Chronic Obstructive Pulmonary Disease: Patient Population: Objectives

Quality Department Guidelines for Clinical Care
Ambulatory
Chronic Obstructive Pulmonary Disease

COPD
Guideline Team Patient population: Adults with chronic obstructive pulmonary disease (COPD).
Team Leader
Objectives:
Davoren A Chick, MD
General Medicine 1. Provide a framework for management of chronic COPD and for the treatment of mild to moderate
Team Members acute exacerbations.
Paul J Grant, MD 2. Improve symptoms, quality of life and lung function while reducing morbidity and mortality for
General Medicine patients with COPD.
R Van Harrison, PhD
Learning Health Sciences Key Points
Amal Othman, MD
COPD is underdiagnosed and misdiagnosed. See Table 1 for an overview of diagnosis and
Family Medicine
management of COPD.
Sarah E Roark, MD
Pulmonary Medicine Do not perform population-wide screening for COPD. [III-C]
Meilan K Han, MD, MS Appropriate comprehensive treatment can improve symptoms and quality of life. [I-A]
Pulmonary Medicine
Consultant
Diagnosis
Tami L Remington, Consider COPD in any patient with dyspnea, chronic cough or sputum production. [I-C] Consider
PharmD early diagnostic case finding in persons with a history of inhalation exposures known to be risk
Pharmacy Services factors for COPD. [I-D]
Pulmonary function testing with post-bronchodilator assessment demonstrating a reduced FEV1/FVC
ratio is required for diagnosis. [I-C]
Initial Release
May 2010 Assess COPD severity by determining extent of airflow limitation (spirometry), symptom severity,
Content Last Reviewed and exacerbation history (Table 5). [I-C]
March 2012
Most Recent Major Treatment
Update
November 2017 Smoking cessation is the single most important intervention to slow the rate of lung function decline,
regardless of disease severity. [I-C]
Chronic medication management includes:
Ambulatory Clinical • Bronchodilators (beta-2 agonists and anticholinergics), selected based on symptoms and severity
Guidelines Oversight (Figure 1 & Table 7), with the goal of improving symptoms and functioning and reducing
Karl T Rew, MD exacerbations. [I-A]
R Van Harrison, PhD • Inhaled corticosteroids – consider adding to bronchodilators for patients with frequent
exacerbations despite bronchodilator therapy [I-A] or with features suggestive of asthma-COPD
Literature search service: overlap. [II-D]
Taubman Health Sciences • Supplemental oxygen if resting oxygen saturation ≤ 88% or PaO2 ≤ 55 mm Hg. [I-A]
Library
Acute exacerbation medication management includes bronchodilators (beta-2 agonists and
anticholinergics) [I-C], systemic corticosteroid therapy [I-A], and antibiotics [II-A] based on
For more information clinical indications (Table 9). Empiric antibiotics are recommended for patients with increased
734-936-9771
sputum purulence plus either increased dyspnea or increased sputum volume. [I-A] Sputum culture
www.uofmhealth.org/provid is not routinely recommended. [III-D]
er/clinical-care-guidelines
Pulmonary rehabilitation should be considered for all patients with functional impairment. [I-A]
© Regents of the Surgical and minimally invasive options include bullectomy, lung volume reduction procedures, and
University of Michigan lung transplantation. [II-B] Life expectancy should be incorporated into shared decision making
These guidelines should regarding the potential benefits of surgery. [II-D] Pulmonary consultation is recommended prior
not be construed as
including all proper
to consideration of invasive options. [I-D]
methods of care or Palliative care should be discussed with patients with advanced COPD. Doing so may help limit
excluding other acceptable
methods of care reasonably
unnecessary and burdensome personal and societal costs and invasive approaches. [I-C]
directed to obtaining the * Strength of recommendation:
same results. The ultimate I = generally should be performed; II = may be reasonable to perform; III = generally should not be performed.
judgment regarding any
specific clinical procedure Levels of evidence for the most significant recommendations
or treatment must be made A = systematic reviews of randomized controlled trials; B = randomized controlled trials; C = systematic review of non-
by the physician in light of randomized controlled trials or observational studies, non-randomized controlled trials, group observation studies (eg,
the circumstances cohort, cross-sectional, case control); D = individual observation studies (case or case series), E = opinion of expert panel.
presented by the patient.
1
Table 1. Overview of Diagnosis and Management of Patients with COPD (Continues on next page)
Diagnosis
Clinical suspicion. Risk factors of exposure to smoking (≥ 10 pack-years) or inhalation irritants. Chronic cough, sputum
production, dyspnea, or acute respiratory symptoms requiring therapy. (See symptoms and signs in Table 2.)
Pulmonary function test. Required for diagnosis. Post-bronchodilator FEV1/FVC < 0.70 is required to demonstrate airflow
obstruction that is not fully reversible. (FEV1 = forced expiratory volume in the first second; FVC = forced vital capacity.)
Alternative diagnoses. If pulmonary function testing is negative or equivocal, consider alternative diagnoses (Tables 3 & 4) or
consider referral to pulmonary specialist.
Alpha-1 antitrypsin level. Assess for deficiency in settings of clinical suspicion: age 45 or less, absence of other risk factors or
severity of disease out of proportion to risk factors, prominent basilar lucency, family history, or bronchiectasis.
Initial Assessment, Patient Education, Prevention, and Treatment
COPD severity assessment (Table 5).
• Assess extent of airflow limitation by spirometry.
• Have the patient assess symptom severity using either the mMRC (Modified Medical Research Council) Dyspnea Scale or
the COPD Assessment Test.
• Assess frequency of past exacerbations.
• For patients with severe disease (FEV1 < 50%), obtain oximetry on room air. A resting oxygen saturation ≤ 88% indicates
very severe disease (Table 8).
• Identify comorbidities likely to affect disease severity and care, eg, “asthma overlap,” cardiovascular disease, diabetes.
Patient education. Provide an educational overview of COPD pathology, causes, diagnosis, staging, exacerbation triggers, and
treatment options (Table 6).
Smoking cessation. Encourage all smokers to quit, and assist them in quitting. (See UMHS Tobacco Treatment Guideline.)
Inhaled irritant control. Identify and review how to avoid triggers and exposures known to cause or aggravate COPD:
smoking, second-hand smoke, occupational fumes and chemicals, indoor air pollution (eg, cooking with biomass fuels),
outdoor air pollution, infection.
Medical therapy. Select bronchodilator and consider inhaled corticosteroid therapy based on COPD severity by stage and by
current frequency of exacerbations (Figure 1). Table 7 provides dose and cost information for medications.
Oxygen therapy. Initiate long-term oxygen for patients with resting oxygen saturation < 88% (Table 8).
Chronic Disease Management
Vaccinate against influenza and pneumococcus.
• Provide annual influenza vaccination for all COPD patients.
• If diagnosed before age 65, provide pneumococcal 23-valent vaccine at the time of diagnosis.
• At age 65, provide pneumococcal 13-valent vaccination (at least 12 months after 23-valent vaccination).
• 12 months after 13-valent vaccination, provide 23-valent pneumococcal vaccine if five years have passed since initial 23-
valent vaccination. (Wait 5 years from initial 23-valent vaccination to provide a booster 23-valent vaccine).
Pulmonary rehabilitation. Refer patients with functional limitations to pulmonary rehabilitation.
Medical therapy. Monitor patient adherence and correct inhaler technique. Prescribe long-acting bronchodilators for patients
with frequent symptoms. For patients with exacerbations requiring systemic steroids or antibiotics within the past year and
FEV1 < 50% predicted, consider adding inhaled corticosteroid therapy (Figure 1). Table 7 provides dose and cost information.
Oxygen therapy. Titrate long-term oxygen for patients with resting oxygen saturation ≤ 88% to achieve resting and exercise
oxygen saturation ≥ 90% (Table 8).
Inhaled irritant control. Provide ongoing smoking cessation counseling and irritant control counseling.
Monitor comorbidities. Consider increased risk for cardiovascular disease, depression, anxiety, and other smoking related
diseases such as osteoporosis and cancer. Monitor blood sugar control for diabetic patients on inhaled corticosteroids. Monitor
for glaucoma and cataracts for patients on inhaled corticosteroids.
Refer to COPD specialist. For patients with alpha-1 antitrypsin deficiency, severe disease (FEV1 ≤ 50% or BODE score ≥ 5),
supplemental oxygen dependence, severe or frequent exacerbations, consider referral for co-management and consideration of
invasive treatment options.
End-of-life planning. Engage patients in shared decision making regarding goals of therapy and advance directives. For patients
with advanced COPD, consider palliative care.
2 UMHS COPD Guideline, November 2017

Table 1. Overview of Diagnosis and Management of Patients with COPD (continued)
Acute Exacerbation Management

Assess exacerbation severity. Determine severity based on history, physical, and pulse oximetry.
Consider etiology. Assess clinically for risk of pneumonia, congestive heart failure, pulmonary embolism, or other causes of
respiratory decline. Consider chest radiograph if clinically indicated.
Determine care setting. Consider hospitalization for patients with marked symptoms, severe underlying disease, significant
complicating comorbidities, respiratory failure, uncertain diagnosis, or insufficient home support.
Medical therapy. Select bronchodilators, antibiotics, and corticosteroid therapy based on clinical indications with the goal of
reducing the frequency of future exacerbations (Table 9).
Oxygen therapy. Titrate oxygen for patients with resting oxygen saturation ≤ 88% to achieve resting oxygen saturation ≥
90% (Table 8).
Follow-up. If symptoms have not returned to baseline, consider repeat spirometry 4-6 weeks following exacerbation. Re-
evaluate necessity of oxygen therapy.
Table 2. Symptoms and Signs Suggesting COPD

Dyspnea that is: Sputum production:
Progressive Chronic sputum production (any pattern) with
Worse with exercise periodic exacerbations
Persistent Exposure to risk factors:
Associated with chest heaviness or air hunger
Tobacco smoke (≥ 10 pack years)
Chronic cough: Occupational dusts and chemicals
May be intermittent Smoke from home cooking and heating fuel
Morning pattern common
May be productive or unproductive
Table 3. Alternative Diagnoses for Chronic Cough and Dyspnea
Asthma Chronic aspiration Cystic fibrosis Sarcoidosis

Bronchiectasis Chronic sinusitis or rhinitis Interstitial lung disease Tuberculosis
Bronchiolitis obliterans Congestive heart failure Lymphangioleiomyomatosis Tumor
Table 4. Factors Differentiating Asthma and COPD*

Factors Asthma COPD
Age of onset Usually < 30 Usually > 40
Antibiotics for exacerbation Poor efficacy Good efficacy
Bronchodilator reversibility Complete or nearly so Partial
Family history Usually Uncommon
History of atopy Often Uncommon
Hypoxemia Rare (extreme distress) Common
IgE elevation Common Uncommon
Leukotriene modifier responsiveness Strong Usually weak
Lung function with therapy Near normal Chronically < normal
Polycythemia Rare Not uncommon
Progressive deterioration Uncommon Typical
Prominent cough Nocturnal, exercise Early morning
Purulent sputum Uncommon Typical
Smoking history Variable Usually
Steroid responsiveness Strong Usually weak
* Asthma-COPD Overlap Syndrome (ACOS) or Asthma-COPD Overlap (ACO) descriptions are emerging to
acknowledge patients with features of both diseases.1 Consider referring such patients to a pulmonologist.
Table 5. Aspects of COPD Severity
Diagnosis of COPD – Chronic Airflow Obstruction (spirometry)

Airflow obstruction post-bronchodilator (not fully reversible) of FEV1/FVC < 0.70
Extent of Airflow Limitation (spirometry)2

FEV1 %
Limitation predicted Symptoms
Mild ≥ 80% Individual may or may not be aware lung function is abnormal.
Moderate 50-79% Patients typically seek medical attention at this stage due to respiratory symptoms or an exacerbation.
Severe 30-49% Dyspnea, reduced exercise capacity, and repeated exacerbations impact quality of life.
Very severe < 30% Quality of life significantly impaired; exacerbations may be life-threatening.
Symptom Severity
Either dyspnea symptoms (mMRC) or symptom impact (CAT) can be used
mMRC (Modified Medical Research Council) Dyspnea Scale3

Score equivalent to point value for highest level question to which respondent answers “Yes.”
Dyspnea Query Score
Are you troubled by shortness of breath when hurrying on level ground or walking up a slight hill? 0
Do you have to walk slower than people of your age on level ground because of shortness of breath? 1
Do you ever have to stop for breath when walking at your own pace on level ground? 2
Do you ever have to stop for breath when walking about 100 yards (or after a few minutes) on level ground? 3
Are you too short of breath to leave the house or short of breath on dressing or undressing? 4
CATTM (COPD Assessment Test)4

For each item below, place a mark (X) in the box that best describes you currently. Be sure to select only one response for each question.
Example: I am very happy       I am very sad Score
I never cough       I cough all the time

I have no phlegm (mucus) in my chest at all       My chest is completely full of phlegm (mucus)
My chest does not feel tight at all       My chest feels very tight
When I walk up a hill or one flight of stairs, I       When I walk up a hill or one flight of stairs, I am
am not breathless very breathless
I am not limited doing any activities at home       I am very limited doing activities at home
I am confident leaving my home despite my       I am not at all confident leaving my home
lung condition because of my lung condition
I sleep soundly       I don’t sleep soundly because of my lung
condition
I have lots of energy       I have no energy at all
Total Score
Exacerbation Risk
During the past year, how many exacerbations occurred? How many of the exacerbations required hospitalization?
Low risk 0-1 exacerbations and 0 hospitalized exacerbations
Increased risk ≥ 2 exacerbations or ≥ 1 hospitalized exacerbation
Other Aspects of Severity

Oxygen, need for continuous – see Table 8
Comorbid conditions, eg, asthma (“asthma overlap”), cardiovascular, heart failure, diabetes, psychiatric disorders) – see text
Note: Aspects of disease severity are adapted from the GOLD 2017 report.2

Figure 1. Overview of COPD Management:
Patient Education, Preventive Care, Pharmacologic Therapy, and Pulmonary Rehabilitation
All patients with a diagnosis of COPD

(post-bronchodilator FEV1/FVC < 0.70)
Provide patient education, smoking cessation
counseling if smoking, influenza and pneumococcal
vaccines, and other relevant preventive care.
Assess:
• Symptoms (mMRC or CAT)
• Exacerbations in the prior year
(Table 5)
If
If If Symptoms: mMRC 0-1, CAT < 10
Symptoms: mMRC 0-1, CAT < 10 Symptoms: mMRC ≥ 2 or CAT > 10 Exacerbations: ≥ 2/year or
Exacerbations: < 2/year & no Exacerbations: with or without hospitalized exacerbation
hospitalized exacerbations then then
then • LAMA, or LAMA + LABA2 • LAMA, or LAMA + LABA, or
• As needed SABD 1, 2 • Pulmonary rehabilitation LABA + ICS
• Pulmonary rehabilitation
If persistent symptoms, If persistent symptoms or

If persistent exacerbations,
exacerbations,
then
then
• LAMA2 then
• LAMA + LABA + ICS
• Pulmonary rehabilitation • LAMA + LABA + ICS
Note: Adapted and expanded from the COPD Pocket Consultant, COPD Foundation Guide for Management of COPD, 2017.5
Abbreviations: ICS = inhaled corticosteroid, LABD = long-acting bronchodilator (includes LABA and LAMA), LABA = long-
acting beta-2 agonist, LAMA = long-acting muscarinic antagonist, SABD = short-acting bronchodilator (includes SABA and
SAMA), SABA = short-acting beta-2 agonist, SAMA = short-acting muscarinic antagonist. (Both LAMA and SAMA are
anticholinergics.)
1
1st line: albuterol (SABA). 2nd line: levalbuterol (SABA); consider if the patient has a history of tachyarrhythmia or is intolerant
to albuterol.
2
If “asthma overlap”, consider combination of ICS + LABA.

Table 6. Patient Education Overview
Acute exacerbation. Recognition of an acute exacerbation and an initial action plan

End of life. Advance directives and end-of-life planning
Inhaler technique. Correct administration technique, and proper oral care for patients using inhaled steroids
Mechanisms. Inflammation, structural changes in the airways, and systemic effects
Medications. Dosing, schedule, rationale
Signs. Exacerbation warning signs (eg, increased dyspnea, sputum production, or cough)
Smoking cessation. Ask, advise, assess, assist, and arrange follow up (the “5 A’s”)
Triggers. Exacerbation triggers (eg, tobacco smoke, occupational dust and chemicals, indoor and outdoor air
pollution) and trigger avoidance (including the importance of preventing infections with vaccination)
Table 7. Medications Commonly Used in Chronic Obstructive Pulmonary Disease

Usual Adult Starting Duration of Cost (30 days) a
Medication Brand Name Dose Action Generic Brand
Inhaled Bronchodilators
Beta-2 agonists
Short-acting beta-2 agonists (SABA)
Albuterol HFA (90 mcg per puff) b ProAir, 2 puffs inhaled every 4-6 4-6 h $10 $61
Proventil, h as needed
Ventolin
Albuterol nebulizer solution 0.083% NA 2.5 mg via nebulizer 4-6 h $20 NA
(2.5 mg/3 mL) every 6-8 h as needed
Levalbuterol HFA (45 mcg per puff) Xopenex 2 puffs inhaled every 4-6 4-6 h $10 $74
b, c
h as needed
Levalbuterol nebulizer solution Xopenex 0.63-1.25 mg via 4-6 h $10 $74
0.021%, (0.63 mg/3 mL), and nebulizer every 6-8 h
0.042% (1.25 mg/3 mL) b, c as needed
Long-acting beta-2 agonists (LABA)
Arformoterol nebulizer solution (15 Brovana 15 mcg via nebulizer 12+ h NA $470
mcg/2 mL) every 12 h
Formoterol nebulizer solution (20 Perforomist 20 mcg via nebulizer 12+ h NA $453
mcg/2 mL) every 12 h
Indacaterol DPI (75 mcg per Arcapta 1 inhalation daily 12+ h NA $231
inhalation) Neohaler
Salmeterol DPI (50 mcg per Serevent Diskus 1 inhalation twice daily 12+ h NA $225
inhalation)
(Continued on next page)

Table 7. Medications Commonly Used in Chronic Obstructive Pulmonary Disease (continued)
Anticholinergics
Short-acting muscarinic antagonist (SAMA)
Ipratropium bromide HFA (17 mcg Atrovent 2 puffs inhaled 4 times a 6-8 h $5 $360
per puff) b day
Ipratropium bromide nebulizer Atrovent 0.25-0.5 mg via nebulizer 6-8 h $5 $360
solution 0.02% (0.5 mg/2.5 mL) every 6-8 h
Long-acting muscarinic antagonists (LAMA)
Aclidinium DPI (400 mcg per Tudorza Pressair 1 inhalation twice daily 12+ h NA $174
inhalation)
Glycopyrrolate DPI (15.6 mcg per Seebri Neohaler 1 inhalation (1 capsule) 12+ h NA $426
capsule) twice daily
Tiotropium bromide DPI (18 mcg Spiriva Handi- 2 puffs (1 capsule) inhaled 24+ h NA $398
per capsule) haler daily
Tiotropium bromide SMI (2.5 mcg Spiriva 5 mcg (2 puffs) inhaled 24+ h NA $398
per puff) Respimat daily
Umeclidinium DPI (62.5 mcg per Incruse Ellipta 1 inhalation daily 12+ h NA $75
inhalation)
Combinations of anticholinergic and long-acting beta-2 agonist (LAMA)
Glycopyrrolate/ formoterol MDI Bevespi 2 puffs inhaled twice daily 12 h NA $361
(9/4.8 mcg per puff) b Aerosphere
Glycopyrrolate/ indacaterol DPI Utibron 1 capsule inhaled twice 24 h NA $368
(15.6/27.5 mcg per capsule) Neohaler daily
Ipratropium/ albuterol nebulizer Duoneb 3 mL via nebulizer 4 6-8 h $5 $37
solution (0.5/2.5 mg per 3 mL) times daily
Ipratropium/ albuterol SMI (20/100 Combivent 1 puff inhaled 4 times a 6-8 h NA $373
mcg per puff) Respimat d day
Tiotropium/ olodaterol SMI (2.5/2.5 Stiolto Respimat 2 puffs inhaled daily 24 h NA $368
mcg per puff)
Umeclidinium/ vilanterol DPI Anoro Ellipta 1 inhalation daily 12+h NA $96
(62.5/25 mcg per puff)
Inhaled corticosteroids e
Beclomethasone dipropionate HFA QVAR 1-4 puffs inhaled twice 12 h NA $169-226
(40 or 80 mcg per inhalation) b, f daily
Budesonide DPI (180 mcg per Pulmicort 1-2 inhalations twice daily 12 h NA $234
inhalation) Flexhaler
Budesonide nebulizer solution (0.5 Pulmicort 0.5-1.0 mg via nebulizer 12 h $6 $332
mg or 1.0 mg per 2 mL) Respules every 12 h
Fluticasone furoate DPI (100 or 200 Arnuity Ellipta 2 inhalations twice daily 24 h NA $185-385
mcg per inhalation)
Fluticasone proprionate HFA b (110 Flovent 1-2 puffs inhaled twice 12 h NA $247-385
or 220 mcg per puff) daily
Fluticasone proprionate DPI (100 or Flovent Diskus 1 inhalation twice daily 12 h NA $247-385
250 mcg per inhalation)
Mometasone DPI (100 mcg or 200 Asmanex 2 inhalations twice daily 12 h NA $226-325
mcg per inhalation) Twisthaler
Mometasone HFA b (100 mcg or 200 Asmanex 2 puffs inhaled twice daily 12 h NA $226-325
mcg per puff)
(Continued on next page)

Table 7. Medications Commonly Used in Chronic Obstructive Pulmonary Disease (continued)
Combinations of inhaled corticosteroid and long-acting bronchodilator
Budesonide/formoterol DPI (160/4.5 Symbicort 2 inhalations twice daily 12 h NA $226
mcg per inhalation) b
Fluticasone/salmeterol DPI (250/50 Advair Diskus 1 inhalation twice daily 12 h NA $151
or 500/50 mcg per inhalation)
Fluticasone/salmeterol HFA (115/21 Advair HFA 2 puffs inhaled twice daily 12 h NA $211
or 230/21 mcg per puff) b
Mometasone/formoterol DPI (100/5 Dulera 2 inhalations twice daily 12 h NA $212
or 200/5 mcg per inhalation) b
Oral medications
Azithromycin (250 mg or 500 mg Zithromax 250 mg orally once daily, $24 $846
tablets) or 500 mg orally three
times weekly
Roflumilast (500 mcg tablet) Daliresp 500 mcg orally daily NA $347
Oral corticosteroids: not routinely recommended
a
Cost = For brand drugs, Average Wholesale Price minus 10%. AWP from Red Book Online 8/10/17. For generic drugs,
Maximum Allowable Cost plus $3 from BCBS of Michigan MAC List, 8/1/17. Prices calculated for 30 day supply unless
otherwise noted.
b
HFA steroid inhalers may be used with a valved holding chamber type spacer.
c
May cause less tremor and tachycardia than albuterol, but at a higher price and with no difference in major clinical outcomes.
d
Not recommended as a first-line agent due to the inability to titrate the short-acting beta agonist component to the lowest
necessary dose while achieving a therapeutic anticholinergic dose.
e
All inhaled corticosteroids should be administered in combination with a long-acting bronchodilator.
f
FDA approved for asthma only. Included here because for some payers it is the only covered inhaled corticosteroid.
DPI = dry powder inhaler; HFA = hydrofluoroalkane metered dose inhaler; SMI = soft mist inhaler

Table 8. Indications for Continuous Use of Oxygen Therapy for Very Severe COPD a
Level of Continuous Use Oxygen

Evidence (at least 15 hours/day, with goal of resting oxygen saturation ≥ 90%)
Strong Resting PaO2 ≤ 55 mm Hg or resting oxygen saturation ≤ 88% b
Weak Resting PaO2 56-59 mm Hg (oxygen saturation 89%)b with any of the
following:
• peripheral edema suggesting congestive heart failure
• evidence of pulmonary hypertension
• polycythemia (hematocrit > 55%)
a
Criteria for Center for Medicare and Medicaid Services coverage.
b
Confirm PaO2 or resting oxygen saturation with two measurements over a 3-week period.
Table 9. Acute Exacerbation: Commonly Used Medications and Doses
Generic Name Brand Names Usual Adult Dose Cost (30 days) a
Generic Brand
Inhaled short-acting beta-2 agonists (SABA) [bronchodilator]

Albuterol HFA (90 ProAir, Proventil, 4-8 puffs inhaled every 20 min x 4 h NA $61 (all)
mcg/puff) Ventolin as needed, then 4-8 puffs inhaled
every 1-4 h as needed
Albuterol nebulizer 2.5-5 mg via nebulizer every 20 min $5 NA
solution; either x 3 doses, then 5-10 mg nebulized
0.083% ready to use every 1-4 h as needed
(2.5 mg/3 mL) or 0.5%
(2.5 mg/0.5 mL)
Levalbuterol tartrate Xopenex 2 puffs inhaled every 4-6 h as $10 $74
HFA (45 mcg/puff) needed
Levalbuterol nebulizer Xopenex 0.63-1.25 mg via nebulizer every 8 $182 $320
solution (1.25 mg/3 h as needed
mL ready to use, or
1.25 mg/0.5 mL)
Inhaled anticholinergic (short-acting muscarinic antagonist = SAMA) b [bronchodilator]
Ipratropium HFA (17 Atrovent 2-4 puffs inhaled every 6 h as NA $395
mcg/puff) needed
Ipratropium nebulizer Atrovent 500 mcg via nebulizer every 6 h as $18 NA
solution (500 mcg/2.5 needed
mL)
Oral corticosteroids c [anti-inflammatory]
Prednisone: 1, 2.5, 5, 10, 40 mg/day for 5-7 days. Regimens $6 $26
20, 50 mg tabs; 1 may vary in dosage strength and
mg/mL liquid duration
Prednisolone: 5 mg tabs; 40 mg/day for 5-7 days. Regimens $13 $35
1 mg/mL, 2 mg/mL 3 may vary in dosage strength and
mg/mL, 4 mg/mL duration
liquid
(Table continues on next page)

Table 9. Acute Exacerbation: Medications and Doses (continued)
Generic Name Brand Name Usual Adult Dosing Cost (30 days) a
Generic Brand
Antibiotics d
Patients without risk factors for poor outcomes e (in order of preference)
Azithromycin Zithromax 500 mg orally on day 1, then 250 mg $8 (tab) $63 (tab)
250, 500 mg tabs; orally daily on days 2-5 $12 (liquid) $131 (liquid)
100, 200 mg/5 mL liquid
Cephalosporins (2nd or 3rd generation)
Cefdinir Omnicef 300 mg orally twice daily $60 (tab) $276 (tab)
300 mg caps; $8 (liquid) $90 (liquid)
125, 250 mg/5 mL liquid
Cefpodoxime NA 200 mg orally twice daily $480 (tab) NA
100, 200 mg tabs; $79 (liquid) NA
100 mg/5 mL liquid
Cefprozil NA 500 mg orally twice daily $122 (tab) NA
250, 500 mg tabs; $60 (liquid) NA
250 mg/5 mL liquid
Doxycycline hyclate Vibramycin capsule 100 mg orally twice daily $38 $645
100 mg tabs
Doxycycline calcium Vibramycin syrup 100 mg orally twice daily NA $452
50 mg/5 mL liquid
Trimethoprim/sulfamethoxazole Bactrim, Septra 160/800 mg (DS tablet) orally twice $14 (all tabs) $104
80/400, 160/800 mg tabs; Sulfatrim (liquid) daily NA
40/200 mg/5 mL liquid $240 (liq) NA (liq)
Patients with risk factors for poor outcomes e (no particular order)
Amoxicillin/clavulanate Augmentin 500 mg orally every 8 h or 875 mg $62 (tab) $208 (tab)
250/125, 500/125, 875/125 mg orally every 12 h $20 (liq) $62 (liq)
tabs; 200/28.5 mg/5 mL,
400/57 mg/5 mL liquid
Levofloxacin Levaquin f 500 mg orally daily $12 (tab) $973 (tab)
250, 500, 750 mg tabs; $17 (liq) $408 (liq)
25 mg/mL liquid
Patients at risk for infection with Pseudomonas aeruginosa g (no particular order)
Levofloxacin Levaquin 750 mg orally daily $21 $1820
250, 500, 750 mg tabs;
25 mg/mL liquid
a
Cost = For brand drugs, Average Wholesale Price minus 10%. AWP from Red Book Online 5/11/17. For generic drugs,
Maximum Allowable Cost plus $3 from BCBS of Michigan MAC List, 5/1/17. Prices calculated for 30 day supply unless
otherwise noted.
b
Ipratropium is preferred for acute exacerbations. Tiotropium does not have acute bronchodilating properties.
c
Oral corticosteroids are not for general maintenance and should be weaned after treatment of the exacerbation.
d
Antibiotics are recommended for patients with increased sputum purulence plus either increased sputum volume or increased
dyspnea. Duration is usually 3 to 7 days, depending on the agent and response to therapy.
e
Risk factors for poorer outcomes with narrower spectrum antibiotics include: age ≥ 65, FEV1 < 50% predicted, > 3
exacerbations/year, and presence of comorbid diseases. Consider broader spectrum antibiotics for these patients.
f
Fluoroquinolones have been associated with disabling and potentially irreversible serious adverse reactions that have occurred
together, including tendinitis and tendon rupture, peripheral neuropathy, and CNS effects. Discontinue levofloxacin
immediately and avoid the use of fluoroquinolones in patients who experience any of these serious adverse reactions.
g
Risk factors for Pseudomonas aeruginosa are:
• Recent hospitalization
• Frequent administration of antibiotics (4 courses over the past year)
• Severe COPD exacerbations
• Isolation of P. aeruginosa during a previous hospitalization or colonization during a stable period

Table 10. BODE (Body-mass index, Obstruction, Dyspnea and Exercise) Score
Variable Points
0 1 2 3
Body Mass Index > 21 ≤ 21
FEV1 % predicted ≥ 65 50-64 36-49 ≤ 35
MMRC dyspnea scale score 0-1 2 3 4
6-minute walk distance (m)* ≥ 350 250-349 150-249 ≤ 149
Note: A BODE score is a general measure of disease severity, combining effects of the listed four factors. Hazard risk for death
from any cause per one-point increase in BODE score is 1.34.6 Patients with scores of ≥ 5 have COPD sufficiently severe to
consider specialty referral.
* The 6-minute walking test (6MWT) is a self-paced test of walking capacity.7 Patients are asked to walk as far as possible in 6
minutes along a flat corridor. The distance in meters is recorded. Standardized instructions and encouragement are commonly
given during this test. The magnitude of desaturation and timing of heart rate recovery are associated with clinical outcomes.
Clinical Background and Rationale for prognosis. Multiple dimensions of disease severity (airflow
Recommendations limitation, symptom severity, exacerbation risk) should help
guide management.
Epidemiology and Impact
Management Issues
COPD is the third-leading cause of death in the United
States, accounting for over 147,000 deaths8 and 700,000 Both physicians and patients under-recognize the potential
hospitalizations annually.9 COPD can have a long pre- benefits of appropriate disease management for COPD. The
symptomatic phase. About 15.7 million Americans have lack of a large FEV1 response to bronchodilation may
been diagnosed with COPD, but an estimated 50% of those contribute to a sense of skepticism regarding the benefits of
with COPD are undiagnosed, so the actual number affected treatment. However, COPD is a chronic inflammatory
is probably much higher.10 disease with systemic manifestations that affect patient
function, quality of life, rate of lung function decline and the
development of comorbidities. FEV1 is not the sole measure
Etiology
of disease response. COPD is responsive to multiple
treatments. Appropriate comprehensive treatment can
The pulmonary manifestations of COPD include an abnormal
improve patients’ quality of life and prognosis.
inflammatory response to noxious inhaled particles or gases.9
The most common causal agent is cigarette smoke, and
cigarette smoking is the single largest risk factor for COPD.11
Second-hand smoke is also a recognized risk factor,12 as are Screening for COPD
environmental and occupational air pollutants.9,13 Deficiency
of alpha-1 antitrypsin is a treatable cause of abnormal Recommendation:
inflammatory response. While uncommon, it can be an
important etiologic factor in early onset and severe disease.14 Do not perform population-wide screening for COPD.
Prognosis Although about half of the individuals with COPD in the

United States are undiagnosed,8 no direct evidence quantifies
COPD is a chronic disease characterized by acute the benefits and harms of COPD screening with
exacerbations. While the disease is heterogeneous with a questionnaires or handheld spirometry, nor does evidence
variable course, airflow limitation is usually progressive, and exist to estimate the treatment benefits in screen-detected
life expectancy falls as disease progresses. Continued populations. Screening in older populations may lead to over-
smoking predicts worse prognosis.15 Persons with frequent diagnosis in “never” smokers. The United States Preventive
exacerbations (two or more per year) experience worse quality Services Task Force recommends against population-based
of life, more rapid loss of lung function, more frequent screening.18
hospitalization, and increased mortality.16,17
While FEV1 (the forced expiratory volume in the first second)

is commonly used to assess airflow limitation, FEV1 does not
always directly correlate with symptom burden, functional
status, or quality of life, and it is imperfect for predicting
Diagnosis of COPD (Table 1) Spirometry
Risk Factors and Clinical History Recommendation:

Perform spirometry to diagnose COPD.
Recommendation:
Consider a diagnosis of COPD in any patient who has Spirometry is the diagnostic “gold standard” because it is the
dyspnea, chronic cough or sputum production. most reproducible, standardized, and objective way of
measuring airflow limitation.26 Spirometry should be ordered
Consider early diagnostic case finding in any patient with risk
with bronchodilator, and the post-bronchodilator values
factors for the disease.
should be used to assess both the presence of airflow
obstruction and its severity. A post-bronchodilator FEV1/FVC
While routine population screening cannot be recommended, < 0.70 confirms the presence of airflow limitation that is not
early diagnostic case finding is encouraged for persons at fully reversible (FVC is the forced vital capacity). The
risk.18 Risk factors for COPD include exposure to chronic severity of post-bronchodilator airflow obstruction is defined
tobacco smoke,19 occupational dusts and chemicals,20 and by the FEV1 (Table 5).27
smoke from home cooking and heating fuels (Table 2).21 The
likelihood of a COPD diagnosis also increases with age. While reversibility with bronchodilator (defined as an
increase in FEV1 of ≥ 200 mL and ≥ 12% absolute value) is
Early diagnosis is encouraged, as the most effective therapy commonly associated with asthma as opposed to COPD, post-
for COPD, in terms of slowing the decline of lung function, is bronchodilator FEV1 improvement of 12% can also be seen in
smoking cessation.19,22 Also, case finding may improve COPD. In such cases of COPD with FEV1 bronchodilation
smoking cessation rates.23 response, the post-bronchodilator FEV1/FVC by definition
remains < 0.70 due to persistent airflow limitation. Therefore,
Recent evidence suggests that explaining a patient’s FEV1 response to bronchodilator should not be solely relied
pulmonary function to them in terms of relative “lung-age” upon to distinguish between asthma and COPD (Table 4).
enhances smoking cessation rates.23
While diffusion capacity and lung volumes obtained using
Differential diagnosis considerations for patients with chronic plethysmography can aid in patient characterization, these
cough and dyspnea can be found in Tables 3 and 4. results are not required for making the diagnosis of COPD.
Symptoms & Signs on Physical Exam (Table 2) Differentiating COPD, Asthma, and Overlap
Syndrome
Recommendation:
Dyspnea, often preceded by a chronic cough with sputum Recommendation:
production, may lead patients to seek care. Physical exam
Use the clinical history and spirometry to differentiate COPD,
is typically helpful only for patients with more severe
asthma, and overlap syndrome.
disease.
Distinguishing between COPD and asthma is important
Dyspnea is the symptom that most frequently leads patients to
because they differ in first-line therapies and chronic
seek medical attention, and dyspnea worsens with increasing
management. A set of clinical factors to help guide clinicians
disease severity.24 With severe disease, dyspnea can be
in distinguishing between asthma and COPD can be found in
debilitating. Chronic cough, often accompanied by sputum
Table 4.
production, may precede the onset of dyspnea. Dyspnea
frequently begins as an intermittent symptom, but later
Fixed airflow obstruction must be demonstrated to make a
becomes persistent. Wheezing and chest tightness are
diagnosis of COPD. Many patients with a diagnosis of COPD
nonspecific symptoms that may or may not be present. In
have not undergone confirmatory testing, suggesting that both
patients with more severe disease, anorexia and anxiety may
under-diagnosis and misdiagnosis are common.2
also develop.
Unfortunately, no single test can reliably distinguish asthma
from COPD.
Physical examination is typically unhelpful in the diagnosis of
COPD.25 Early airflow limitation is typically detectable via
Some patients have features of both asthma and COPD. The
spirometry before it is evident on physical exam. In patients
Global Initiative for Asthma (GINA) and Global Initiative for
with more severe disease, the physical exam may reveal
Chronic Obstructive Lung Disease (GOLD) recognize
decreased breath sounds, decreased air movement, wheezing,
Asthma COPD Overlap (ACO) or Asthma COPD Overlap
and rhonchi. Hyperinflation, as indicated by a “barrel” chest,
Syndrome (ACOS) as characterized by “persistent airflow
accessory muscle use and weight loss, typically indicates
limitation with several features usually associated with
more advanced disease.
asthma and several features usually associated with COPD.”1

Imaging and exacerbation risk helps individualize planning for each
patient.2 While these dimensions of COPD severity are
Recommendation: somewhat interrelated, individuals vary appreciably on their
status across these dimensions and on progression along each
Do not image to diagnose early or moderate COPD. of these dimensions. All of these dimensions should be
considered when assessing disease severity in an individual
Generally, COPD can be documented by spirometry before it patient.
is seen on chest radiograph. A chest radiograph may suggest
a diagnosis of COPD, particularly if it demonstrates The upper part of Table 5 shows levels of airflow limitation
hyperinflation, but it should not be considered diagnostic of (mild to very severe) by spirometry.
the disease.
The middle part of Table 5 shows two approaches to assessing
Current evidence is not sufficient to recommend routine chest symptom severity. Patients use the Modified Medical
imaging with computed tomography (CT) in early or Research Council (mMRC) Dyspnea Scale to rate their
moderate COPD. In patients with severe disease, high shortness of breath.3,30 Patients use the COPD Assessment
resolution CT is required to evaluate the appropriateness of Test (CATTM) to rate their health status impairment in 8 areas
therapies such as lung volume reduction surgery or transplant. likely to be affected by COPD, and then the score is totaled.4,31
The utility of chest CT in patients with COPD is an area of Either method of assessing symptom severity can be used,
active investigation.2 However, it should be noted that many although the mMRC Dyspnea scale has a narrower focus. The
individuals with COPD also meet criteria for lung cancer choice can be made based on local preference and likely
screening with CT, due to their smoking history.18 relevance to a specific patient.
Alpha-1 Antitrypsin The lower part of Table 5 addresses exacerbation risk and
other aspects of severity. Having had ≥ 2 exacerbations in the
Recommendation: past year or ≥ 1 exacerbation resulting in hospitalization is
associated with increased risk for future exacerbations.17
Perform alpha-1 antitrypsin testing in patients with early onset Other aspects of severity include oxygen therapy and
COPD or a family history of early onset COPD. Consider comorbid conditions.
alpha-1 antitrypsin testing in the presence of prominent
basilar lucency, unexplained liver disease, or the absence of
other risk factors for COPD.
Recognition of Comorbid Diseases
While alpha-1 antitrypsin deficiency has some association
with COPD,28 testing is controversial. Some of the Comorbid Disease
controversy derives from quality of data regarding efficacy of
treatment with alpha-1 antitrypsin augmentation therapy. Recommendation:
Recognize and diagnose comorbid diseases affecting the
In the absence of clear empirical data, we recommend management and health of patients with COPD.
following the GOLD Guidelines to test alpha-1 antitrypsin in
persons with COPD who:2 Patients with COPD are frequently at increased risk for:
• are of Caucasian descent under 45 years of age or • cardiovascular disease, heart failure, hypertension
• have a strong family history of COPD. • diabetes
• osteoporosis
Consider broader testing based on clinician judgment. The • cancer
American Thoracic Society and European Respiratory Society • psychiatric disorders including anxiety and depression32
joint statement recommends testing for:29
• symptomatic adults with emphysema, COPD, or asthma Cigarette smoking, an established risk factor for COPD, also
with airflow obstruction that is incompletely reversible places patients at risk for other diseases due to its systemic
after aggressive treatment with bronchodilators effects.
• adolescents with persistent airflow obstruction
• asymptomatic individuals with persistent airflow COPD itself is an independent risk factor for cardiovascular
obstruction and no risk factors. disease, even after controlling for smoking.33 This risk may be
related to systemic inflammation.
Assess COPD Severity
Cardiovascular Conditions
Recommendation:
Assess the extent of airflow limitation (using spirometry), Recommendation:
symptom severity, and exacerbation risk (Table 5) to Beta-blockers necessary for cardiovascular conditions can be
monitor patient status and guide therapy. prescribed for most patients with comorbid COPD.
Separately assessing airflow limitation, symptom severity,

Data from several studies demonstrate that beta-blockers further guidance regarding depression management, see the
necessary for cardiovascular conditions can be safely UMHS Depression Clinical Guideline.
prescribed for most patients with COPD, particularly beta-1
cardioselective blockers (eg, atenolol, metoprolol) or
combined beta and alpha blockers (eg, carvedilol).34,35 Management
Heart Failure Overview of COPD Management
Recommendation: Managing COPD includes patient education, preventive care,
For inpatients with COPD, a low BNP (< 100) can help rule medications, pulmonary rehabilitation, and oxygen therapy.
out heart failure and a high BNP (> 500) can help rule in Using symptoms and exacerbations as a guide, Figure 1
heart failure. provides an approach to incorporating all of these
management activities except oxygen therapy, which is
addressed separately below. The rationale for each
Clinicians may have difficulty distinguishing between heart
recommendation is explained in the relevant sections below.
failure and COPD in certain clinical settings. Baseline BNP
measurements may be elevated in COPD patients compared
to those without COPD, but are not as high as measurements Patient Education
in patients with heart failure. In patients with COPD, a low
BNP (less than 100) can help rule out significant heart failure, Recommendation:
while a very high BNP (greater than 500) can help rule in heart Provide patient-focused education to support disease self-
failure.36,37 Values between 100 and 500 must be interpreted management including: smoking cessation, avoidance of
with caution, keeping in mind the entire clinical picture. For exacerbations, appropriate inhaler technique, healthy
further guidance regarding the management of heart failure, behaviors, and end-of-life planning (Table 6).
see the University of Michigan Health System (UMHS) Heart
Failure Clinical Guideline. While evidence for clinical benefit due to self-management
support is lacking,42 patients should understand their disease,
Diabetes and Osteoporosis risk factors for progression, and their roles in optimizing their
health and wellness. Education should include identification
Recommendation: and reduction of exposures to inhalant irritants and
appropriate use of inhalers.2 Patients should be informed that
Inhaled corticosteroids have only a small effect on serum
smoking cessation has the greatest capacity to influence the
glucose in diabetics and on bone mineral density related to
natural history of COPD. Prospective end-of-life discussions
osteoporosis.
help patients understand advance directives and therapies near
the end of life.
Inhaled corticosteroid use is associated with only a small
(approximately 2 mg/dL) dose-dependent increase in serum
Patients enrolled in pulmonary rehabilitation at UMHS
glucose concentration in diabetic patients. For further
receive instruction in self-management skills that enhance
guidance regarding diabetes management, see the UMHS
self-efficacy and support chronic disease management.
Diabetes Clinical Guideline.
While inhaled corticosteroids may carry a theoretical risk for

Preventive Care
decreasing bone mineral density (BMD), several studies
Preventive care focuses on avoiding irritants that can
following BMD over 3 years indicate the risk is minimal.38
aggravate COPD. The most common “triggers” are smoking,
For further guidance regarding osteoporosis management, see
second-hand smoke, occupational fumes and chemicals,
the UMHS Osteoporosis Clinical Guideline.
indoor air pollution (eg, cooking with biomass fuels), outdoor
air pollution, and infections.
Psychiatric Disorders
Smoking cessation and second-hand smoke.
Recommendation:
Identify psychiatric disorders in COPD patients and treat with Recommendation:
cognitive behavioral therapy, mind-body interventions,
Advise smokers to quit and assist them in quitting. Assess for
and non-sedating therapies when possible.
exposure to second-hand smoke and counsel its avoidance.
Depression and anxiety are highly prevalent in COPD
Smoking cessation is the single most important intervention
patients, and both predict a worse quality of life.39 Cognitive
to slow the rate of lung decline and reduce respiratory
behavioral therapy may improve psychological outcomes, and
symptoms, regardless of the severity of the patient’s disease.
mind-body interventions (such as mindfulness, yoga, and
The beneficial impact of smoking cessation on the natural
relaxation) may decrease physical suffering.40 Due to the risk
history of COPD is greater the earlier in the disease that
of respiratory suppression, non-selective benzodiazepine
cessation is achieved.22
anxiolytic sedation should be avoided when possible.41 For
Smoking cessation should be encouraged at each visit. The Inactivated influenza vaccination significantly reduces
combination of pharmacologic and psychosocial treatment for exacerbations and influenza-related respiratory infections.51
smoking cessation has been shown to be superior to Influenza vaccine reduces serious illness and death from
psychosocial treatment alone in patients with COPD.43 influenza in COPD patients by approximately 50%.52
Smoking cessation counseling is a billable diagnosis for
patients with COPD.44 For further guidance on smoking Medications for Chronic Care
cessation, see the UMHS Tobacco Treatment Guideline.
Figure 1 presents an overview of medical management for
Second-hand smoke exposure appears to have an adverse COPD based on symptom severity and exacerbation risk. It
impact on health outcomes in COPD, independent of personal focuses on commonly used medications: short- and long-
smoking.45 It is a modifiable risk factor. acting bronchodilators and inhaled corticosteroids. Specific
recommendations regarding their use and the use of additional
Occupational fumes and air pollution. medications are presented below.
Recommendation: Benefits of medication.

Advise patients to identify and avoid occupational fumes and
air pollution. Recommendation:
Medical therapy improves symptoms and functional status.
Occupational pulmonary irritant exposure causes 12-17% of However, no existing medications for COPD have been
COPD cases.46 Therefore, limiting exposure to industrial shown to modify long-term decline in lung function.
fumes and dust is recommended. Limiting exposure can help Oxygen is the only treatment proven to impact mortality.
slow the progression of disease and improve symptoms.
Occupational exposures include organic and inorganic dusts, Medications commonly used in COPD include
chemical agents, and fumes. bronchodilators (both short- and long-acting beta-2 agonists
and anticholinergics) and anti-inflammatory agents (inhaled
Patients with COPD should be counseled to avoid exposure to glucocorticoids). Detailed dosing and cost information by
high air pollution to the extent that avoidance is reasonable. drug is presented in Table 7.
Emergency room visits have been shown to increase among
patients with COPD following days of high air pollution. Beta-2 agonists and anticholinergics.
Long-term exposure to air pollution may be associated with
increased risk for both COPD hospitalizations and COPD Recommendation:
mortality.47
Treatment with bronchodilators provides clinical benefit
Patients should be counseled to avoid indoor air pollution as despite limited change in spirometric measures.
well. Use of biomass fuels (eg, wood, crop materials, coal,
animal dung) for indoor cooking is a significant risk factor for Both beta-2 agonists and anticholinergics are bronchodilators.
COPD, especially in developing countries.48 They are indicated in the treatment of any COPD patient who
is symptomatic. Current evidence suggests that the long-
Vaccination. acting muscarinic antagonist (LAMA) anticholinergics should
be considered first-line agents for baseline bronchodilator
Recommendation: control, particularly in patients with severe airflow
obstruction.53,54
Provide annual influenza vaccination to all COPD patients.
Provide 23-valent pneumococcal vaccine at the time of Dual bronchodilator therapy should be considered for patients
COPD diagnosis. At age 65, provide 13-valent who have persistent symptoms despite use of a single
pneumococcal vaccine (at least 1 year after 23-valent bronchodilator, and for patients with frequent exacerbations.2
vaccination.) Provide 23-valent booster pneumococcal Combining different types of bronchodilators may increase
vaccination at least 1 year after 13-valent vaccination and the degree of bronchodilation with equivalent or fewer side
at least 5 years after the initial 23-valent vaccination. effects.55 Several combinations of long-acting beta agonist
with long-acting muscarinic antagonist (LABA/LAMA)
Patients with COPD are at increased risk for complications bronchodilators are now available. Evidence suggests lung
from pulmonary infections (eg, hospitalization, increased use function and quality of life improvements are greater for
of antibiotics). Therefore, the CDC Advisory Committee on combination than for single agent bronchodilators.2,56 Dual
Immunization Practices recommends all patients receive LABA/LAMA bronchodilators have also been demonstrated
pneumococcal and influenza vaccines beginning at the time of to reduce exacerbation frequency to a greater extent than
diagnosis.49 inhaled corticosteroid/long-acting beta agonist (ICS/LABA)
combination therapy.
Injectable polyvalent pneumococcal vaccination reduces risk
for community acquired pneumonia and disease exacerbation To treat asthma-COPD overlap patients, avoid monotherapy
in patients with COPD.50 with long-acting beta agonists and consider earlier
introduction of inhaled corticosteroid therapy in conjunction in pulmonary related deaths was noted in the ICS/LABA
with a LABA and/or a LAMA. combination therapy group as compared to placebo.63 In
patients with COPD being treated with ICS, particularly those
Data from several studies demonstrate that beta-blockers age 65 and older, consider the possible increased risk of
necessary for cardiovascular conditions can be safely pneumonia and maintain a lower threshold for considering a
prescribed for most patients with COPD, particularly beta-1 diagnosis of pneumonia when patients present with increased
cardioselective blockers (eg, atenolol, metoprolol) or symptoms.
combined beta and alpha blockers (eg, carvedilol).34,35
ICS may also increase a patient’s risk for cataracts or
Both long-acting beta-2 agonists and anticholinergics have glaucoma.2 Consider regular eye exams for patients using
safety concerns. these medications. Patients using ICS should also be warned
about the possibility of oral candidiasis and vocal changes.
• Long-acting beta-2 agonists (LABA). An FDA advisory
Rinsing the mouth after administration of ICS should be
panel recommended that LABAs not be used as single-
encouraged.
agent therapy in asthma (see UMHS Asthma Guideline).
However, for patients with COPD, LABAs may still be
Decrease in bone density is a theoretical risk of this class of
used as single-agent therapy without an inhaled
medication, but available long-term data suggest there is no
corticosteroid. While LABAs may increase blood
meaningful association between ICS use and decreased bone
pressure and heart rate, data for COPD patients from the
mineral density in this patient population.38
TORCH study57 (a three-year trial in COPD patients of
fluticasone proprionate and salmeterol combination
Phosphodiesterase-4 inhibitors (roflumilast).
versus fluticasone alone, salmeterol alone, or placebo),
found no increased risk of all-cause death or
cardiovascular death in the salmeterol group. These data Recommendation:
further underscore the importance of distinguishing Consider roflumilast to reduce the frequency of acute
asthma from COPD. exacerbations in patients with chronic bronchitis,
recognizing that side effects may limit adherence.
• Anticholinergics. Anticholinergic drugs may worsen
symptoms and signs associated with narrow-angle
glaucoma, prostatic hyperplasia, or bladder-neck Evidence is developing regarding both the role of
obstruction and should be used with caution in patients phosphodiesterase-4 inhibitors in stable COPD management
with any of these conditions. Concerns about and which patients are most likely to benefit, including
cardiovascular effects have diminished. Initially a meta- patients with a history of chronic bronchitis and frequent or
analysis suggested that inhaled anticholinergics severe exacerbations.2 Roflumilast should be considered in
(ipratropium and tiotropium) were associated with conjunction with consultation with a pulmonologist. Discuss
significantly increased risk of cardiovascular death, MI, side effects including GI intolerance prior to prescribing.
or stroke among patients with COPD.58 However, since
then, data from the UPLIFT study (a four-year, placebo Antibiotics.
controlled trial of tiotropium) found no significant
increase in myocardial infarction or stroke in the Recommendation:
tiotropium treated group.59 Do not routinely use prophylactic antibiotics, but consider
referral to a COPD specialist for chronic macrolide therapy
Inhaled glucocorticosteroids (ICS). in selected patients.
Recommendation: Chronic macrolide therapy with oral azithromycin has been

Add ICS to bronchodilator therapy in patients with features of shown to decrease the frequency of COPD exacerbations.64 A
asthma overlap. Consider adding ICS in patients with follow-up systematic review also suggests an improvement in
frequent (at least annual) severe COPD exacerbations acute exacerbations and decreased hospitalization with
despite maximal bronchodilation. chronic macrolide therapy.65 In patients with persistent
exacerbations despite maximal inhaled therapies, consider
ICS should not be used as monotherapy in COPD. However, referral to a specialist in COPD management (eg,
ICS can provide additive benefit to bronchodilators in pulmonologist) for consideration of additional therapies
reducing the frequency of exacerbations and improving health including macrolide antibiotics.
status.60 Withdrawal from treatment with ICS can lead to a
short term increase in exacerbations in some patients.2 Leukotriene modifiers.
An increase in the frequency of pneumonia has been reported Recommendation:

in COPD patients using ICS, particularly in patients age 65 Consider using leukotriene modifiers in patients with
and older.2,61,62 The frequency of reported pneumonia appears asthma/COPD overlap syndrome.
to be approximately double in several studies comparing
ICS/LABA combinations versus placebo in COPD. However,
in the largest published mortality study in COPD, no increase
Leukotriene modifiers have not been adequately tested in
COPD and cannot be recommended solely for COPD at this The primary goal of oxygen therapy is to maintain vital organ
time. function by ensuring adequate oxygen delivery. This is
achieved by increasing the baseline PaO2 to at least 60 mm Hg
Oral glucocorticosteroids. (or resting oxygen saturation to at least 90%).67,69
Recommendation: In patients with very severe COPD, long-term oxygen therapy

has been shown to improve the following outcomes:70-73
Do not routinely use oral steroids for treatment of chronic
• mortality
COPD. However, oral steroids can be used for acute
• quality of life
exacerbations of COPD, as discussed below.
• cardiovascular morbidity (ie, pulmonary hypertension)
• depression
Theophylline. • cognitive function
• exercise capacity
Recommendation: • frequency of hospitalization
Do not routinely use theophylline for control of chronic
COPD symptoms. Indications for continuous oxygen use are summarized in
Table 8. Once oxygen therapy is initiated, if the clinical
Theophylline is effective for symptom control in COPD. picture changes, oxygen requirement may need to be
However, due to its narrow therapeutic window and side reevaluated. Medicare requires annual recertification of a
effect profile, inhaled bronchodilators are preferred. patient’s continuing need for oxygen therapy.
Pulmonary Rehabilitation Currently the Center for Medicare and Medicaid Services
covers oxygen use both for patients who meet the evidence-
based criteria in Table 8, as well as for individuals with PaO2
Recommendation:
≤ 55 mm Hg (resting oxygen saturation ≤ 88%) either with
Consider pulmonary rehabilitation for any patient with COPD activity or at night. For these patients with moderate
who experiences significant dyspnea or exercise hypoxemia but significant breathlessness despite maximizing
limitation, regardless of severity of airflow limitation. other medical therapies, a trial of oxygen therapy may be
appropriate.
The American Thoracic Society and European Respiratory
Society66 define pulmonary rehabilitation as “a Exercise and nocturnal oxygen therapy.
comprehensive intervention based on a thorough patient
assessment followed by patient-tailored therapies that include, Recommendation:
but are not limited to, exercise training, education, and
Oxygen therapy during exercise or during sleep may benefit
behavior change, designed to improve the physical and
selected patients.
psychological condition of people with chronic respiratory
disease and to promote the long-term adherence to health-
enhancing behaviors.” The Long-term Oxygen Treatment Trial74 randomized COPD
subjects who had a moderate exercise-induced desaturation
Pulmonary rehabilitation improves exercise capacity, during the six-minute walk test (SpO2 ≥ 80% for ≥ 5 minutes
dyspnea, and quality of life.67 Pulmonary rehabilitation after a and < 90% for ≥ 10 seconds) or a moderate resting
recent hospitalization for COPD has been shown to decrease desaturation (pulse oximetry 89-93%) to supplemental
hospital readmissions, decrease mortality, and improve both oxygen versus no supplemental oxygen. This study found no
exercise capacity and health related quality of life.68 difference in time to death or first hospitalization, nor in the
rates of all hospitalizations or COPD exacerbations. The study
Medicare covers pulmonary rehabilitation for patients with also found no consistent between-group differences in
COPD who have moderate or greater disease severity, based measures of quality of life, lung function, or the distance
on FEV1 % predicted. (Table 5.) Medicare patients who walked in 6 minutes. Patients in the supplemental-oxygen
continue to smoke must also be enrolled in a smoking group who had a COPD exacerbation 1-2 months before
cessation program. enrollment, those greater than 71 years at enrollment, and
those with lower quality of life at enrollment did experience
longer time to death or first hospitalization, although these
Oxygen Therapy
effects did not remain significant when adjusted for multiple
comparisons. However, a lack of evidence for benefit should
Continuous oxygen.
not be confused with a lack of clinical effectiveness in some
patients. A trial of oxygen therapy may still be warranted in
Recommendation: selected patients who have moderate exertional hypoxemia
Provide continuous oxygen therapy for COPD patients if and intractable breathlessness despite appropriate evidence-
resting oxygen saturation is ≤ 88% and confirmed twice based treatment.
over a 3-week period.

Follow Up Chronic Care Medication Management
Frequency Recommendation:
Adjust medical therapy based on symptom severity as
Recommendation: summarized in Figure 1 and as described above under
Initial chronic care visits should occur at least every 6 months. “Medications for Chronic Care.”
Visits may be once a year for currently nonsmoking
patients with mild disease who are stable on treatment and If patients remain symptomatic at subsequent follow-up visits
only rarely have exacerbations. despite adherence to medications, intensifying
pharmacotherapy should be considered.
No consensus exists on the recommended frequency of office
visits for chronic COPD care. Frequency of follow-up may be Oxygen Therapy Management
guided by:
• Worsening symptoms not associated with an exacerbation Recommendation:
• Frequency of acute exacerbations Reassess patients who are on oxygen for resting hypoxemia
• Smoking status (resting oxygen saturation ≤ 88%).
• Adherence to treatment plan
• Social support systems For patients on long-term oxygen therapy, an annual
• Presence of other comorbid chronic diseases reevaluation of oxygen saturation is recommended to
determine if oxygen is therapeutic and still clinically
6.2. Factors to Reassess indicated.
Recommendation: All patients prescribed oxygen must be recertified every 12

At follow-up visits, reassess: months in order to qualify for Medicare and Medicaid
• Risk of exposure to pulmonary irritants coverage. Recertification includes an in-person encounter
• Symptoms: severity, control, new, stable or worsening (eg, with the treating physician, a documented exam, and a resting
sputum production, dyspnea, cough, activities of daily oxygen saturation of < 88%, with improvement of the
living) hypoxemia on oxygen.76
• History of exacerbations and possible causes
• Smoking cessation, if applicable Functional Assessment and Rehabilitation
• Current medications, dosages, adherence, and proper use
• Inhaler technique Recommendation:
• Vaccinations If not already initiated, consider pulmonary rehabilitation for
all patients with significant dyspnea or exercise limitation.
Evidence regarding comprehensive self-management is
limited. One study that compared self-management to routine
Nutrition
monitoring did not demonstrate long-term benefits in terms of
quality of life or self-efficacy over usual care alone in COPD
Recommendation:
patients in general practice.75
For patients with COPD and malnourishment, consider a
Spirometry referral for nutritional counseling and supplementation.
Recommendation: Insurance coverage for dietician referral for this purpose

varies.
Monitor symptoms and functional status to guide spirometry
use in disease monitoring.
Reassessment after Severe Acute Exacerbation
No clear consensus exists on the appropriate frequency of
Recommendation:
spirometry to guide therapy after the initial diagnosis of
COPD. Systematic reviews found insufficient evidence for Reassess patients after hospital discharge for an acute COPD
using spirometry to guide therapy. When patients report exacerbation.
symptomatic changes, follow-up spirometry may be
warranted to detect clinically significant changes of lung
function that may alter clinical therapeutic options.

Assessment should include:
• Spirometry about 3 months after the patient’s return to Ordering a chest radiograph is generally not recommended.
stability. Significant declines in baseline lung function can However, it may be reasonable for patients who are age 65 or
occur with exacerbations. older, use inhaled steroids, or have fever.
• Ability to cope in their home environment
• Inhaler technique and understanding of treatment regimen The utility of sputum gram stain and culture in the outpatient
• Need for oxygen setting is limited given the length of time before results are
• Medical regimen optimization for prevention of future available as well as the low reliability of the results.2 Patients
exacerbations who have recently been on antibiotics or who are not
responding to therapy may be exceptions.
Acute Exacerbation Spirometry, arterial blood gas, and electrocardiogram are

in the Outpatient Setting generally not recommended in the outpatient assessment of a
patient with an acute COPD exacerbation.
This guideline focuses on management of an exacerbation
Pharmacotherapy
treated in the outpatient setting. For information regarding
exacerbation in the inpatient setting, see Care of the
Hospitalized Patient with Acute Exacerbation of COPD. Recommendation:
Outpatient management of acute COPD exacerbation involves
Diagnosis treatment with bronchodilators, systemic corticosteroids,
and antibiotics.
Recommendation:
Specific drugs and dosing are described in Table 9. Their use
Diagnose an acute exacerbation of COPD based on clinical
is summarized below.
findings. Consider causes of COPD exacerbation and
alternate diagnoses.
Bronchodilators.
No single definition of acute COPD exacerbation is Recommendation:
universally accepted. However, it can reasonably be described
as an acute change in a patient’s baseline dyspnea, cough, or Use bronchodilators as first-line therapy.
sputum that is beyond the normal day-to-day variability and
is sufficient to warrant a change in medication. Bronchodilators improve respiratory symptoms and FEV1
during acute COPD exacerbations. The dose and/or frequency
Causes of acute COPD exacerbation include:2,77 of short-acting beta-2 agonists, either via inhaler or nebulizer,
• Infections (both viral and bacterial) should be increased. The inhaled anticholinergic ipratropium,
• Environmental conditions which is a short-acting muscarinic antagonist (SAMA), can be
• Air pollution added if not already used, although the effectiveness of
• Lack of compliance with long-term oxygen therapy combination therapy in the setting of acute exacerbation is
• Unknown questionable.78 The clinical response to medication
administration via MDI with spacer is similar to that for
Alternate diagnoses need to be considered, including: inhalation via nebulizer for persons who can adequately
• Pneumonia demonstrate bronchodilator technique (even while
• Congestive heart failure dyspneic).79
• Pneumothorax
• Pleural effusion Systemic corticosteroids.
• Pulmonary embolism
• Cardiac arrhythmia Recommendation:
Provide oral corticosteroids to reduce recovery time, improve
Assessment lung function (FEV1), and improve hypoxemia (PaO2).
Recommendation:
Prednisone 40 mg orally daily is recommended for not more
Assess the patient’s clinical history, physical exam, and than 5-7 days,2,80 particularly in patients with an FEV1 < 50%
oxygen saturation. predicted.
Do not routinely perform a chest radiograph or a sputum gram
stain & culture.
Outpatient assessment for an acute exacerbation of COPD

starts with the clinical history and physical examination.
Obtaining an oxygen saturation via pulse oximetry is
recommended.
Antibiotics. Noninvasive and Surgical Therapy
for Severe Disease
Recommendation:
Treat selected patients with empiric antibiotic therapy. Noninvasive Ventilation
The benefit of antibiotics for patients with severe COPD Recommendation:

exacerbations requiring mechanical ventilation is well Refer patients with a history of hospitalization for respiratory
established. The role of antibiotics for the treatment of failure and with severe chronic hypercapnia to a
moderate exacerbations in the outpatient setting is more pulmonologist for consideration of noninvasive
controversial. A few studies have shown that antibiotics ventilation.
reduce treatment failure rate and may increase the time to the
next exacerbation.2,81 Some studies suggest that patients who
Long-term noninvasive positive pressure ventilation,
present with purulent sputum may benefit most from
delivered nasally or by mask, may decrease mortality and
antibiotic treatment. COPD guideline documents vary in their
reduce risk for re-hospitalization in selected patients.2,82
recommendations.
For treatment of outpatients with a COPD exacerbation, we Lung Volume Reduction

recommend using antibiotics in patients where at least two of
the following have increased: Recommendation:
• Dyspnea
• Sputum volume Refer patients with very severe COPD who are willing to
• Sputum purulence consider invasive therapy to a pulmonologist for
consideration of surgical bullectomy, bronchoscopic lung
Antibiotic choice should be selected for presumptive therapy volume reduction procedures, or lung volume reduction
based on local resistance patterns. Sputum cultures are surgery.
generally not recommended unless the patient has recently
been taking antibiotics. For patients who meet the above Bullectomy may be considered for patients with localized
criteria for antibiotics, the selection of a specific antibiotic giant bullae that are associated with compression of adjacent
depends on risk factors for poor outcomes with narrower lung tissue.2 One-way valve endobronchial lung volume
spectrum antibiotics (eg, age ≥ 65, FEV1 < 50% predicted, ≥ reduction has been shown to improve walk distance, but with
3 exacerbations/year, presence of comorbid diseases) and increased risk of complications.83,84 Bronchoscopic placement
unusual circumstances (Table 9). of multiple lung volume reduction coils in affected lobes can
improve dyspnea and 6 minute walk distance,85 but may
Indications for hospitalization. increase major complications.86
Recommendation: Lung volume reduction surgery may be considered after

consultation with a pulmonary specialist for patients with
Initiate an emergency department evaluation or hospital bilateral upper lobe disease and reduced exercise capacity (as
admission based on clinical judgment of COPD measured by formal cardiopulmonary exercise testing) despite
exacerbation severity, lack of response to treatment, maximal medical therapy and pulmonary rehabilitation.87
history, and contextual factors. Data demonstrate improvements in exercise capacity,
dyspnea, and quality of life; survival outcomes are favorable
Consider emergency department evaluation or hospital for those with upper lobe emphysema and reduced exercise
admission based on clinical judgment: capacity.87 Cost-effectiveness of this approach is not
• Marked increase in symptoms such as dyspnea at rest demonstrated for even the most favorable subgroup (ie,
• Severe underlying COPD COPD patients with upper lobe emphysema and reduced
• Frequent exacerbations exercise capacity) unless outcomes are expected to remain
• Significant comorbidities (eg, older age, pneumonia, favorable for 10 years.88 Therefore, life expectancy should be
congestive heart failure, diabetes mellitus, renal or liver incorporated into shared decision making regarding the
failure) potential benefits of surgery.
• Worsening hypoxemia or hypercapnia
• Changes in mental status Lung Transplantation
• Inadequate response to outpatient therapy
• Uncertain diagnosis Recommendation:
• Insufficient home support
Consider lung transplantation evaluation for patients with
severe COPD without comorbid conditions that would
otherwise limit their lifespans.
Lung transplantation may be considered for patients who have

BODE scores from 7-10 (Table 10) without comorbid
conditions that would otherwise limit their expected lifespans. Referral to COPD Subspecialist
Consideration of transplantation potential requires co-
management with a pulmonary specialist for detailed Recommendation:
assessment of baseline pulmonary physiology and potential
contraindications.89 Consider referring COPD patients with severe asthma or other
complicating conditions to a subspecialist for co-
management and consideration of invasive treatment
Complementary and Alternative Medicine options.
As COPD worsens, care considerations and decisions become

Recommendation:
increasingly complex. Consider referring patients with:
Yoga, tai chi, qigong, and nutritional supplements have not • Severe disease (FEV1 ≤ 50% predicted or BODE score ≥
been demonstrated to be of greater symptomatic benefit 5)
than a standard healthy diet, walking, and breathing • Severe or frequent exacerbations
exercises for persons with COPD. • Dependence on supplemental oxygen
While complementary and alternative medical therapies have Also consider referral for the following conditions that may
been proposed for the treatment of COPD, little evidence of require complex management:
significant specific clinical benefit exists. For example, yoga, • Alpha-1 antitrypsin deficiency
tai chi, and qigong have been investigated as interventions to • Concurrent cardiac disease, suspected asthma, or another
reduce dyspnea and improve quality of life, but benefits have pulmonary disease that complicates diagnosis or
not been demonstrated to be greater than those of standard management
nonpharmacologic interventions such as walking or breathing • Suspected upper airway obstruction (eg, upper airway
exercise and education.90-92 While usual advice regarding a wheezing or stridor) – consider referral to otolaryngology
healthy diet is generally endorsed, specific nutrient or pulmonary medicine
supplements have no proven benefit. Pulmonary function • Symptoms that are not responsive to optimal therapy or are
testing demonstrated statistically significant worsening out of proportion to obstructive findings
immediately following osteopathic manipulative therapy, as
• Symptoms that are present in the absence of formal
measured by FEV1 and residual volume,93 and a systematic
spirometric obstruction criteria
review of osteopathic manipulative therapy for COPD
• Frequent (at least twice per year) exacerbations or
revealed no evidence of benefit from a small number of low
pneumonia complicate management
quality studies.94
• Lung volume reduction surgery or lung transplantation is
considered (eg, BODE score 7-10, giant bullae, severe
disease). Early referral for monitoring and preparation is
Palliative Care recommended if FEV1 < 50% and the patient is likely to be
a future candidate.89
Recommendation: • Intensive care pulmonary hospitalization or mechanical
Engage patients in shared decision making regarding goals of ventilation is required
therapy, including end-of-life planning and advance
directives.
Related National Guidelines
Severe COPD increases risk of respiratory failure and is a and Performance Measures
leading cause of death. Given the progressive nature of the
disease, a palliative focus for care should be discussed with National Guidelines
patients desiring less aggressive therapy, avoidance of
endotracheal intubation, or comfort care measures This guideline is generally consistent with the:
(symptomatic care) at the end of life. The discussion may limit • GOLD 2017 Global Strategy for the Diagnosis,
unnecessary and burdensome personal and societal costs and Management, and Prevention of Chronic Obstructive
invasive approaches.95,96 Therapies with proven effectiveness Pulmonary Disease.2
for management of dyspnea at the end of life include opioids • The COPD Pocket Consultant: COPD Foundation Guide
and oxygen. for Management of COPD (2017).5
• Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention of
acute exacerbations of COPD (2015).97
• US Preventive Services Task Force (USPSTF). Screening
for chronic obstructive pulmonary disease (2016).98
• VA/DOD Clinical Practice Guideline for the Management
of Chronic Obstructive Pulmonary Disease (2014).99

Performance Measures • Primary care physicians: Davoren A. Chick, MD, General
Medicine, Paul J. Grant, MD, General Internal Medicine,
National programs that have clinical performance measures and Amal E. Othman, MD, Family Medicine.
for COPD care include the following: • Specialists in COPD care: Meilan K. Han, MD, Pulmonary
Medicine, Sarah E. Roark, MD, Pulmonary Medicine.
National Committee for Quality Assurance: Healthcare • Guideline development methodologist: R. Van Harrison,
Effectiveness Data and Information Sets (HEDIS). (Many PhD, Learning Health Sciences.
payers use HEDIS measures of performance.) • Literature search services were provided by
informationists at the Taubman Health Sciences Library,
Spirometry in the assessment and diagnosis of new COPD. University of Michigan Medical School.
The percentage of members 40 years of age and older with
a new diagnosis of COPD or newly active COPD, who UMHS endorses the Standards of the Accreditation Council
received appropriate spirometry testing to confirm the for Continuing Medical Education that the individuals who
diagnosis. present educational activities disclose significant
relationships with commercial companies whose products or
Corticosteroids in pharmacotherapy management of a services are discussed. Contributions of team members with
COPD exacerbation. The percentage of COPD relevant financial relationships are reviewed by team
exacerbations for members 40 years of age and older who members without relevant financial relationships to assure the
had an acute inpatient discharge or ED visit on or between information is presented without bias.
January 1–November 30 of the measurement year and who
were dispensed appropriate medications. Dispensed a Individuals with no relevant personal financial relationships:
systemic corticosteroid (or there was evidence of an active Davoren A. Chick, MD, Paul J. Grant, MD, R. Van Harrison,
prescription) within 14 days of the event. PhD, Amal E. Othman, MD, Tami L Remington, PharmD,
and Sarah E. Roark, MD
Bronchodilators in pharmacotherapy management of a
COPD exacerbation. The percentage of COPD Individuals with relevant personal financial relationships:
exacerbations for members 40 years of age and older who MeiLan K. Han, MD
had an acute inpatient discharge or ED visit on or between Consultant Novartis, Nycomed
January 1–November 30 of the measurement year and who
were dispensed appropriate medications. Dispensed a Speaker’s bureau Boehringer Ingelheim,
bronchodilator (or there was evidence of an active GlaxoSmithKline, CLS Boehring
prescription) within 30 days of the event. Advisory board CLS Boehring
Centers for Disease Control and Prevention: Advisory Systematic Review of Literature
Committee on Immunization Practices (ACIP). (Some payers
use ACIP recommendations for immunization as measures of A detailed description of the systematic search and review of
performance.) literature upon which this guideline is based is presented in
the associated UMHS document “Guideline for Chronic
Pneumococcal vaccination. Adults aged 19-64 with COPD, Obstructive Pulmonary Disease, 2017: Literature Review
administer PPSV23. At age ≥ 65 years, administer PC13 at Methods and Results.” The following section highlights major
least 1 year after PPSV23, followed by another dose of aspects of the literature search and review process.
PPSV23 at least 1 year after PCV13 and at least 5 years after
the last dose of PPSV23. Literature search. The team began the search of literature by
accepting the results of a systematic literature review
Influenza vaccination. Vaccination is recommended for all performed in 2014:
persons aged ≥ 6 months. (Individuals with COPD are at VA/DOD Clinical Practice Guideline for the Management
higher risk for complications of influenza.) of Chronic Obstructive Pulmonary Disease. The
Management of Chronic Obstructive Pulmonary Disease
Working Group, Department of Veterans Affairs and
Guideline Development Department of Defense. Dec. 2014. (Searched literature
Methodology from January 2005 through February 2014.)
To update those results, we performed a systematic search of

Funding
literature on Medline and in the Cochrane Database of
Systematic Reviews for the time period 1/1/14 – 9/8/16.
The development of this guideline was funded by UMHS.
The major search term was chronic obstructive pulmonary
Guideline Development Team and Disclosures disease. The searches were for guidelines, controlled trials
(including meta-analyses), and cohort studies, for literature on
The multidisciplinary guideline development team consisted
humans in the English language. Within these parameters
of:
individual searches were performed for the following topics:

A. Etiology: Smoking, particulate inhalation exposures, A = systematic reviews of randomized controlled trials with
alpha-1 antitrypsin deficiency, life expectancy based on or without meta-analysis
FEV1/BODE B = randomized controlled trials
B. Screening: Questionnaires, pulmonary function C = systematic reviews of non-randomized controlled trials
testing/spirometry or observational studies, non-randomized controlled
C. Diagnosis: History (risk factors, symptoms), physical trials, group observation studies (cohort, cross-
exam sectional, case-control)
D. Diagnostic studies: PFTs, alpha-1 antitrypsin level, chest D = individual observation studies (case study or case
X-ray, 6-minute walk test, chest CT series)
E. Diagnostic classification: GOLD classes, MRC or E = expert opinion regarding benefits and harm
mMRC dyspnea scale, BODE index
F. Definition and diagnosis: Acute exacerbation Beginning with best evidence identified by the VA/DoD
G. Other diagnoses not included in C–F above systematic literature review, team members checked
H. Comorbid diseases (increased risk) publications identified in the more recent search (1/1/14 –
I. Prevention: Smoking cessation, vaccination (influenza, 9/8/16) to determine whether better evidence was available.
pneumococcus) Team members also had the option of considering very recent
J. Prevention: Irritant avoidance literature (published since 9/8/16) in determining whether
K. Pharmacologic treatment: Bronchodilators, inhaled even better evidence was available.
corticosteroids
L. Treatment: Supplemental oxygen The process of review and assessment is described in more
M. Treatment: Pulmonary rehabilitation detail in Section V of the accompanying Literature Review
N. Nutrition Methods and Results
O. Treatment: Complementary and alternative medicine
P. Treatment: Mental health, psychosocial support Best evidence. The best evidence regarding specific topics
Q. Treatment: Acute exacerbation – outpatient management, was summarized in evidence tables listing articles, study
hospitalization designs, patient populations, main outcome variables, results,
R. Referral to pulmonary subspecialist and notes regarding methodological issues and harms. The
S. Surgical treatment: Lung volume reduction surgery, lung evidence tables are presented in Section VI of the
transplantation accompanying Literature Review Methods and Results.
T. Treatment: Follow up care, monitoring, chronic disease
management Recommendations. The guideline team reviewed the
U. Treatment: Palliative care evidence and determined the importance of performing or
V. Other “treatments” not in I–U above not performing key aspects of care (listed on the first page of
W. Other not in A–V above this guideline). In the absence of empirical evidence, the
guideline team based recommendations on their expert
A more formal presentation of the inclusion and exclusion opinion.
criteria is in Section II of the accompanying Literature Review
Methods and Results. The strength of recommendations regarding care were
categorized as:
The detailed search strategies are presented in Section III of I = Generally should be performed
the accompanying Literature Review Methods and Results. II = May be reasonable to perform
III = Generally should not be performed
The search was conducted in components of a formal problem
structure (outlined above). The search was supplemented with Review and Endorsement
very recent clinical trials known to expert members of the
panel. The search was a single cycle. The number of A draft of this guideline was reviewed in clinical conferences
publications identified is presented in Section IV of the and by distribution for comment within departments and
accompanying Literature Review Methods and Results. divisions of UMHS to which the content is most relevant:
Emergency Medicine, Family Medicine, General Medicine,
Literature review and assessment. Members of the Geriatric Medicine, Obstetrics & Gynecology (Women’s
guideline team reviewed the publications identified to be Health), and Pulmonary & Critical Care Medicine. The draft
relevant to specific topics in order to select those with best was revised based on comments from these groups.
evidence. Criteria to identify overall best evidence included
relevance of the study setting and population, study design, The final version of this guideline was endorsed by the
sample size, measurement methods (variables, measures, data Clinical Practice Committee of the University of Michigan
collection), intervention methods (appropriateness, Medical Group and by the Executive Committee for Clinical
execution), appropriateness of analyses, and clarity of Affairs of the University of Michigan Hospitals and Health
description. Centers.
In considering level of evidence based on study design, the

classification was:

References smoking to COPD, chronic bronchitis and emphysema. BMC
Pulm Med. 2011;11:36-2466-11-36.
1. 2017 GINA report, global strategy for asthma 12. Fischer F, Kraemer A. Meta-analysis of the association
management and prevention. http://ginasthma.org/asthma- between second-hand smoke exposure and ischaemic heart
copd-and-asthma-copd-overlap-syndrome-acos/. Accessed diseases, COPD and stroke. BMC Public Health.
March 14, 2017. 2015;15:1202.
2. GOLD 2017 Global Strategy for the Diagnosis, 13. Ryu JY, Sunwoo YE, Lee S, et al. Chronic obstructive
Management, and Prevention of Chronic Obstructive pulmonary disease (COPD) and vapors, gases, dusts, or
Pulmonary Disease. Global initiative for chronic obstructive fumes (VGDF): A meta-analysis. Copd: Journal of Chronic
lung disease (GOLD) 2017. Obstructive Pulmonary Disease. 2015;12(4):374-380.
3. Fletcher CM. Standardized questionnaire on respiratory 14. Silverman EK, Sandhaus RA. Clinical practice. Alpha1-
symptoms: A statement prepared and approved by the MRC antitrypsin deficiency. N Engl J Med. 2009;360(26):2749-
committee on the aetiology of chronic bronchitis (MRC 2757.
breathlessness score). British Medical Journal. 1960;2:1662.
15. Vestbo J, Agusti A, Wouters EF, et al. Should we view
4. Jones PW, Harding G, Berry P, Wiklund I, Chen WH, chronic obstructive pulmonary disease differently after
Kline Leidy N. Development and first validation of the ECLIPSE? A clinical perspective from the study team.
COPD assessment test. Eur Respir J. 2009;34(3):648-654. American Journal of Respiratory & Critical Care Medicine.
2014;189(9):1022-1030.
5. Yawn BP, Thomashow B, Mannino DM, Han MK,
Kalhan R, Rennard S, Cerreta S, Crapo JD, Wise R. The 16. Beeh KM, Glaab T, Stowasser S, et al. Characterisation
2017 update to the COPD foundation COPD Pocket of exacerbation risk and exacerbator phenotypes in the
Consultant Guide. Chronic Obstr Pulm Dis. 2017;4(3):177- POET-COPD trial. Respir Res. 2013;14:116-9921-14-116.
185. doi: https://doi.org/10.15326/jcopdf.4.3.2017.0136.
2017;4(3):177-185. 17. Hurst JR, Vestbo J, Anzueto A, et al. Susceptibility to
exacerbation in chronic obstructive pulmonary disease. N
6. Celli BR, Cote CG, Marin JM, et al. The body-mass Engl J Med. 2010;363(12):1128-1138.
index, airflow obstruction, dyspnea, and exercise capacity
index in chronic obstructive pulmonary disease. N Engl J 18. Guirguis-Blake JM, Senger CA, Webber EM, Mularski
Med. 2004;350(10):1005-1012. RA, Whitlock EP. Screening for chronic obstructive
pulmonary disease: Evidence report and systematic review
7. Holland AE, Spruit MA, Troosters T, et al. An official for the US preventive services task force. JAMA.
European Respiratory Society/American Thoracic Society 2016;315(13):1378-1393.
technical standard: Field walking tests in chronic respiratory
disease. Eur Respir J. 2014;44(6):1428-1446. 19. Kohansal R, Martinez-Camblor P, Agusti A, Buist AS,
Mannino DM, Soriano JB. The natural history of chronic
8. Mannino DM, Gagnon RC, Petty TL, Lydick E. airflow obstruction revisited: An analysis of the Framingham
Obstructive lung disease and low lung function in adults in offspring cohort. Am J Respir Crit Care Med. 2009;180(1):3-
the United States: Data from the National Health and 10.
Nutrition Examination Survey, 1988-1994. Arch Intern Med.
2000;160(11):1683-1689. 20. Hnizdo E, Sullivan PA, Bang KM, Wagner G.
Association between chronic obstructive pulmonary disease
9. Decramer M, Janssens W, Miravitlles M. Chronic and employment by industry and occupation in the US
obstructive pulmonary disease. Lancet. population: A study of data from the Third National Health
2012;379(9823):1341-1351. and Nutrition Examination Survey. Am J Epidemiol.
2002;156(8):738-746.
10. Centers for Disease Control and Prevention. Chronic
Obstructive Pulmonary Disease (COPD). 21. Liu S, Zhou Y, Wang X, et al. Biomass fuels are the
https://www.cdc.gov/copd/index.html#4 . Accessed probable risk factor for chronic obstructive pulmonary
September 9, 2017. disease in rural south China. Thorax. 2007;62(10):889-897.
11. Forey BA, Thornton AJ, Lee PN. Systematic review with 22. Dhariwal J, Tennant RC, Hansell DM, et al. Smoking
meta-analysis of the epidemiological evidence relating cessation in COPD causes a transient improvement in

spirometry and decreases micronodules on high-resolution population-based study and a systematic review of the
CT imaging. Chest. 2014;145(5):1006-1015. literature. Chest. 2005;127(6):1952-1959.
23. Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on 34. Etminan M, Jafari S, Carleton B, FitzGerald JM. Beta-
smoking quit rate of telling patients their lung age: The blocker use and COPD mortality: A systematic review and
Step2quit randomised controlled trial. BMJ. meta-analysis. BMC Pulm Med. 2012;12:48-2466-12-48.
2008;336(7644):598-600.
35. Zeng LH, Hu YX, Liu L, Zhang M, Cui H. Impact of
24. Miravitlles M, Worth H, Soler Cataluna JJ, et al. beta2-agonists, beta-blockers, and their combination on
Observational study to characterise 24-hour COPD cardiac function in elderly male patients with chronic
symptoms and their relationship with patient-reported obstructive pulmonary disease. Clin Interv Aging.
outcomes: Results from the ASSESS study. Respiratory 2013;8:1157-1165.
Research. 2014;15:122.
36. Prosen G, Klemen P, Strnad M, Grmec S. Combination
25. Holleman DR,Jr, Simel DL. Does the clinical of lung ultrasound (a comet-tail sign) and N-terminal pro-
examination predict airflow limitation? JAMA. brain natriuretic peptide in differentiating acute heart failure
1995;273(4):313-319. from chronic obstructive pulmonary disease and asthma as
cause of acute dyspnea in prehospital emergency setting.
26. Walker PP, Mitchell P, Diamantea F, Warburton CJ, Crit Care. 2011;15(2):R114.
Davies L. Effect of primary-care spirometry on the diagnosis
and management of COPD. Eur Respir J. 2006;28(5):945- 37. Zhao SQ, Hu YM, Li Q, et al. The clinical value of rapid
952. assay for plasma B-type natriuretic peptide in differentiating
congestive heart failure from pulmonary causes of dyspnoea.
27. Han MK, Muellerova H, Curran-Everett D, et al. GOLD Int J Clin Pract. 2008;62(2):214-220.
2011 disease severity classification in COPDGene: A
prospective cohort study. Lancet Respir Med. 2013;1(1):43- 38. Sarwar G, Bisquera A, Peel R, Hancock S, Grainge C,
50. Attia J. The effect of inhaled corticosteroids on bone mineral
density measured by quantitative ultrasonography in an older
28. Rahaghi FF, Sandhaus RA, Brantly ML, et al. The population. Clin Respir J. 2016.
prevalence of alpha-1 antitrypsin deficiency among patients
found to have airflow obstruction. COPD. 2012;9(4):352- 39. Blakemore A, Dickens C, Guthrie E, et al. Depression
358. and anxiety predict health-related quality of life in chronic
obstructive pulmonary disease: Systematic review and meta-
29. American Thoracic Society, European Respiratory analysis. International Journal of Copd. 2014;9:501-512.
Society. American Thoracic Society/European Respiratory
Society statement: Standards for the diagnosis and 40. Farver-Vestergaard I, Jacobsen D, Zachariae R. Efficacy
management of individuals with alpha-1 antitrypsin of psychosocial interventions on psychological and physical
deficiency. Am J Respir Crit Care Med. 2003;168(7):818- health outcomes in chronic obstructive pulmonary disease: A
900. systematic review and meta-analysis. Psychotherapy &
Psychosomatics. 2015;84(1):37-50.
30. Nishimura K, Izumi T, Tsukino M, Oga T. Dyspnea is a
better predictor of 5-year survival than airway obstruction in 41. Vozoris NT. Do benzodiazepines contribute to
patients with COPD. Chest. 2002;121(5):1434. respiratory problems? Expert Rev Respir Med.
2014;8(6):661-663.
31. Karloh M, Fleig Mayer A, Maurici R, Pizzichini MM,
Jones PW, Pizzichini E. The COPD assessment test: What 42. Majothi S, Jolly K, Heneghan NR, et al. Supported self-
do we know so far?: A systematic review and meta-analysis management for patients with COPD who have recently been
about clinical outcomes prediction and classification of discharged from hospital: A systematic review and meta-
patients into GOLD stages. Chest. 2016;149(2):413-425. analysis. International Journal of Copd. 2015;10:853-867.
32. Decramer M, Rennard S, Troosters T, et al. COPD as a 43. Stead LF, Koilpillai P, Fanshawe TR, Lancaster T.
lung disease with systemic consequences--clinical impact, Combined pharmacotherapy and behavioural interventions
mechanisms, and potential for early intervention. COPD. for smoking cessation. Cochrane Database Syst Rev.
2008;5(4):235-256. 2016;3:CD008286.
33. Sin DD, Wu L, Man SF. The relationship between 44. Schauer GL, Wheaton AG, Malarcher AM, Croft JB.
reduced lung function and cardiovascular mortality: A Health-care provider screening and advice for smoking
cessation among smokers with and without COPD: 2009-

2010 national adult tobacco survey. Chest. 2016;149(3):676- antagonists in COPD. Pulm Pharmacol Ther.
684. 2010;23(4):257-267.
45. Eisner MD, Balmes J, Katz PP, Trupin L, Yelin EH, 56. Wedzicha JA, Banerji D, Chapman KR, et al.
Blanc PD. Lifetime environmental tobacco smoke exposure Indacaterol-glycopyrronium versus salmeterol-fluticasone
and the risk of chronic obstructive pulmonary disease. for COPD. N Engl J Med. 2016;374(23):2222-2234.
Environ Health. 2005;4(1):7.
57. Calverley PM, Anderson JA, Celli B, et al. Salmeterol
46. Bang KM, Syamlal G, Mazurek JM. Prevalence of and fluticasone propionate and survival in chronic
chronic obstructive pulmonary disease in the U.S. working obstructive pulmonary disease. N Engl J Med.
population: An analysis of data from the 1997-2004 national 2007;356(8):775-789.
health interview survey. COPD. 2009;6(5):380-387.
58. Singh S, Loke YK, Furberg CD. Inhaled anticholinergics
47. Gan WQ, FitzGerald JM, Carlsten C, Sadatsafavi M, and risk of major adverse cardiovascular events in patients
Brauer M. Associations of ambient air pollution with chronic with chronic obstructive pulmonary disease: A systematic
obstructive pulmonary disease hospitalization and mortality. review and meta-analysis. JAMA. 2008;300(12):1439-1450.
Am J Respir Crit Care Med. 2013;187(7):721-727.
59. Tashkin D, Celli B, Senn S, et al. A 4-year trial of
48. Romieu I, Riojas-Rodriguez H, Marron-Mares AT, tiotropium in chronic obstructive pulmonary disease
Schilmann A, Perez-Padilla R, Masera O. Improved biomass (UPLIFT trial). Rev Port Pneumol. 2009;15(1):137-140.
stove intervention in rural Mexico: Impact on the respiratory
health of women. Am J Respir Crit Care Med. 60. Nannini LJ, Poole P, Milan SJ, Holmes R, Normansell R.
2009;180(7):649-656. Combined corticosteroid and long-acting beta(2)-agonist in
one inhaler versus placebo for chronic obstructive
49. Kim DK, Bridges CB, Harriman KH, Advisory pulmonary disease. Cochrane Database Syst Rev.
Committee on Immunization Practices (ACIP), ACIP Adult 2013;(11):CD003794. doi(11):CD003794.
Immunization Work Group. Advisory Committee on
Immunization Practices recommended immunization 61. Yang IA, Clarke MS, Sim EH, Fong KM. Inhaled
schedule for adults aged 19 years or older - United States, corticosteroids for stable chronic obstructive pulmonary
2016. Am J Transplant. 2016;16(6):1930-1932. disease. Cochrane Database Syst Rev. 2012;(7):CD002991.
doi(7):CD002991.
50. Walters JA, Tang JN, Poole P, Wood-Baker R.
Pneumococcal vaccines for preventing pneumonia in chronic 62. Spencer S, Karner C, Cates CJ, Evans DJ. Inhaled
obstructive pulmonary disease. Cochrane Database Syst Rev. corticosteroids versus long-acting beta(2)-agonists for
2017;1:CD001390. chronic obstructive pulmonary disease. Cochrane Database
Syst Rev. 2011;(12):CD007033. doi(12):CD007033.
51. Poole PJ, Chacko E, Wood-Baker RW, Cates CJ.
Influenza vaccine for patients with chronic obstructive 63. Vestbo J, Anderson JA, Brook RD, et al. Fluticasone
pulmonary disease. Cochrane Database Syst Rev. furoate and vilanterol and survival in chronic obstructive
2006;(1)(1):CD002733. pulmonary disease with heightened cardiovascular risk
(SUMMIT): A double-blind randomised controlled trial.
52. Vu T, Farish S, Jenkins M, Kelly H. A meta-analysis of Lancet. 2016;387(10030):1817-1826.
effectiveness of influenza vaccine in persons aged 65 years
and over living in the community. Vaccine. 2002;20(13- 64. Albert RK, Connett J, Bailey WC, et al. Azithromycin
14):1831-1836. for prevention of exacerbations of COPD. N Engl J Med.
2011;365(8):689-698.
53. Sestini P, Renzoni E, Robinson S, Poole P, Ram FS.
Short-acting beta 2 agonists for stable COPD. Cochrane 65. Yao GY, Ma YL, Zhang MQ, Gao ZC. Macrolide
Database Syst Rev. 2000;(3)(3):CD001495. therapy decreases chronic obstructive pulmonary disease
exacerbation: A meta-analysis. Respiration. 2013;86(3):254-
54. Karner C, Chong J, Poole P. Tiotropium versus placebo 260.
for chronic obstructive pulmonary disease. Cochrane
Database of Systematic Reviews. 2014;7:009285. 66. Garvey C, Bayles MP, Hamm LF, et al. Pulmonary
rehabilitation exercise prescription in chronic obstructive
55. Cazzola M, Molimard M. The scientific rationale for pulmonary disease: Review of selected guidelines: An
combining long-acting beta2-agonists and muscarinic official statement from the American Association of

Cardiovascular and Pulmonary Rehabilitation. J Cardiopulm MLN/MLNProducts/Downloads/Home-Oxygen-Therapy-
Rehabil Prev. 2016;36(2):75-83. Text-Only.pdf. Updated October 2016. Accessed May 2017.
67. COPD Working Group. Long-term oxygen therapy for 77. Sapey E, Stockley RA. COPD exacerbations . 2:
patients with chronic obstructive pulmonary disease Aetiology. Thorax. 2006;61(3):250-258.
(COPD): An evidence-based analysis. Ont Health Technol
Assess Ser. 2012;12(7):1-64. 78. McCrory DC, Brown CD. Anti-cholinergic
bronchodilators versus beta2-sympathomimetic agents for
68. Puhan MA, Gimeno-Santos E, Scharplatz M, Troosters acute exacerbations of chronic obstructive pulmonary
T, Walters EH, Steurer J. Pulmonary rehabilitation following disease. Cochrane Database Syst Rev.
exacerbations of chronic obstructive pulmonary disease. 2002;(4)(4):CD003900.
Cochrane Database Syst Rev. 2011;(10):CD005305.
doi(10):CD005305. 79. Dolovich MB, Ahrens RC, Hess DR, et al. Device
selection and outcomes of aerosol therapy: Evidence-based
69. Cranston JM, Crockett AJ, Moss JR, Alpers JH. guidelines: American College of Chest Physicians/American
Domiciliary oxygen for chronic obstructive pulmonary College of Asthma, Allergy, and Immunology. Chest.
disease. Cochrane Database Syst Rev. 2005;127(1):335-371.
2005;(4)(4):CD001744.
80. Leuppi JD, Schuetz P, Bingisser R, et al. Short-term vs
70. Nocturnal Oxygen Therapy Trial Group. et al. conventional glucocorticoid therapy in acute exacerbations
Continuous or nocturnal oxygen therapy in hypoxemic of chronic obstructive pulmonary disease: The REDUCE
chronic obstructive lung disease: A clinical trial. Ann Intern randomized clinical trial. JAMA. 2013;309(21):2223-2231.
Med. 1980;93(3):391-8.
81. Wedzicha JA Ers C, Miravitlles M, Hurst JR, et al.
71. Long term domiciliary oxygen therapy in chronic Management of COPD exacerbations: A European
hypoxic cor pulmonale complicating chronic bronchitis and Respiratory Society/American Thoracic Society guideline.
emphysema. Report of the Medical Research Council Eur Respir J. 2017;49(3):10.1183/13993003.00791-2016.
Working Party. Lancet. 1981;317(8222):681-686. Print 2017 Mar.
72. Tanni SE, Vale SA, Lopes PS, Guiotoko MM, Godoy I, 82. Murphy PB, Rehal S, Arbane G, et al. Effect of home
Godoy I. Influence of the oxygen delivery system on the noninvasive ventilation with oxygen therapy vs oxygen
quality of life of patients with chronic hypoxemia. J Bras therapy alone on hospital readmission or death after an acute
Pneumol. 2007;33(2):161-167. COPD exacerbation: A randomized clinical trial. JAMA.
2017;317(21):2177-2186.
73. Nonoyama ML, Brooks D, Guyatt GH, Goldstein RS.
Effect of oxygen on health quality of life in patients with 83. Klooster K, ten Hacken NHT, Hartman JE, Kerstjens
chronic obstructive pulmonary disease with transient HAM, van Rikxoort EM, Slebos D. Endobronchial valves
exertional hypoxemia. Am J Respir Crit Care Med. for emphysema without interlobar collateral ventilation. N
2007;176(4):343-349. Engl J Med. 2015;373(24):2325-2335.
74. Long-Term Oxygen Treatment Trial Research Group, 84. Davey C, Zoumot Z, Jordan S, et al. Bronchoscopic lung
Albert RK, Au DH, et al. A randomized trial of long-term volume reduction with endobronchial valves for patients
oxygen for COPD with moderate desaturation. N Engl J with heterogeneous emphysema and intact interlobar fissures
Med. 2016;375(17):1617-1627. (the BeLieVeR-HIFi trial): Study design and rationale.
Thorax. 2015;70(3):288-290.
75. Bischoff EW, Akkermans R, Bourbeau J, van Weel C,
Vercoulen JH, Schermer TR. Comprehensive self 85. Deslee G, Klooster K, Hetzel M, et al. Lung volume
management and routine monitoring in chronic obstructive reduction coil treatment for patients with severe emphysema:
pulmonary disease patients in general practice: Randomised A European multicentre trial. Thorax. 2014;69(11):980-986.
controlled trial. BMJ. 2012;345:e7642.
86. Sciurba FC, Criner GJ, Strange C, et al. Effect of
76. The Medicare Learning Network®. Home oxygen endobronchial coils vs usual care on exercise tolerance in
therapy. https://www.cms.gov/Outreach-and- patients with severe emphysema: The RENEW randomized
Education/Medicare-Learning-Network- clinical trial. JAMA. 2016;315(20):2178-2189.
87. Naunheim KS, Wood DE, Mohsenifar Z, et al. Long-

term follow-up of patients receiving lung-volume-reduction
surgery versus medical therapy for severe emphysema by the

national emphysema treatment trial research group. Ann recommendation statement. JAMA. 2016;315(13):1372-
Thorac Surg. 2006;82(2):431-443. 1377.
88. Ramsey SD, Shroyer AL, Sullivan SD, Wood DE. 99. Department of Veterans Affairs Department of Defense.
Updated evaluation of the cost-effectiveness of lung volume VA/DoD clinical practice guideline for the management of
reduction surgery. Chest. 2007;131(3):823-832. chronic obstructive pulmonary disease. 2014.
89. Orens JB, Estenne M, Arcasoy S, et al. International

guidelines for the selection of lung transplant candidates:
2006 update--a consensus report from the Pulmonary
Scientific Council of the International Society for Heart and
Lung Transplantation. J Heart Lung Transplant.
2006;25(7):745-755.
90. Ding M, Zhang W, Li K, Chen X. Effectiveness of t'ai

chi and qigong on chronic obstructive pulmonary disease: A
systematic review and meta-analysis. Journal of Alternative
& Complementary Medicine. 2014;20(2):79-86.
91. Wu W, Liu X, Wang L, Wang Z, Hu J, Yan J. Effects of

tai chi on exercise capacity and health-related quality of life
in patients with chronic obstructive pulmonary disease: A
systematic review and meta-analysis. International Journal
of Copd. 2014;9:1253-1263.
92. Ngai Shirley PC, Jones Alice YM, Tam Wilson Wai S.
Tai chi for chronic obstructive pulmonary disease (COPD). .
2016(6).
93. Noll DR, Johnson JC, Baer RW, Snider EJ. The
immediate effect of individual manipulation techniques on
pulmonary function measures in persons with chronic
obstructive pulmonary disease. Osteopath Med Prim Care.
2009;3:9-4732-3-9.
94. Heneghan NR, Adab P, Balanos GM, Jordan RE. Manual

therapy for chronic obstructive airways disease: A
systematic review of current evidence. Man Ther.
2012;17(6):507-518.
95. Weber C, Stirnemann J, Herrmann FR, Pautex S,

Janssens JP. Can early introduction of specialized palliative
care limit intensive care, emergency and hospital admissions
in patients with severe and very severe COPD? A
randomized study. BMC Palliative Care. 2014;13:47.
96. Au DH, Udris EM, Engelberg RA, et al. A randomized

trial to improve communication about end-of-life care
among patients with COPD. Chest. 2012;141(3):726-735.
97. Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention

of acute exacerbations of COPD: American College of Chest
Physicians and Canadian Thoracic Society Guideline. Chest.
2015;147(4):894-942.
98. US Preventive Services Task Force (USPSTF), Siu AL,

Bibbins-Domingo K, et al. Screening for chronic obstructive
pulmonary disease: US Preventive Services Task Force

Chronic Obstructive Pulmonary Disease: Patient Population: Objectives

Uploaded by

Copyright:

Available Formats

Chronic Obstructive Pulmonary Disease: Patient Population: Objectives

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Chronic Obstructive Pulmonary Disease: Patient Population: Objectives

Uploaded by

Copyright:

Available Formats

Quality Department Guidelines for Clinical Care

Chronic Obstructive Pulmonary Disease

2 UMHS COPD Guideline, November 2017

Acute Exacerbation Management

Table 2. Symptoms and Signs Suggesting COPD

Table 3. Alternative Diagnoses for Chronic Cough and Dyspnea

Asthma Chronic aspiration Cystic fibrosis Sarcoidosis

Table 4. Factors Differentiating Asthma and COPD*

Diagnosis of COPD – Chronic Airflow Obstruction (spirometry)

Extent of Airflow Limitation (spirometry)2

mMRC (Modified Medical Research Council) Dyspnea Scale3

CATTM (COPD Assessment Test)4

I never cough       I cough all the time

Other Aspects of Severity

4 UMHS COPD Guideline, November 2017

All patients with a diagnosis of COPD

If persistent symptoms, If persistent symptoms or

5 UMHS COPD Guideline, November 2017

Acute exacerbation. Recognition of an acute exacerbation and an initial action plan

Table 7. Medications Commonly Used in Chronic Obstructive Pulmonary Disease

6 UMHS COPD Guideline, November 2017

7 UMHS COPD Guideline, November 2017

Oral corticosteroids: not routinely recommended

8 UMHS COPD Guideline, November 2017

Level of Continuous Use Oxygen

Strong Resting PaO2 ≤ 55 mm Hg or resting oxygen saturation ≤ 88% b

Table 9. Acute Exacerbation: Commonly Used Medications and Doses

Inhaled short-acting beta-2 agonists (SABA) [bronchodilator]

9 UMHS COPD Guideline, November 2017

10 UMHS COPD Guideline, November 2017

Prognosis Although about half of the individuals with COPD in the

While FEV1 (the forced expiratory volume in the first second)

Risk Factors and Clinical History Recommendation:

12 UMHS COPD Guideline, November 2017

Separately assessing airflow limitation, symptom severity,

While inhaled corticosteroids may carry a theoretical risk for

Recommendation: Benefits of medication.

Recommendation: Chronic macrolide therapy with oral azithromycin has been

An increase in the frequency of pneumonia has been reported Recommendation:

Recommendation: In patients with very severe COPD, long-term oxygen therapy

17 UMHS COPD Guideline, November 2017

Recommendation: All patients prescribed oxygen must be recertified every 12

Recommendation: Insurance coverage for dietician referral for this purpose

18 UMHS COPD Guideline, November 2017

Acute Exacerbation Spirometry, arterial blood gas, and electrocardiogram are

Outpatient assessment for an acute exacerbation of COPD

The benefit of antibiotics for patients with severe COPD Recommendation:

For treatment of outpatients with a COPD exacerbation, we Lung Volume Reduction

Recommendation: Lung volume reduction surgery may be considered after

Lung transplantation may be considered for patients who have

As COPD worsens, care considerations and decisions become

21 UMHS COPD Guideline, November 2017

To update those results, we performed a systematic search of

22 UMHS COPD Guideline, November 2017

In considering level of evidence based on study design, the

23 UMHS COPD Guideline, November 2017

24 UMHS COPD Guideline, November 2017

25 UMHS COPD Guideline, November 2017

26 UMHS COPD Guideline, November 2017