sleep apnea: what the internist needs to...
TRANSCRIPT
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