
90
100
110
120
% Predicted normal neck circumference
Davies RJ et al. Eur Respir J 1990;3.
130
140
Risk Factor: Age
35
30
25
% with
AHI > 5
20
Female
15
Male
10
5
0
30-39 Yrs
Adapted from Young T et al.
N Engl J Med 1993;328.
40-49 Yrs
50-60 Yrs
Risk Factor: Gender
Apnea/Hypopnea Index
120
100
80
60
Male
Female
40
20
0
0
20
40
60
80
100
Skinfold Sum (mm)
Millman RP et al. Chest 1995;107.
120
140
Apneas & Hypopneas per hour of sleep
Risk Factor: Anatomic Abnormality
6
75
4
8
5
50
45
40
3
35
7
30
2
25
1
20
15
10
5
0
Nose Open
Suratt PM et al. Chest 1986;90.
Nose Occluded
Risk Factor: Family History
Likelihood of Sleep Apnea as Function of Family Prevalence
4
3.5
Odds Ratio
3
2.5
(Adjusted for
age, race, sex,
BMI)
2
1.5
1
0.5
0
1
Relative
Adapted from Redline S et al.
Am J Resp Crit Care Med 1995;151.
2
Relatives
3
Relatives
Risk Factor: Sedatives
150
100
(% control)
Peak Integrated activity
Phrenic Nerve
Hypoglossal Nerve
50
Diazepam Injection
0
0 5
15
30
Minutes after injection
60
Sanders MH. In: Principles and Practice of Sleep Medicine. Philadelphia: W.B. Saunders Company, 1994.
Risk Factor: Alcohol
Before Alcohol
Phrenic
Hypoglossal
Blood Alcohol = 83 mg/dl
Phrenic
Hypoglossal
Blood Alcohol = 134 mg/dl
Phrenic
Hypoglossal
Bonara M et al. Am Rev Respir Dis 1984;130 © American Lung Association.
Risk Factor: Smoking
Adjusted Odds Ratio for Sleep Apnea (AHI > 15)
in Former & Current Smokers vs Nonsmokers
5
4
Odds Ratio
3
(Adjusted for age,
race, sex, BMI)
2
1
0
Former
Smokers
Current
Smokers
Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.
Diagnosis: History
• Snoring (loud, chronic)
• Nocturnal gasping and choking
– Ask bed partner (witnessed apneas)
• Automobile or work related accidents
• Personality changes or cognitive problems
• Risk factors
• Excessive daytime sleepiness
Sleep Apnea: Is Your Patient at Risk? NIH Publication, No 95-3803.
Diagnosis:
Assessing Daytime Sleepiness
• Often unrecognized by patient
– Ask family members
• Must ask specific questions
– Fatigue vs. sleepiness
– Auto crashes or near misses
– Sleep in inappropriate settings
• Work
• Social situations
Diagnosis: Physical Examination
• Upper body obesity / thick neck
> 17” males
> 16” females
• Hypertension
• Obvious upper airway abnormality
Exam: Tonsillar Hypertrophy
Normal Oropharynx
Shepard JW Jr et al. Mayo Clin Proc 1990;65.
Oropharynx With Tonsillar Hypertrophy
Exam: Oropharynx
Patient With the Crowded Oropharynx
Exam: Oropharynx
Class I
Class II
Class III
Class IV
Physical Examination
Structural Abnormalities
Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.
Diagnosis: Pediatric Apnea
• Presentation
–
–
–
–
Behavioral problems / irritability
Poor school performance
Enuresis
Snoring
• Cause
– Adenotonsillar hypertrophy
– Craniofacial abnormality
– Frequently not obese
Pediatric Sleep Apnea
Child with Sleep Apnea
Child’s Enlarged Palatine & Adenoidal Tonsils
Why Get a Sleep Study?
• Signs and symptoms poorly predict
•
•
disease severity
Appropriate therapy dependent on severity
Failure to treat leads to:
– Increased morbidity
– Motor vehicle crashes
– Mortality
• Other causes of daytime sleepiness
What Test Should be Used?
• In-laboratory full night
polysomnography
– Split night studies
• Home diagnostic systems
– Oximetry to full polysomnography
Polysomnography
Polysomnogram
Full-Night In-Laboratory
Polysomnography
• Pro
– Full set of variables obtained
– Equipment problems can be repaired
– Technician can address patient problems
• Con
– Cost
– Accessibility
– Patient sleeps away from home
Split-Night In-Laboratory
Polysomnography
• Pro
– Reduced cost
– Patient may be studied only once
– Reduces time to treatment initiation
• Con
– Diagnostic time may be inadequate
– Treatment time limited
– Protocol decisions to start CPAP may be difficult to
make during data acquisition
Home Study Tracing
Home Study
• Pro
– Potentially less expensive
– Patient sleeps at home
• Con
– Generally fewer signals are recorded
– Equipment cannot be adjusted
– Technician cannot assist patient
Diagnostic Conclusions
• Signs and symptoms
– Excessive daytime sleepiness
– Hypertension and other cardiovascular sequelae
• Sleep study results
– Apnea / hypopnea frequency
– Sleep fragmentation
– Oxyhemoglobin desaturation
Treatment Objectives
• Reduce morbidity and mortality
– Reduce sleepiness
– Decrease cardiovascular consequences
• Improve quality of life
Therapeutic Approach
• Risk counseling
– Motor vehicle crashes
– Job-related hazards
– Judgment impairment
• Apnea and co-morbidity treatment
– Behavioral
– Medical
– Surgical
The High-Risk Driver
• Educate patient
• Document warning
• Resolve apnea quickly
• Follow-up
– Effectiveness
– Compliance
Behavioral Interventions
• Encourage patients to:
– Lose weight
– Avoid alcohol and sedatives
– Avoid sleep deprivation
– Avoid supine sleep position
– Stop smoking
Weight Loss
• Should be prescribed for all obese
patients
• Can be curative but has low success rate
• Other treatment is required until optimal
weight loss is achieved
Weight Loss and Sleep Apnea
6
5
4
3
Mean Change in
AHI, Events/hr
2
1
0
-1
-2
-3
-4
-20 to
<-10%
Adapted from Peppard PE et
al. JAMA 2000;284.
-10 to <5%
-5% to
<+5
+5 to
+10%
Change in Body Weight
+10% to
+20
Weight Loss and Sleep Apnea
100
40
80
20
60
15
40
10
20
5
Baseline
Smith PL et al.
Ann Intern Med 1985;103.
Weight Loss
Baseline
Weight Loss
Apnea Frequency
Mean Fall Sa02
(EPISODES/HOUR)
(PERCENT)
Sleep-Position Training
Medical Interventions
• Positive airway pressure
– Continuous positive airway pressure (CPAP)
– Bi-level positive airway pressure
• Oral appliances
• Other (limited role)
– Medications
– Oxygen
Positive Airway Pressure
Positive Airway Pressure
Benefits of CPAP: Mortality
96%
86%
Campos-Rodriguez, et al., Chest 2005; 128:624
91%
Benefits of CPAP: Sleepiness
CPAP Treatment
Latency to Sleep (min)
15
12
9
1 night
14 nights
42 nights
6
3
0
Pre
Adapted from Lamphere J
et al. Chest 1989;96.
Post
Benefits of CPAP: Performance
35
Obstacles hit in 30 min.
30
25
20
15
10
5
0
Before CPAP
(n=6)
Adapted from Findley L et al. Clin Chest Med 1992;13.
After CPAP
(n=6)
No Apnea
(n=12)
Positive Airway Pressure: Problems
Mask Discomfort
Patient Acceptance
Claustrophobia
Aerophagia
Chest Discomfort
CPAP for OSA: Benefits
•
•
•
•
•
•
•
•
•
•
Improved cognitive function
Improved quality of life
Reduced daytime sleepiness
Reduced risk of automobile accidents
Reduced health care costs
Reduced blood pressure
Reduced cardiac arrhythmias
Improved glucose tolerance
Reduced mortality rate
Reversal of impotence
Positive Airway Pressure:
Problems
CPAP Compliance
• Patient report: 75%
• Objectively measured use
> 4 hrs for > 5 nights / week: 46%
• Asthma-medicine compliance: 30%
CPAP Compliance
70
1 month
3 month
Mean percentage days
CPAP used
60
50
40
30
20
10
0
20 Minutes
4 Hours
Time CPAP used
Adapted from Kribbs NB et al. Am Rev Respir Dis 1993;147.
7 hours
CPAP Compliance: Predictors
• Predict Good
Compliance
– Increased AHI
– Increased daytime
sleepiness
– Perception of benefit
• Predict Poor
Compliance
– Lack of EDS
– Lack of perceived
benefit
– Nasal obstruction
– Side effects
– Claustrophobia
Strategies to Improve
Compliance
• Patient Education
• Frequent and early follow-up
• Machine-patient interfaces
•
•
•
•
– Masks
– Nasal pillows
– Chin straps
Humidifiers
Ramp
Desensitization
Pressure relief CPAP or Bi-level pressure
CPAP Masks
CPAP Ramping
Effect of Recurrent Use of Ramping on Nocturnal Saturation
Pressman MR et al. Am J Respir Crit Care 1995;151 © American Lung Association.
Bi-level Positive Airway Pressure
Positive Pressure Therapy
CPAP
15
10
Pressure
5
0
Insp
Flow
Exp
Bi-level
Compliance: CPAP Vs. Bi-Level
PAP
Compliance: CPAP vs Bi-level Positive Pressure
CPAP
Bi-level
Mean
hours of
use
86
75
64
53
42
31
20
Visit
1
2 weeks
Visit
1
2
4-8 weeks
Visit
23
8-12 weeks
Visit
34
24-28 weeks
Visit
45
52 weeks
Reeves-Hoché MK et al. Am J Respir Crit Care Med 1995;151 © American Lung Association.
Monitoring Compliance
• Most PAP units measure ‘mask-on’ times
• Adherence data can be downloaded into
compliance reports
• Objective monitoring recommended in
treatment guidelines
• Objective monitoring required by CMS
Monitoring Compliance
Oral Appliances
• Indications
– Snoring and apnea (not severe)
• Efficacy
– Variable with 52% of patients with
AHI<10/hr on treatment
• Side effects
– TMJ discomfort, dental misalignment,
and salivation
Oral Appliances
Variables that Effect Efficacy
• Severity of OSA: higher success with mild to
•
•
•
moderate disease (AHI <30-40)
Degree of protrusion: more effective with
increased protrusion
Positionality of SDB: more effective in
patients with supine-dependent OSA
BMI: more effective in patients with lower
BMI
Sleep 2006;29:244
Oral Appliance: Mechanics
Supplemental Oxygen
• Not a primary treatment for sleep apnea
• Does not improve daytime sleepiness
• May prolong apneas
• Reduces oxygen desaturation during
apneas
• Reduces arrhythmias
Pharmacologic Treatment
• Limited Role
– Protriptyline or fluoxetine
– Decongestants
– Nasal steroids
– Antihistamines
– Other
Surgical Alternatives
• Reconstruct upper airway
–
–
–
–
–
Uvulopalatopharyngoplasty (UPPP)
Radiofrequency tissue volume reduction
Genioglossal advancement
Nasal reconstruction
Tonsillectomy
• Bypass upper airway
– Tracheostomy
Sites of Airway Narrowing
18%
82%
Adapted from Morrison DL et al. Am Rev Respir Dis 1993;148.
Collapse at soft
palate only
Multiple sites of
collapse
Uvulopalatopharyngoplasty (UPPP)
• Usually eliminates snoring
• 41% chance of achieving AHI < 20
• No accurate method to predict surgical
success
• Follow-up sleep study required
Uvulopalatopharyngoplasty (UPPP)
Primary Care Management
• Risk counseling
• Behavior modification
• Monitor symptoms and compliance
– Monitor weight and blood pressure
– Ask about recurrence of symptoms
– Evaluate CPAP use and side effects
Sleep Apnea: Is Your Patient at Risk? NIH Publication No.95-3803.
Primary Care Management
• Reasons for lack of improvement
– Noncompliance
– Alcohol and sedative use
– Depression
– Poor sleep habits
– Nonapneic sleep disorder
• Persistent or recurrent symptoms
– Consider referral to sleep specialist
Sleep Medicine in the Future
• The prevalence and importance of
•
•
•
•
•
sleep apnea are attracting attention
Training and credentialing have
changed
Diagnostic approaches are simplifying,
and multiplying
Reimbursement will continue to fall.
Treatment approaches are changing
The field is vulnerable
Portable Monitoring (or oximetry)
is to in-lab PSG as…
• CXR is to CT scan (lung cancer)
• Pre-post spirometry is to methacholine
challenge (asthma)
• Fasting glucose is to oral glucose
challenge test (diabetes)
Outcomes of Home-Based Diagnosis and
Treatment of Obstructive Sleep Apnea
Chest 2010; 138: 257-263
• Home testing and autoCPAP resulted in
the same results in sleepiness, adherence,
blood pressure and QoL as in-lab testing.
• “It is really not about the technology; it is
about the initial and then chronic care of
the patient….” (Dr N Collop, editorial)
CPAP as a Therapeutic Trial
(Senn O Chest 2006, n= 33)
• Autotitrating CPAP, 4-15 cm H20, was used as
•
the therapeutic trial
A successful trial was “yes” to
– Are you willing to continue CPAP treatment?
– Was objective CPAP use > 2 hours/night?
• All underwent PSG; sleep apnea was
•
•
considered an AHI of > 10
Excluded were those with CHF, OHS, underlying
lung disease, prior CPAP Rx, psych or illness,
language problems
Those who were diagnosed with OSA on basis
of TT had same outcomes as in-lab diagnosed.
Autotitrating CPAP
(Ayas N, Sleep 2004)
• Most commonly, increases pressure to eliminate
•
•
•
•
•
vibration of palate and soft tissue.
Now costs about the same as “straight” CPAP.
May improve compliance.
Results in lower pressure over all.
Can obviate the need for in-lab titration, in many
cases.
Is supplanting in-lab titration
Oral Appliances
(Kushida C, Sleep 2006)
 Indicated for patients with mild-to-moderate
obstructive sleep apnea who




prefer oral appliances to CPAP
do not respond to CPAP
are not appropriate candidates for CPAP
fail treatment attempts with CPAP (Kushida Sleep 2006)
 Not as effective as CPAP
 Lower blood pressure 3-4 mmHg (Otsuka Sleep
Breath 2006)
 Outperformed surgery in the only head-to
head trial.
Preferred to CPAP in head-to-head trials.
Do Oral Appliances Work?
Cochrane Database Syst Rev. 2006 Jan 25;(1):CD001106.
“CPAP is effective in reducing symptoms of
sleepiness and improving quality of life
measures in people with moderate and
severe obstructive sleep apnoea (OSA). It is
more effective than oral appliances in
reducing respiratory disturbances in these
people but subjective outcomes are more
equivocal. Certain people tend to prefer oral
appliances to CPAP where both are effective.
This could be because they offer a more
convenient way of controlling OSA.”
Sleep Apnea
Questions?