Sleep Apnea: What the internist needs to knowimupdateskw.com/presentation/dr-douglas/sleep-apnea... · 2019. 3. 24. · Treatment (PAP) benefits for OSA Sleepiness, QOL, cognition,

Sleep Apnea: What the internist needs to know

Updates in Internal Medicine:March 8th, 2019

Douglas Beach, MD, MPH

Pulmonary, Critical Care, and Sleep Medicine

Beth Israel Deaconess Medical Center

Objectives

Understand why sleep apnea is important particularly in terms of co-morbid conditions.

Understand what diagnostic tests do we use and why

Learn treatment options and the impact of treating sleep apnea on co-morbid conditions

CASE 1: Ms. M

56 y/o woman with rhinitis, hyperlipidemia and HTN seen for routine follow up. No complaints. Gained 5 pounds since last year. Less active due to knee injury. Nonsmoker. Works FT.

Meds: statin, HCTZ, atenolol, lisinopril, fluticasone nasal spray

VS: BP 165/91, HR 80, RR 12, SpO2 97%BMI 31 kg/m2

Should you be thinking about sleep apnea?

Why should you care about sleep apnea?

Most common sleep d/o

Prevalence estimates in US adults 18-23 million (moderate-severe)

1/5 mild, 1/15 moderate to severe

20-30% ♂ 10-15% ♀

> 80% remains undiagnosed

Increases with Age, BMI

Major driver of health care cost

Somers et al. Am Coll Cardiol 2008; Young et al. AJRCCM 2002; Tishler et al. JAMA 2003; Kapur et al. Sleep Breath 2002; Peppard et a. Am J Epidemiol 2013

Sleep

apnea

Sleep

fragmentation

Arousals

Sleep deprivation

Hypoxemia

Hypercapnia

Intrathoracic

pressure

Functional consequences

Functional consequences

Excessive daytime sleepinessInsomniaDecreased QOLMVAs and workplace accidentsCognitive deficits

Malhotra and White. Lancet 2002; Somers et al. JACC 2008; Redline et al. AJRCCM

2010; Yaffe et al. JAMA 2011; Kang et al, Science 2009. Bratton et al.,JAMA 2015.

Mechanisms

Sympathetic activation

Inflammation

Endothelial dysfunction

Hypercoagulability

Left atrial enlargement

Fatty acid lypolysis

Oxidative stress

Disease manifestations

Sleep

apnea

Sleep

fragmentation

Arousals

Sleep deprivation

Hypoxemia

Hypercapnia

Intrathoracic

pressure

Disease manifestations

Impaired glucose tolerance

Type 2 DM

HTN (systemic, pulmonary)

Atherosclerosis

Cerebral vascular disease

MI

CHF

Arrhythmias

Sudden cardiac death

Cognitive disorders

Malhotra and White. Lancet 2002; Somers et al. JACC 2008; Redline et al. AJRCCM

2010; Yaffe et al. JAMA 2011; Mehra et al., AJRCCM 2006; O’Connor et al., AJRCCM

2009; Kang et al, Science 2009; Buchner S et al. Eur Heart J. 2014;Circulation 2016.

Shared featuresOSA Metabolic

Syndrome

Hypertension*** **

Central obesity** ***

Insulin resistance** ***

Sympathetic

activation *** *Inflammation

** **Endothelial

dysfunction ** **Batsis JA et al. Clin Pharmacol Ther 2007

OSA prevalence in CVS patients

60%Stroke

Bazzano et al. Hypertension 2007; Haentjens et al. Arch Intern Med 2007; Pedrosa et al. Hypertension 2011; Redline et al. AJRCCM 2010; Mehra et al. AJRCCM 2006;

Bratton et al.,JAMA 2015.

CASE 1: Ms. M

56 y/o woman with rhinitis, hyperlipidemia and HTN seen for routine follow up. No complaints. Gained 5 pounds since last year. Less active due to knee injury. Nonsmoker. Works FT.

Meds: statin, HCTZ, atenolol, lisinopril, Flonase

VS: BP 165/91, HR 80, RR 12, SpO2 97%BMI 31 kg/m2

Should you be thinking about sleep apnea?(If not, why not?)

OSA: No perfect screening tool

History and physical examEpworth sleepiness scaleSTOP-BANGOvernight oximetry

Physical exam can suggest increased risk VS

Nasal and upper airway exam

Neck circumference

Signs of heart failure or other comorbid conditions

History can provide clues

even when overt sleep

symptoms are not present

Oropharyngeal, nasal, craniofacial features

Retrognathia/Micrognathia

Tooth wear

Dental malocclusion

Mallampati Classification

Likelihood of dozing or falling asleep1) Sitting and reading

2) Watching TV

3) Sitting, inactive in a public place

4) As a passenger in a car for an hour without a break

5) Lying down to rest in the afternoon when circumstances permit

6) Sitting and talking to someone

7) Sitting quietly after a lunch without alcohol

8) In a car, while stopped for a few minutes in the traffic

Total: 0–10 Normal range10–12 Borderline12–24 Abnormal

Epworth sleepiness scale

0 = would never doze

1 = Slight chance of dozing

2 = Moderate chance of dozing

3 = High chance of dozing

1) Do you snore loudly?2) Are you tired or sleepy during the

daytime? 3) Are you observed to stop breathing?4) Do you have high blood pressure?5) BMI ≥ 35 kg/m2

6) Age > 50 yo?7) Neck circumference > 40 cm?8) Gender male?

STOP-BANG questionnaire

Risk of OSA High if yes to ≥ 3 items Low if yes to < 3 items

Chung et al. Anesthesiology 2008.

CASE 1: MS. M

56 y/o woman with rhinitis, hyperlipidemia and HTN seen for routine follow up. No complaints. Gained 5 pounds since last year. Less active due to knee injury. Nonsmoker. Works FT.

Meds: statin, HCTZ, atenolol, lisinopril, Flonase

VS: BP 165/91, HR 80, RR 12, SpO2 97%BMI 31 kg/m2

On your questioning, reports loud snoring - bed partner sleeps in separate room. Never fully refreshed. Wakes 4 time/night to urinate. ESS 12

Exam: 16 inch/40 cm neck, MM 3, slight retrognathia.

Diagnosis

1.) What test would you recommend?

A. Overnight oximetry

B. Overnight attended PSG

C.Overnight portable limited channel sleep study (HST)

D.Arterial blood gas

E. Echocardiogram

1.) What test would you recommend?

A. Overnight oximetry

B. Overnight attended PSG

C.Overnight portable limited channel sleep study (HST)

D.Arterial blood gas

E. Echocardiogram

Patient selection for home study

Appropriate patients No contraindications (pulmonary, CHF, neuro)

High pretest probability

No other sleep disorder suspected

Assess non-CPAP treatment (for example: oral

appliance/positional therapy)

Portable Monitoring Task Force, Clinical Guidelines for the Use of Unattended Portable

Monitors in the Diagnosis of Obstructive Sleep Apnea in Adult Patients. JCSM 2007.

Should NOT get HST

Evaluate –

parasomnias, narcolepsy, REM behavior disorder

Dementia/physical issues limiting proper use without tech supervision

Not preferred but can be used if patient otherwise refuses or is unable to come to sleep lab

• CHF/Advanced pulmonary disease

• Suspected hypoventilation (HCO3 ≥ 28, persistent hypoxia)

• Suspected OSA with severe insomnia

What if the HST returns as “no sleep apnea”?

False negatives are possible

Disease burden is underestimated vs. in-lab PSG

AHI calculated based on recording, not time of sleep

Only apneas and events with 4% or 3% desaturations are scored

No EEG so events causing arousals are missed

Artifacts/missing data

Screening for Obstructive Sleep Apnea in Adults. US Preventive Services Task Force

Recommendation Statement. JAMA 2017.

Portable monitors: Home sleep tests

Lower cost, convenient

Limited: no EEG or EMG information

Snore

Nasal flow

Thorax effort

SpO2

HR

Apnea hypopnea index, AHI 4% Apneas + hypopneas / hour sleep

Marker of disease severity/hypoxia

Apnea hypopnea index, AHI 3% (i.e. 3% desaturation or associated with EEG arousal) Sometimes referred to as “alternative criteria”

Respiratory disturbance index, RDI All resp events / hour, regardless of desaturation

Marker of sleep fragmentation/UARS

Sleep apnea definitions

OSA severity based on AHI Mild: 5-15

Moderate: 15-30

Severe: ≥ 30

2.) What if Ms. M had excessive sleepiness (ESS 20/24), and the HST showed no sleep apnea?

A. Order an MSLT, since she probably has narcolepsy

B. Ask her to sleep more

C.Start a stimulant

D.Refer to sleep clinic

E. Repeat the HST or in-lab PSG

2.) What if Ms. M had EDS (ESS 20/24), and the HST showed no sleep apnea?

A. Order an MSLT, since she probably has narcolepsy

B. Ask her to sleep more

C.Start a stimulant

D.Refer to sleep clinic

E. Repeat the HST or in-lab PSG

Polysomnogram (PSG)

PSG multistage hypnogram

Oximetry banding vs. V-shaped

Desat

Obstructive apnea

Rapid eye movements

EEG arousal

Tachycardia

A. Auto continuous positive airway pressure (APAP)

B. Oral appliance

C. Weight loss

D. Stimulant medication

E. Nocturnal oxygen

3.) Ms. M’s HST shows OSA (AHI

32/hr, O2 nadir 79%). What

treatment(s) would you recommend?

A. Auto continuous positive airway pressure (APAP)

B. Oral appliance

C. Weight loss

D. Stimulant medication

E. Nocturnal oxygen

3.) Ms. M’s HST shows OSA (AHI

32/hr, O2 nadir 79%). What

treatment(s) would you recommend?

Patient education

Treat predisposing or modifiable factors

Weight loss

Treatment of nasal congestion

Avoidance of supine sleep

Avoidance of alcohol/sedatives

Treatment selection (symptomatic, moderate to severe OSA)

PAP

Treatment approach

APAP vs. in-lab titration

If only OSA is found, EVEN if severe, APAP is appropriate, but might change the settings

• 5-15 cm H20 usual empiric setting

• Higher if obese (8-20) cm H20

In-lab titration recommended if HST shows

• Baseline hypoxia

• Concern for hypoventilation

• Central / complex sleep apneas or periodic breathing

Randy Glasbergen

www.glasbergen.com

Positive airway pressure

Continuous-CPAP, Bilevel-BPAP, Auto-titrating-APAP

Gold standard / first-line therapy

Johnson and Johnson. Medical Devices: Evidence and Research. 2015.

Busetto et al. Chest. 2005; Philips et al. AJRCCM 2013.

Treatment (PAP) benefits for OSA Sleepiness, QOL, cognition, depression

Effect > more severe OSAbetter adherence

Hypertension

LVEF in CHF

Cardiac remodeling

Glucose parameters (data is variable)

Pulmonary hypertension

Bazzano et al. Hypert 2007; Haentjens et al. Arch Int Med. 2007; Patel et al.

Arch Int Med. 2003; Colish J et al.,Chest 2012; Babu et al. Arch Int Med. 2005;

Bratton et al.,JAMA 2015; Lee et al. Circulation 2016.

CVS events increased in untreated OSA

Marin et al. Lancet 2005

CPAP improves 24-hour BPAfter treatment

Time from wake and sleep onset (hours)

Me

an

blo

od

pre

ss

ure

(m

mH

g)

85

90

95

100

105

110

115

120

sub-therapeutic

therapeutic

wake 4 8 12 16 sleep 4 8

Before treatment

Me

an

blo

od

pre

ss

ure

(m

mH

g)

85

90

95

100

105

110

115

120

Time from wake and sleep onset (hours)

wake 4 8 12 16 sleep 4 8

sub-therapeutic

therapeutic

Pepperell et al. Lancet 2002.

Diagnosing/treating SDB reduces

readmission rates in cardiac patients

Kauta SR et a., JCSM 2014;10:1051-59.

N

CASE 2: EJ

49 y/o man with obese BMI (32 kg/m2), HTN, who has moderate OSA (AHI 4% 16). He presented with loud snoring, EDS, frequent awakenings, and naps. He was started on APAP 8-14 cm with a full face mask.

He returns to clinic and states that he is doing well with APAP. He reports nightly use. He still feels tired and notes no improvement in his sleep continuity. He does not have problems with his mask and does not report leaking as a problem.

A.Send him to see a sleep specialist

B.Schedule a lab titration

C. Start a stimulant medication

D. Look at his machine data

E. Ask about his sleep schedule

F. All of the above

1.) What should you do?

Online data trackingAirView (ResMed)

Encore (Respironics): APAP data

Interface Leak, mouth breathing, nasal patency, skin breakdown

PressurePositional disease, weight change, need for repeat titration

AerophagiaFlex, expiratory pressure relief, Bilevel

Another disorder / overlap conditions

Central or complex sleep apnea

Trouble shooting poor adherence

Alternative / adjunctive treatments

Oral appliances

Surgical treatment

Surgical weight loss

Adaptive-servo ventilation (non-systolic CHF with central/complex disease)

Nasal EPAP (Provent)

Upper airway stimulation

Expiratory positive airway pressure

(EPAP)

FDA approved

~$70/month

Improvement in ESS and AHI

maintained at 3 months compared to sham

Berry et al., Sleep. 2011.

Upper airway (hypoglossal nerve)

stimulation for OSA

Strollo et al. NEJM 2014

When / who to refer to sleep specialist?

Inconclusive testing

Severe OSA

Hypoxia out of proportion to degree of OSA

Shift workers/overlap conditions

Treatment intolerant / nonadherent

Suboptimal treatment response

Take Home Points

OSA is common / does not discriminate but prevalence is highest in co-comorbid conditions. Screen high risk patients!

Treatment impacts co-morbid conditions

Trouble shoot – if patient is intolerant or not improving, there is usually a reason.

Look at device data – efficacy, not just use duration matters

Involve sleep specialist

Thanks!

Special thanks to:

Melanie Pogach, MD

BIDMC Sleep Disorders Center