Quality Indicators for the Care of Chronic Obstructive Pulmonary

Disease in Vulnerable Elders

Eric Kleerup, MD

Key words: chronic obstructive pulmonary disease;

smoking cessation; vulnerable elderly; quality indicators;
oxygen therapy; bronchodilators; corticosteroids

hronic obstructive pulmonary disease (COPD) produces persistent respiratory symptoms of cough,
sputum production, wheezing, and, in later stages, dyspnea,
poor exercise tolerance, and symptoms and signs of
right-sided heart failure. The Global Initiative for Chronic
Obstructive Lung Disease, (GOLD)1 defines COPD as:
A disease state characterized by airflow limitation that is not fully
reversible. The airflow limitation is usually both progressive and
associated with an abnormal inflammatory response of the lungs
to noxious particles or gases.1

Small-airway disease (obstructive bronchiolitis) and

parenchymal destruction (emphysema) result in airflow
limitation perceived as dyspnea. Parenchymal destruction
also reduces the surface area for gas exchange, contributing
to exercise limitation late in disease. Many, although not
all, patients with COPD have chronic bronchitis (mucous
hypersecretion), a condition defined as the presence of
cough and sputum production for at least 3 months in each
of 2 consecutive years. A predominance of CD81 cells,
macrophages, and neutrophils characterize inflammation in
COPD. In contrast, CD41 (helper) cells and eosinophils
predominate in asthmatic airways.
Although COPD begins soon after the onset of smoking
(a habit that typically begins in the teenage years), primarily
older persons experience the effects of its morbidity and
mortality. Symptomatic COPD affects more than 5% to 8%
of the adult population. In 2000, 9.6% of those aged 65 to
74 and 10.6% of those aged 75 and older had self-reported
From the Division of Pulmonary, Critical Care Medicine and Hospitalists,
David Geffen School of Medicine at the University of California, Los Angeles,
California.
Address correspondence to Eric Kleerup, MD, 10833 Le Conte Ave., CHS
37-131, Los Angeles, CA 90095-1690. E-mail: ekleerup@mednet.ucla.edu
DOI: 10.1111/j.1532-5415.2007.01332.x

JAGS 55:S270S276, 2007

r 2007, Copyright the Authors
Journal compilation r 2007, The American Geriatrics Society

physician-diagnosed lifetime emphysema or chronic bronchitis.2 Approximately 3.2 million Americans aged 65 and
older have COPD.3 In 2000, the annual COPD death rate
was 43.1 per 100,000 population for those aged 55 to 64,
171.2 for those aged 65 to 74, and 449.7 for those aged 75
and older.2 Chronic lower respiratory diseases are the
fourth leading cause of death in women (269.4) and
the third leading cause in men (353.4) in the United States
for people aged 65 and older.4 COPD is increasing in prevalence and incident mortality worldwide.1,5 Between 1980
and 2000, the overall death rate for COPD increased 67%.
COPD as a primary diagnosis resulted in 4.2 million
physician office and hospital outpatient visits and 5.5 million emergency department visits for patients aged 65 and
older in 2000. The estimated annual rate of hospitalization
for COPD is higher for people aged 65 and older than
for younger patients. COPD also affects quality of life for
many people. Eight percent of COPD patients self-report
activity limitationFtwice the rate of those without
COPD.2 COPD is projected to be the fifth leading cause
of disability-adjusted life years lost worldwide by 2020.
Finally, decreased pulmonary function is an independent
risk factor for coronary heart disease.6

METHODS
Articles were identified through reference mining and from
the authors files on COPD in older persons. A total of 111
articles were considered in this review, and 13 guidelines
were identified using a Web search. Three additional articles
were included after peer review.
RESULTS
Of the 13 potential quality indicators, 10 were judged valid
according to the expert panel process, and one new
indicator was developed (see the quality indicators on pages S464S487 of this supplement); three indicators were
rejected. The literature summaries that support each of the
indicators judged to be valid in the expert panel process are
described.
Evaluate Respiratory Symptoms
1. IF a vulnerable elder (VE) presents with noncardiac
exertional dyspnea, chronic cough ( 6 months), wheeze

0002-8614/07/$15.00

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OCTOBER 2007VOL. 55, NO. S2

or two or more episodes per year of bronchitis, THEN he or

she should have spirometry, BECAUSE an early diagnosis
of COPD may lead to more-effective interventions.

Supporting Evidence
Early intervention with smoking cessation reduces the progression of COPD and mortality.7,8 Theoretically, making a
diagnosis of early COPD could lead to better intervention
with smoking cessation. Physiological feedback such as
spirometry may improve quitting rate or abstinence, but
this remains unproved.9 No clinical trial has demonstrated
that screening spirometry leads to better clinical outcomes,
but a recent review concluded that there was insufficient
evidence that case-finding spirometry screening for COPD
substantially improves smoking cessation rates, allowed
early treatment that altered the effectiveness of existing
therapies for COPD, or forecasted future respiratory impairment better than symptoms, especially dyspnea.10,11
The diagnosis of COPD generally occurs late in
the natural history of the disease. Incompletely reversible
spirometric obstruction essentially defines COPD. According
to the GOLD guidelines, COPD is a disease state characterized by airflow limitation that is not fully reversible. The
airflow limitation is usually both progressive and associated
with an abnormal inflammatory response of the lungs
to noxious particles or gases.1 Diagnosis and staging
of COPD severity in the GOLD guidelines (Table 1) uses
postbronchodilator forced expiratory volume in 1 second
(FEV1). The major COPD guidelines1,12,13 and a National
Institutes of Health consensus statement14 recommend
spirometry for smokers aged 45 and older or individuals
with respiratory symptoms such as chronic cough, episodic
wheezing, and exertional dyspnea to detect airways
obstruction due to asthma or COPD.
Table 1. Classification of Severity of Chronic Obstructive
Pulmonary Disease
Stage

0: At risk
I: Mild

II: Moderate

III: Severe

IV: Very severe

Characteristics

Normal spirometry
Chronic symptoms (cough, sputum production)
FEV1/FVC o70%
FEV1 80% predicted
With or without chronic symptoms
(cough, sputum production)
FEV1/FVC o70%
50% FEV1 o80% predicted
With or without chronic symptoms
(cough, sputum production)
FEV1/FVC o70%
30% FEV1 o50% predicted
With or without chronic symptoms
(cough, sputum production)
FEV1/FVC o70%
FEV1 o30% predicted or FEV1
o50% predicted plus chronic respiratory failure

Note: Classification based on postbronchodilator FEV1 (forced expiratory

volume in 1 second).
 Arterial partial pressure of oxygen less than 8.0 kPa (60 mmHg) with or
without arterial partial pressure of carbon dioxide greater than 6.7 kPa
(50 mmHg) while breathing air at sea level.
FVC 5 forced vital capacity.

QUALITY INDICATORS FOR COPD IN VULNERABLE ELDERS

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More than 80% of individuals aged 65 to 94 can perform adequate spirometry.15 Those who cannot perform
adequate spirometry have lower activity of daily living (5.5
vs 5.8), instrumental activity of daily living (5.9 vs 6.8), and
Mini-Mental State Examination (25 vs 28) scores.15
Because almost all errors in spirometry result in a false
low value, using it for its negative predictive value obviates
many of the concerns about quality or misinterpretation of
results.16 Population screening in Poland found that
fewer than 60% of individuals aged 40 and older with a
10 pack-year history of smoking had normal spirometry.17
In a general practice study in Brussels of patients aged 35 to
70, 7.4% had previously unknown obstructive lung disease
(asthma or COPD), and 42% would not have been detected
according to questionnaire without spirometry.18
FEV1 (odds ratio (OR) of death 5 2.08 per 10% decrease, 95% confidence interval (CI) 5 1.612.63) and
forced expiratory flow between 25% and 75% of FVC
(FEF2575%) (OR of death 5 2.40, 95% CI 5 1.543.76) are
the best spirometric predictors of mortality from COPD.19
The BODE index combines Body mass index, FEV1
(Obstruction), Dyspnea, and Exercise capacity to predict
mortality in COPD better than spirometry alone.20 Using
the GOLD criteria of FEV1/forced vital capacity (FVC) of
less than 70% leads to overdiagnosis of obstruction because
of an age-related decline in FEV1/FVC, and the lower limit
of normal approach is likely preferable.21
A cost-effective alternative is to screen with a peak flow
meter (sensitivity 72.7%, 95% CI 5 67.078.6; specificity
81.1%, 95% CI 5 79.782.5) and confirm with spirometry,22,23 although peak expiratory flow is effort dependent,
and the false-positive rate in comparison with spirometry is,
at a minimum, 17.1%.22,23 On physical examination,
wheeze (likelihood ratio present:absent, 2.9:0.8), and
forced expiratory time of 9 seconds or longer (likelihood
ratio present:absent, 4.6:0.8) are insufficient even in
combination to diagnose obstruction.24
Parenchymal destruction (emphysema) identified using
high-resolution computed tomography may not be associated with airway obstruction as measured using spirometry
in early COPD.25 Screening using high-resolution computed tomography has not been evaluated for COPD, but its
presence might be noted on screening scans for lung cancer
or coronary artery calcifications.

Smoke-Free Environment
2. IF a VE with COPD lives with others who smoke, THEN
the patient, smoker, or both should be counseled to eliminate smoking in the home, BECAUSE this encourages
smoking abstinence and reduces recidivism in former smokers and may reduce COPD exacerbations.
Supporting Evidence
Most often, the argument for a smoke-free environment is
based on the risk for employees (e.g., bartenders, flight
attendants) developing disease, and this may be valid
for healthcare institutions. It is likely that environmental
tobacco smoke is a risk factor for lung cancer, COPD,
asthma severity, and hospitalizations,2629 although there is
debate as to whether spousal smoking is a risk factor.30
VEs who reside in an institution that permits smoking may be viewed as the equivalent of employees regarding

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ERIC KLEERUP

exposure, and hence a smoke-free environment is rational.

Someone with existing COPD may be more sensitive to
environmental tobacco smoke and have less lung reserve,
although there are no experimental data to prove or refute
this concept.31 The World Health Organization (WHO)
Framework Convention on Tobacco Control provides for
protection from exposure to tobacco smoke in indoor
workplaces, public transport, indoor public places, and as
appropriate, other public places.32 The WHO recommends
progressive provision of a supportive environment for
smoking cessation, ranging from a minimum of 100%
smoke-free hospitals to an ideal of 100% of all public places
and workplaces smoke free with enforcement.33
In the home, the argument is more difficult, although
still rational. Twenty-two percent of ex-smokers hospitalized for COPD exacerbations were exposed to environmental tobacco smoke at home.34 In those contemplating
quitting smoking, a complete household ban of smoking resulted in greater probability of a quitting attempt (OR 5 2.0,
95% CI 5 1.03.9) and decreased relapse (hazard ratio
(HR) 5 0.5, 95% CI 5 0.20.9).35 A relative with COPD or
lung cancer does not necessarily motivate smokers to quit
smoking.36

Smoking Status
3. IF a VE with COPD is new to a primary care practice,
THEN smoking status should be documented, and if the
patient ever smoked, smoking status should be assessed
annually, BECAUSE smoking worsens COPD and identification of current smokers among patients with COPD
is a prerequisite to offering smoking cessation assistance.
Counseling can contribute to smoking cessation, and
quitting smoking stops the progression of COPD and
reduces mortality.
Supporting Evidence
Tobacco smoking causes COPD. Smoking cessation is the
only proven intervention that prevents progression of
COPD and reduces mortality.7,8 Clinicians and healthcare delivery systems must institutionalize the consistent
identification, documentation and treatment of every tobacco user at every visit, according to the U.S. Public
Health Service (USPHS) Report, Treating Tobacco Use
and Dependence: A Clinical Practice Guideline (www.
surgeongeneral.gov/tobacco/default.htm).37 The Ambulatory
Care Quality Alliance recommends the percentage of patients
who were queried about tobacco use as a clinical performance
measure for ambulatory care.38
Identification of active smokers is key to implementing
a smoking cessation intervention. More than 20% of current smokers had not been asked their smoking status in
2003 by their healthcare provider.39 Smokers seldom volunteer smoking status or recidivism if they are precontemplative regarding quitting. Having a tobacco use status
identification system in place results in an increase in the
rate of clinician intervention with patients who smoke from
38.5% to 65.6% (OR 5 3.1, 95% CI 5 2.24.2).37 A small
number of studies suggest that this translates to an increase
in patient-reported abstinence from 3.1% to 6.4%
(OR 5 2.0, 95% CI 5 0.84.8).37 Caution must be exercised, because self-report of smoking abstinence does not
correlate with biological verification 24% to 40% of the

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time.40 Current smoking status alone is neither sensitive to

nor specific for the detection of COPD,41 but smoking cessation also has many benefits outside the realm of COPD. In
elderly people, 10.1% of men and 8.6% of women are current smokers.42 Of daily smokers, 35% of Americans aged
65 to 74 and 27% aged 75 and older attempted to quit in
the prior year.43

Smoking Cessation
4. IF a VE with COPD is a current smoker, THEN counseling to quit smoking should be documented annually,
BECAUSE smoking cessation is the only intervention that
prevents further decline in lung function in patients with
early COPD, and it reduces the risk of death, heart disease,
and lung cancer.
Supporting Evidence
Tobacco smoking causes COPD. Smoking cessation is the
only intervention shown to prevent progression of COPD
and reduces mortality.7,8
All major COPD guidelines recommend smoking cessation. The USPHS Clinical Practice Guideline37 concludes
that it is essential that clinicians and healthcare delivery
systems institutionalize the consistent identification, documentation, and treatment of every tobacco user seen in
a healthcare setting. The Ambulatory Care Quality Alliance
recommends the percentage of patients who received advice
to quit smoking as a clinical performance measure for ambulatory care.38
Brief tobacco-dependence treatment is effective, and
every patient who uses tobacco should be offered at least
brief treatment. There is a strong doseresponse relationship between the intensity of tobacco-dependence counseling and its effectiveness. Three types of counseling and
behavioral therapies are especially effective and should be
used with all patients attempting tobacco cessation:
 Provision of practical counseling (problem solving and
skills training): OR 5 1.5, 95% CI 5 1.31.8
 Provision of social support as part of treatment (intratreatment social support): OR 5 1.3, 95% CI 5 1.11.6
 Help in securing social support outside of treatment
(extratreatment social support): OR 5 1.5, 95%
CI 5 1.12.1
In general, increasing the intensity and duration of smoking
cessation intervention counseling improves success, with a
plateau after longer than 30 minutes.37 Likewise, increasing
the number of sessions increases the effectiveness.37 Nonphysician caregivers can also provide counseling. A combination of physician advice, group support, skills training,
and nicotine replacement therapy achieved a quit rate of
35% at 1 year and a sustained quit rate of 22% at 5 years,
perhaps the highest reasonable expectation.7
The British National Institute for Clinical Excellence
guidelines suggest that nicotine replacement results in an
increase in 12-month abstinence from 10% to 17%
(OR 5 1.69, 95% CI 5 1.571.82) and bupropion from
9% to 19% (OR 5 2.05, 95% CI 5 1.452.91) over counseling alone.44 The USPHS Clinical Practice Guideline37
recommends that, except in the presence of contraindica-

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OCTOBER 2007VOL. 55, NO. S2

tions, one or more of the following should be used with all

patients attempting to quit smoking:
 Bupropion sustained release (SR) (OR 5 2.1, 95%
CI 5 1.53.0)
 Nicotine gum (OR 5 1.5, 95% CI 5 1.31.8)
 Nicotine inhaler (OR 5 2.5, 95% CI 5 1.73.6)
 Nicotine nasal spray (OR 5 2.7, 95% CI 5 1.84.1)
 Nicotine patch (OR 5 1.9, 95% CI 5 1.72.2)
Varenicline, recently released in the United States, may
be superior to bupropion SR (OR 5 1.77, 95% CI 5 1.19
2.63) and counseling alone (OR 5 2.66, 95% CI 5 1.72
4.11).45 The estimated cost of smoking cessation therapy
per life year gained is less than d3,000 (US$5,200).44
Use of two forms of nicotine replacement (e.g., patch
and gum) is more effective than a single agent (OR 5 1.9,
95% CI 5 1.32.6).37 There does not appear to be synergy
between bupropion and nicotine replacement.46,47 Assuming a 30% 1-year quit rate, for every 10,000 smokers treated with bupropion SR, 19 lives are saved, and 86 cases of
smoking-attributed morbidity are averted in a 5-year
period, whereas the risk of experiencing potentially serious
adverse events (seizures or hypersensitivity pneumonitis)
during treatment is 0.22%.48
In elderly people, 10.1% of men and 8.6% of women
are current smokers.42 Of daily smokers, 35% of Americans aged 65 to 74 and 27% aged 75 and older attempted to
quit in the prior year.43 There is little information specific to
elderly people for smoking cessation interventions.

Screening for Hypoxemia

5. IF a VE with COPD does not use supplemental oxygen
and has a postbronchodilator FEV1 of less than 50%
predicted (or unknown), THEN oxygenation (pulse oximetry
or arterial blood gas) should be assessed annually,
BECAUSE correction of resting hypoxemia extends life.
Supporting Evidence
Long-term supplemental oxygen reduces mortality in patients with COPD with hypoxemia at rest (arterial partial
pressure of oxygen (PaO2) o55 mmHg (8.0 kPa) with cor
pulmonale or PaO2 o50 mmHg (7.3 kPa)).4951 With
supplemental oxygen 15 hours per day, 5-year survival improved from 45% to 66%,50 and 12-hour use was inferior
to continuous (19-hour) use (OR for death 5 1.94).49
Hypoxemia in COPD also correlates with poorer cognitive function52 and periventricular white matter lesions
on brain magnetic resonance imaging.53 Long-term oxygen
therapy improves health-related quality of life.54 FEV1 less
than 50% predicted has a specificity of 91% and a negative
predictive value of 96% for identifying patients with COPD
with significant hypoxemia.55 The role of evaluating
oxygenation during sleep, exercise, or continuously during
daily activities is unclear.
Rapid-Acting Bronchodilator
6. IF a VE has COPD (GOLD stage I), THEN he or she
should be prescribed a rapid-acting bronchodilator,
BECAUSE short-acting bronchodilation can relieve dyspnea.

QUALITY INDICATORS FOR COPD IN VULNERABLE ELDERS

S273

Supporting Evidence
Guidelines recommend short-acting bronchodilators for relief of dyspnea in all but patients with the mildest COPD
and for the treatment of acute exacerbations.1,12,13,56 Food
and Drug Administration approval of bronchodilators for
COPD is based on FEV1 response, which is present in approximately 80% of patients with COPD with a mean age
of 64.57 Short-acting bronchodilators improve dyspnea,
hyperinflation, and exercise tolerance.58,59 Common
inhaled rapid-acting bronchodilators include albuterol,
ipratropium, and formoterol (a rapid onset long-acting
beta agonist).
In 1996, fewer than half of patients with COPD
received prescriptions for short-acting bronchodilators.60
Adherence to prescribed regimens is poor, even in
controlled clinical trials.61
The true risk of cardiovascular events attributable to
beta agonists6264 and anticholinergic agents65 remains
unclear and is certainly confounded by disease severity.
Inhaler Device Training
7. IF a VE with COPD is given a new inhaler device, spacer,
or nebulizer, THEN training to use the device should be
documented, BECAUSE specific training improves technique and optimizes the delivery of the drug to the lungs.
Supporting Evidence
When used correctly, inhalers used for treatment of lung
disease usually work well. Poor technique reduces deposition of medication in the airways, potentially reducing efficacy.66 One-quarter of patients make an error in using their
inhaler.67,68 Misuse appears to occur with similar frequency
in older patients (aged 5475).67 Training patients to use
inhalers takes time and expertise, but it reduces errors.
Patients trained by respiratory therapists made only 2.4
errors of 15 possible, compared with 6.7 errors made by
patients in the control group (Po.001).69
In monitoring pharmacological therapy at each visit,
the GOLD guidelines recommend evaluating inhaler technique with a question such as Please show me how you use
your inhaler.1 The British National Institute for Clinical
Excellence guidelines give a grade D (expert opinion) to the
evidence for initial inhaler training and rechecking at each
physician visit,13 although these guidelines state, Inhalers
should be prescribed only after patients have received
training in the use of the device and have demonstrated
satisfactory technique.
Long-Acting Bronchodilator
8. IF a VE with moderate to very severe COPD (GOLD
stage IIIV) has symptoms not controlled by as-needed
bronchodilator use or had two or more exacerbations in the
previous year, THEN a long-acting bronchodilator should
be prescribed, BECAUSE long-acting bronchodilators provide more-consistent relief of symptoms than repetitively
dosed short-acting bronchodilators and reduce the risk of
exacerbations.
Supporting Evidence
Long-acting inhaled anticholinergic medications reduce
COPD exacerbations, hospitalizations, and symptoms (typ-

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ERIC KLEERUP

ical mean age 64). Tiotropium reduces COPD exacerbation

(OR 5 0.74, 95% CI 5 0.660.83) and related hospitalizations (OR 5 0.64, 95% CI 5 0.510.82) with similar patterns evident for quality-of-life and symptom scales.70
Increases in FEV1 and FVC from baseline were significantly
larger with tiotropium than with placebo, ipratropium, and
long-acting beta-2 agonists over 6 to 12 months.70
Long-acting beta-2 agonists, including salmeterol
and formoterol, also improve FEV1, symptoms, and
exercise tolerance and reduce exacerbations (mean age
6264).7173 In individuals with a less than 15% increase
in FEV1 after albuterol, the success of long-acting beta
agonists is less clear.74
Exacerbations account for 35% to 45% of healthcare
costs for COPD.75 Long-acting bronchodilators (e.g., salmeterol, formoterol) are cost effective or have only slightly higher
cost than routine use of short-acting bronchodilators because
of the lower exacerbation rates.7678
The true risk of cardiovascular events attributable to
beta-agonists6264 and anticholinergic agents65 remains unclear and is certainly confounded by disease severity.
The choice between long-acting bronchodilators remains
unclear. For 3-year mortality, the risk compared with placebo, of long-acting beta-agonist alone (HR 5 0.857, 95%
CI 5 0.7101.035), inhaled corticosteroid plus long-acting
beta agonist (HR 5 0.811, 95% CI 5 0.6700.982), and
inhaled corticosteroid alone (HR 5 1.056, 95%, CI 5 0.883
1.264) in subjects with COPD with FEV1 less than 60%
does not appear to indicate any greater risk for long-acting
beta-agonists.79
Guidelines recommend long-acting bronchodilators for
persistent symptoms in COPD patients.1,12,13,56

Inhaled Corticosteroids
9. IF a VE with severe to very severe COPD (GOLD stage
IIIIV) had two or more exacerbations requiring antibiotics
or oral corticosteroids in the previous year, THEN (in addition to a long-acting bronchodilator) inhaled steroids (if
not taking oral steroids) should be prescribed, BECAUSE
inhaled corticosteroids reduce the frequency of exacerbations and mortality, and long-acting bronchodilators reduce
exacerbations and improve symptoms.
Supporting Evidence
Inhaled corticosteroids (steroids) reduce the risk of exacerbations in COPD 25% to 30% (relative risk (RR) 5 0.76,
95% CI 5 0.720.80).80,81 Exacerbation frequency (5% vs
15%) and severity are higher in GOLD Stage III and IV
COPD than in Stage I. The combination of inhaled steroids
and long-acting beta-agonists (RR 5 0.70, 95% CI 5 0.62
0.78) and likely long-acting anticholinergics further reduces
the risk of exacerbation. This is most apparent with lower
FEV1 values consistent with GOLD Stage III and IV. The
combined analysis of seven studies (mean age 59)8288 of
inhaled steroids in COPD shows lower mortality
(HR 5 0.73, 95% CI 5 0.550.96).89 Those who died were
older (64 vs 58; Po.001), had lower postbronchodilator
FEV1 (48% vs 59%; Po.001), and were more often male
(P 5.002). A more-direct study of mortality showed
no mortality benefit for inhaled steroids alone for overall
mortality at 3 years (HR 5 1.056, 95% CI 5 0.8831.264),
in spite of a reduction in exacerbations (HR 5 0.82, 95%

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CI 5 0.760.89), perhaps because of an increase in pneumonia incidence.79 Patients without exacerbations cannot
manifest a reduction in rate, and it is likely that they are at
lower risk for future exacerbations without intervention.
Individually, five large studies failed to show that inhaled corticosteroids reduced the rate of decline in lung
function in COPD.8286 Two meta-analyses show clinically
miniscule improvements in rate of decline in FEV1.90
Loss of bone mineral density and skin bruising remain a
concern for long-term use of inhaled corticosteroids.91,92
Exacerbations account for 35% to 45% of healthcare
costs for COPD.75 Inhaled corticosteroid treatment in patients with Stage III or IV COPD was estimated to cost
$17,000 per quality-of-life year gained, and treatment of
only Stage IV patients was estimated to cost $11,100 per
quality-of-life year gained.93

Long-Term Oxygen Therapy

10. IF a VE with COPD has an arterial partial pressure
of oxygen (PaO2) less than 55 mmHg or an oxygen saturation of less than 88% (not during an exacerbation),
THEN long-term oxygen therapy should be offered, BECAUSE long-term oxygen therapy prolongs life.
11. IF a VE with COPD is prescribed long-term oxygen
therapy, THEN encouragement to use it for 18 hours per day
or longer (including portable oxygen) should be documented,
BECAUSE 18 hours or longer is superior to shorter durations, and lack of portable oxygen may prevent patients
from meeting the goal of 18 hours or longer or discourage
them from continuing activities outside the home.
Supporting Evidence
Long-term supplemental oxygen of more than 15 hours daily
to maintain a PaO2 of greater than 60 mmHg reduces mortality in patients with COPD (baseline FEV1 o30% of predicted) with a PaO2 less than 55 mmHg (RR 5 0.61, 95%
CI 5 0.460.82).4951 With supplemental oxygen 15 hours
per day, the 5-year survival improved from 45% to 66%,50
and 12-hour use was inferior to continuous (19-hour) use
(OR for death 5 1.94).49 In other trials, in which resting mean
PaO2 was 60 mmHg or higher, no survival advantage was
seen (RR 5 1.16; 95% CI 5 0.851.58).94 Trials of patients
desaturating with exercise are underway.95
Most survey studies document poor adherence to the
recommended daily duration of oxygen use. In a Danish
study, 35% of patients used oxygen less than 15 hours
per day.96 In the Netherlands, patients averaged 13 hours
per day of oxygen use.97
ACKNOWLEDGMENTS
Patricia Smith provided technical assistance.
Financial Disclosure: The ACOVE project was supported by a contract from Pfizer Inc to RAND. Eric
Kleerup has conducted or is conducting studies of COPD or
smoking cessation for Almirall, Altana, Boehringer-Ingelheim, Dey, GlaxoSmithKline, Nabi, Novartis, Pfizer, and
Schering-Plough. Pfizer represents 15% of these grants.
Author Contribution: Eric Kleerup conducted the
literature review, analysis, and manuscript preparation
within the framework developed by RAND for the ACOVE
project.

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OCTOBER 2007VOL. 55, NO. S2

Sponsors Role: The funding source had no role in

the design, analysis, or interpretation of the study or in the
preparation of the manuscript for publication.

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