Sleep Apnea and Commercial Drivers A CLINICAL PERSPECTIVE

Sleep Apnea and Commercial Drivers A CLINICAL PERSPECTIVE Outline 1. Presentation of OSA 2. Pathophysiology of OSA 3. Effects on the Body 4. ...
Author: Moses Baker
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Sleep Apnea and Commercial Drivers A CLINICAL PERSPECTIVE

Outline 1.

Presentation of OSA

2.

Pathophysiology of OSA

3.

Effects on the Body

4.

Effects on Alertness

5.

Testing for OSA

6.

Outcomes

7.

Summary

Clinical Presentation

Recognizing and Managing Sleep Apnea in Primary Care. Journal of Clinical Psychiatry. 2009; 11 No 6: 330-338

Upper Airway Anatomy- Oropharynx 

Composed of numerous muscles and soft tissue but lacks rigid or bony support



Collapsible portion



Ability to change shape and close momentarily for speech and swallowing



Opportunity for collapse at inappropriate times, such as during sleep The Proceedings of the American Thoracic Society, 5:144-153 (2008)

Pathophysiology 

What causes OSA?  During sleep, generalized decrease of muscle tone of the upper airway  Most pronounced in REM  In patients with a small airway, repetitive airway collapse can cause numerous dips in oxygen levels  Repeated airway collapse can cause numerous brief awakenings which lead to daytime fatigue

Pathophysiology •

Apnea: Complete



cessation of airflow

Hypopnea: 30%

reduction in airflow plus at least 4% oxygen desaturation



Respiratory Effort-Related Arousal: Mild

airflow reduction which results in an arousal but no desaturation

Patent Upper Airway No obstruction

Partially Blocked Upper Airway Likely snoring •

Hypopnea



Respiratory EffortRelated Arousal

Obstructed Upper Airway Apnea •

Possible O2 desaturations

Obstructive Sleep Apnea. NEJM 2006; 334 No 2: 99-104

Outline 1.

Presentation of OSA

2.

Pathophysiology of OSA

3.

Effects on the Body

4.

Effects on Alertness

5.

Testing for OSA

6.

Outcomes

7.

Summary

Sleep Heart Health Study- Hypertension

Sleep Heart Health Study: Sleep Disordered Breathing and Cardiovascular Risk: Cross Sectional Results of the Sleep Heart Health Study AJRCCM. 2001; Vol 163, 19-25

SHHSMortality Compared to those without OSA all-cause OR for mortality in mild OSA was 0.93, 1.17 in moderate OSA, and 1.46 in severe OSA

Sleep Disordered Breathing and Mortality: A Prospective Cohort Study

Tracy Morgan •

Limousine van rear-ended by Wal-Mart driver



Driver charged with vehicular homicide



Driver had not slept “in excess of 24 hours”

Cognitive impairment from going without sleep for 24 = BAC of 0.10%

Drowsy Driving- Screening 

“Obstructive sleep apnea increases the risk of motor vehicle crashes by 500 to 700 percent and raises medical costs. Schneider Trucking recently reported that introduction of a screening and treatment program for obstructive sleep apnea among drivers in its trucking fleet reduced fatiguerelated truck crashes by 30 percent, cut medical costs in treated drivers by 58 percent, and increased its driver retention rate.” Charles Czeisler, MD, professor of sleep medicine division at Harvard Medical School, in a Boston Globe editorial, 2009

Driving Risks for patients with Untreated OSA

The Association between Sleep Apnea and the Risk of Traffic Accidents, NEJM. 1999; 340: 847-51

Driving Risks- Accident Severity 

783 patients, 783 matched controls



71% male, average AHI of 22, Epworth 10



Reviewed records for motor vehicle crashes in 3 yrs prior to sleep study



Relative Risk of 2.6 for mild,1.9 for moderate, 2.0 for severe OSA



MVC associated with personal injury, RR: 4.8, 3.0, 4.3



80% of severe MVCs involved patients with OSA Mulgrew et al, Thorax, 2008, 63: 536-541

Outline 1.

Presentation of OSA

2.

Pathophysiology of OSA

3.

Effects on the Body

4.

Effects on Alertness

5.

Testing for OSA

6.

Outcomes

7.

Summary

Testing for OSA Polysomnography • Attended, in-lab • 12-13 channels Home Sleep Testing • 4-8 channels

Polysomnography •

Pros Gold Standard Assess for multiple sleep disorders/abnormalities

Polysomnography •

Cons Expensive- $750-$1900 ‘Unnatural'

Polysomnography Monitors nasal pressure, airflow, heart rate, O2 sat, respiratory effort • Brain wave activity (EEG) • Eye movements (REM sleep) • Leg movements • Muscle tone • (End-tidal CO2 monitoring)

Home Sleep Testing Monitors nasal pressure, airflow, heart rate, O2 sat, respiratory effort • May measure peripheral arterial tone rather than nasal pressure/airflow

Really a sleep apnea test as does not measure ‘sleep’ (no EEG leads)

CleveMed SleepView Home Sleep Testing



Traditional HST unit



Type III unit



8 Channels



Chain-of-Custody feature available

WatchPAT 200

Cost Comparison In-lab PSG • $750-$1900 HST •

$200-$400

Polysomnography •

• • •

Allows diagnosis of OSA, CSA, periodic limb movements, nocturnal seizures, parasomnias, +/obesity-hypoventilation syndrome Provides sleep staging Diagnostic and therapeutic capability: able to initiate treatment (PAP, O2) Opportunity for education

Polysomnography With CPAP/BiPAP in place, used to demonstrate resolution of obstructive sleep apnea-hypopnea syndrome • Necessary for DOT certification/re-certification

Home Sleep Testing •

• • •

Allows diagnosis of OSA and CSA Does NOT provide sleep staging Unable to initiate treatment (PAP, O2) Less opportunity for patient education

As cannot verify sleep, may underestimate severity of apnea

Multiple Sleep Latency Test Measure of propensity to fall asleep • Five naps at 2-hr intervals •

Preceded by PSG the night before

• In a quiet, dark room, patient instructed to close eyes and to try to fall asleep • Used to showed resolution of excessive sleepiness following night of treatment with CPAP/BiPAP

Multiple Sleep Latency Test Now has a role in assessing treatment response, i.e. effectiveness of PAP • May be used in place of MWT Mean sleep latency= 10.4 +/- 4.3 min

Maintenance of Wakefulness Test “The MWT is a validated objective measure of the ability to stay awake for a defined period of time.” AASM • Four 40-min trials at 2-hr intervals while seated on bed in dimly lit room • Drug testing in a.m. • Instructions: stay awake as long as possible

Maintenance of Wakefulness Test “The primary purpose of the MWT is to document ability to stay awake following intervention.” AASM • Ideally performed after overnight PSG • Mean sleep latency 30.4 min +/- 11.2 min • Recent guidelines included use of MSLT to document adequate treatment response • No guarantee that results translate to work setting

HST vs. PSG in Diagnosis of OSA for Commercial Motor Vehicle Drivers Clinical •



Severe COPD, CHF, uncontrolled arrhythmia- PSG Comorbid sleep disorder- PSG

Regulatory • •

Guidelines indicate PSG to verify sleep Chain-of-Custody issues (changing)

Cost?

Treatment 



Mild 

Weight loss



Sleeping off your back



Ensuring nasal patency (nasal steroids)



Wedge pillow



Anti-snore shirt



Mandibular re-positioning device



CPAP



Stimulants

Moderate 

CPAP



Upper airway surgery



Stimulants (modafanil or methylphenidate) for residual fatigue

Treatment  Severe  CPAP/BiPAP  Maxillomandibular

Advancement surgery  Nocturnal supplemental O2 for patients unable to tolerate PAP  Stimulants  Minimization or avoidance of sedatives/narcotics, especially IV

Treatment Works Evidence shows decreases in mortality •

Protective in patients with AHI>20 CPAP and tracheostomy • Kryger et al, CHEST, 1988 •



CPAP decreases CV mortality •

Young et al, SLEEP, 2008

Treatment Works Cochrane Database Review on use of CPAP to treat OSA, 2006 Moderate-severe OSA •

Decreased sleepiness



Improved quality of life

Decreased blood pressure

Sleep Heart Health Study- Hypertension

Treatment Works •

Evidence also shows improvements in alertness • Risk of driving accidents normalizes with PAP treatment

MVCs reduced with CPAP 210 patients, mean age of 52 BMI 35.5, AHI 54 3 yrs before/after treatment with CPAP Untreated pts: more MVCs than controls CPAP→ MVCs reduced to level of controls  Treated

OSA pts no more accidents than ‘normals’

George CF, Thorax, 2001

MVCs reduced with CPAP 50 2

consecutive patients

 36

using CPAP regularly over 2 yrs

yrs after treatment with CPAP

 Compliant

Untreated

vs. non-compliant pts

pts: more MVCs than controls CPAP→ MVCs reduced to zero  Treated

OSA pts had no accidents

Findley et al, Amer J Resp Crit Care Med, 2000

Summary 1.

Presentation of OSA

2.

Pathophysiology of OSA

3.

Effects on the Body

4.

Effects on Alertness

5.

Testing for OSA

6.

Outcomes

Summary OSA results from upper airway collapse related to anatomical features and, often, obesity 2. OSA causes HTN; increases risk of cardiovascular morbidity; increases all-cause mortality and risk of driving accidents 3. In-lab PSG is recommended test for CMV drivers; growing role for Home Sleep Tests 4. Treatment is effective; compliance is marginal 1.

Summary 1. 2.

Treatment restores alertness to normal levels Most evidence focuses on CPAP

Questions?