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The information contained in this ICSI Health Care Guideline is intended primarily for health profes-sionals and the following expert audiences:

physicians, nurses, and other health care professional and provider organizations; health plans, health systems, health care organizations, hospitals and integrated health care

delivery systems; medical specialty and professional societies; researchers; federal, state and local government health care policy makers and specialists; and employee benefit managers.

This ICSI Health Care Guideline should not be construed as medical advice or medical opinionrelated to any specific facts or circumstances. If you are not one of the expert audiences listedabove you are urged to consult a health care professional regarding your own situation and anyspecific medical questions you may have. In addition, you should seek assistance from a healthcare professional in interpreting this ICSI Health Care Guideline and applying it in your individualcase.

This ICSI Health Care Guideline is designed to assist clinicians by providing an analytical frameworkfor the evaluation and treatment of patients, and is not intended either to replace a clinicians

judgment or to establish a protocol for all patients with a particular condition. AnICSI Health Care

Guideline rarely will establish the only approach to a problem.

Copies of this ICSI Health Care Guideline may be distributed by any organization to theorganizations employees but, except as provided below, may not be distributed outside of theorganization without the prior written consent of the Institute for Clinical Systems Improvement,Inc. If the organization is a legally constituted medical group, the ICSI Health Care Guideline maybe used by the medical group in any of the following ways:

copies may be provided to anyone involved in the medical groups process for developing andimplementing clinical guidelines;

the ICSI Health Care Guideline may be adopted or adapted for use within the medical grouponly, provided that ICSI receives appropriate attribution on all written or electronic documents;and

copies may be provided to patients and the clinicians who manage their care, if the ICSI HealthCare Guideline is incorporated into the medical groups clinical guideline program.

All other copyright rights in this ICSI Health Care Guideline are reserved by the Institute for ClinicalSystems Improvement. The Institute for Clinical Systems Improvement assumes no liability forany adaptations or revisions or modifications made to this ICSI Health Care Guideline .

Health Care GuidelineICSIINSTITUTE FOR CLINICAL

SYSTEMS IMPROVEMENT

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Health Care Guideline:

Chronic Obstructive Pulmonary Disease

These clinical guidelines aredesigned to assist clinicians

by providing an ana lyticalframework for the evaluationand treatment of patients, andare not intended either toreplace a clinician's judgmentor to establish a protocol forall patients with a particularcondition. A guideline willrarely establish the onlyapproach to a problem.

Sixth Edition

January 2007

Work Group LeaderJames Mickman, MDPulmonology & Critical Care

Medicine, HealthPartners

Medical Group

Work Group Members

Family Medicine

Allen Horn, MD

CentraCare Clinic

G. Paul Kerestes, MD

Allina Medical Clinic

Nursing and Health

Education

Catherine Youngman, RNHealthPartners Medical

Group

Pharmacy

Stefanie Larson, RPH

Park Nicollet Health Services

Pulmonary & Critical Care

Medicine

Delmar Gillespie, MD

Mayo Clinic

Charlene McEvoy, MD

HealthPartners Regions

Hospital

Respiratory Therapy

Scott Copeman, RRT, RCP

Mayo Clinic

Jeff Norton, CRT, RCP

Fairview Health Services

Measurement and

Implementation Advisor

Teresa Hunteman, RRT,

CPHQ

ICSI

Facilitator

Linda Setterlund, MA

ICSI

www.icsi.org

I ICSINSTITUTE FOR CLINICAL

SYS TEMS IMPROVEMENT

Copyright 2007 by Institute for Clinical Systems Improvement 1

A = AnnotationSymptoms of or risk factors for COPD

1

A

Ask about tobacco

use/exposure at every visit

2

A

Establish diagnosis of COPD Medical history Physical examination Spirometry (pre- and

post-bronchodilator) Chest radiograph

3

A

Acuteexacerbation?

4

A

Evaluation

5

A

Treatment

6

A

Establish severity of stable COPD Mild Moderate Severe

10

A

Positive response totreatment?

7

A

Step-care pharmacologicapproach for managing

stable COPD

11

A

Other pharmacologic

treatment

12

A

Non-pharmacologic treatment applicable to all levels of severity Encourage exercise Education Pulmonary rehab program for

moderate, severe disease

13

A

Assess for hypoxemia andhypercapnia and treat if

indicated

14

A

Long-term management Schedule regular follow-up visits Evaluation and monitoring of comorbidities Refer to pulmonary specialist Surgical options for severe disease Discuss health care directives (advance

directives) and goals of care

15

A

yes

yes

Admit to hospital out of guideline

9

A

Arrange forfollow-up

8

no

A

no

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Algorithms and Annotations ................................................................................................................1-41

Algorithm ..............................................................................................................................................1

ForewordScope and Target Population ..........................................................................................................3

Clinical Highlights and Recommendations ....................................................................................3

Priority Aims ..................................................................................................................................3

Related ICSI Scientic Documents ................................................................................................4

Brief Description of Evidence Grading ..........................................................................................4

Disclosure of Potential Conict of Interest ....................................................................................4

Annotations ...........................................................................................................................................5-36

Appendices ............................................................................................................................................37-41Appendix A Estimated Comparative Daily Dosage for

Inhaled Corticosteroids ..............................................................................................................37

Appendix B Medicare Standard for Oxygen Coverage ...............................................................38

Appendix C Summary of Structure and Services Pulmonary Rehabilitation Program ..............................................................................................39-41

Supporting Evidence ..............................................................................................................................42-59

Evidence Grading System .....................................................................................................................43-44References .............................................................................................................................................45-51

Conclusion Grading Worksheets ...........................................................................................................52-59

Conclusion Grading Worksheet A Annotation #11 (Pharmacological Management) .................52-59

Support for Implementation ................................................................................................................60-65

Priority Aims and Suggested Measures ................................................................................................61-62

Measurement Specications...........................................................................................................63

Key Implementation Recommendations ...............................................................................................64

Knowledge Products and Resources .....................................................................................................64Other Resources Available ....................................................................................................................65

Table of Contents

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Foreword

Scope and Target Population

Although chronic obstructive pulmonary disease (COPD) can occur in adults of any age, especially smokers,

it most commonly occurs in people 45 years and older. The target population for this guideline is people

with symptoms of stable COPD as well as acute exacerbations of COPD.

Clinical Highlights and Recommendations

Assess patients for symptoms and risk factors for COPD, including asking about tobacco use/exposure

at every visit. (Annotations #1, 2)

Establish diagnosis and severity of COPD through spirometry, pre- and post-bronchodilator and chest

radiograph, in addition to history and physical examination. (Annotation #3)

After establishing severity, assess patient needs for pharmacologic and non-pharmacologic treatmentand provide appropriate therapy as indicated. (Annotations #11, 12, 13)

Management of COPD should include an education plan suited to the patient's specic needs, encourage-

ment of exercise, tobacco use cessation and other behavioral changes, and monitoring of immunization

status. (Annotations #2, 13)

A trial of inhaled steroids is indicated for symptoms not controlled by scheduled bronchodilators.

(Annotation #11)

A course of systemic steroids is benecial for COPD exacerbations. (Annotation #6)

Tiotropium offers signicant advantages compared to other bronchodilators to patients whose symptoms

are not controlled by albuterol. (Annotation #11)

For patients with severe symptoms, despite maximal medical therapy, lung volume reduction surgery

and transplantation may be an option. (Annotation #15)

Patients should be regularly assessed for hypoxemia; appropriate oxygen therapy should be prescribed

accordingly. (Annotation #14)

Physicians should discuss advance directives/health care directives and goals of care as early as possible.

(Annotation #15)

Priority Aims

1. Increase the quality and use of spirometry testing in the diagnosis of patients with COPD.

2. Increase the number of patients with COPD who receive information on the options for tobacco cessa-

tion and information on the risks of continued smoking.3. Reduce COPD exacerbation requiring emergency department (ED) evaluation or hospital admission.

4. Increase the appropriate use of pharmacotherapy prescribed for patients with COPD.

5. Increase patients' education and management skills with COPD.

6. Increase the number of patients with COPD presenting with an acute exacerbation who have an oxymetric

evaluation.


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Related ICSI Scientic Documents

Related Guidelines

Diagnosis and Management of Asthma

Emergency and Inpatient Management of Asthma

Respiratory Illness in Adults and Children

Tobacco Use Cessation and Prevention in Adults

Palliative Care

Technology Assessment Reports

Lung Volume Reduction Surgery for Emphysema (#23, 2003)

Case Management for Chronic Illness, the Frail Elderly, and Acute MI (#44, 1998)

Pulmonary Rehabilitation for Chronic Obstructive Pulmonary Disease ( #32, 1997)

Patient and Family Guidelines

Chronic Obstructive Pulmonary Disease for Patients and Families

Evidence Grading

Individual research reports are assigned a letter indicating the class of report based on design type: A, B,

C, D, M, R, X.

Key conclusions are assigned a conclusion grade: I, II, III, or Grade Not Assignable.

A full explanation of these designators is found in the Supporting Evidence section of the guideline.

Disclosure of Potential Conict of InterestIn the interest of full disclosure, ICSI has adopted the policy of revealing relationships work group members

have with companies that sell products or services that are relevant to this guideline topic. The reader should

not assume that these nancial interests will have an adverse impact on the content of the guideline, but they

are noted here to fully inform readers. Readers of the guideline may assume that only work group members

listed below have potential conicts of interest to disclose.

No work group members have potential conicts of interest to disclose.

ICSI's conflict of interest policy and procedures are available for review on ICSI's Web site athttp://www.icsi.org.

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Algorithm Annotations

1. Symptoms of or Risk Factors for COPDCOPD may be indicated by the presence of one of the following symptoms:

Chronic cough (duration greater than three months) with or without sputum production

Dyspnea with or without wheezing

COPD should also be considered if the patient has one or more of the following risk factors:

History of tobacco use or prolonged exposure to secondhand or environmental smoke

Asthma

Environmental exposure to occupational dust and chemicals (e.g., cadmium)

Alpha1- antitrypsin deciency

Chronic respiratory infections

2. Ask About Tobacco Use/Exposure at Every Visit

Key Points:

Tobacco cessation and oxygen therapy are the only interventions proven to

prolong survival of patients with COPD.

Ten to fteen percent of long-term smokers develop COPD with accelerated rates of decline in FEV1. Advice

and support from physicians and other health professionals are potentially powerful inuences on tobacco

cessation. According to the U.S. Surgeon General, tobacco use is one of the most important public health

issues of our time. The National Cancer Institute, which is the primary federal agency for tobacco control,

states that the keys to patient awareness and education about tobacco cessation in a clinical setting are:

ASK about tobacco use at every visit

ADVISE all users to stop

ASSESS users' willingness to make a quit attempt

ASSIST users' efforts to quit

ARRANGE follow-up

Reinforcement of tobacco cessation and follow-up for patients with COPD are extremely important. Phar-

macotherapy, social support and skills training/problem solving are the key treatments for tobacco cessa-

tion. Nicotine patches, nasal sprays, inhalers and oral medication are all available to help patients achieve

cessation (Dale, 2001; Institute for Clinical Systems Improvement, 2000; U.S. Department of Health andHuman Services, 2000).

For more information about tobacco cessation, please refer to the ICSI Tobacco Use Prevention and Cessa-

tion for Adults and Mature Adolescents guideline and the U.S. Department of Health and Human Services

Clinical Practice Guideline, Treating Tobacco Use and Dependence.

Supporting evidence is of classes: A, R


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3. Establish Diagnosis of COPD

Key Points:

The American Thoracic Society (ATS) denes COPD as follows:

COPD is a disease characterized by the presence of airow obstruction due tochronic bronchitis or emphysema; the airow obstruction is generally progres-

sive, may be accompanied by airway hyperreactivity and may be partially

reversible.

Chronic bronchitis is dened as the presence of chronic productive cough

for three months in each of two successive years in a patient in whom other

causes of chronic cough have been excluded.

Emphysema is dened as an abnormal permanent enlargement of the air spaces

distal to the terminal bronchioles, accompanied by destruction of their wallsand without obvious brosis.

The diagnosis of COPD should be suspected based on the patient's medical history and physical examina-

tion, but requires spirometry to determine the degree of airow limitation.

Signs/symptoms for which COPD may be suspected:

Wheezing, prolonged expiratory phase of respiration, rhonchi and cough

Dyspnea (exertional or at rest)

Chronic sputum production

Hyperination of the chest with increased anterior-posterior (A-P) diameter

Use of accessory muscles of respiration

Pursed-lip breathing

Signs of cor pulmonale:

- Increased pulmonic component of the second heart sound

- Neck vein distention

- Lower extremity edema

- Hepatomegaly

NOTE: nger clubbing is not characteristic of COPD and should alert the clinician to another

condition such as idiopathic pulmonary brosis (IPF), cystic brosis, lung cancer or asbes-

tosis.

Airow obstruction is measured by spirometry and shows a reduced forced expiratory volume in one second

(FEV1) and FEV

1/FVC (forced vital capacity) ratio. Measuring pre- and post-bronchodilator spirometry

is important to identify those patients with partial reversibility of airow obstruction. Partial reversibility

is dened as improvement in airow by 12% of baseline and 200 mL after administration of a bronchodi-

lator.

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Bronchitis and Emphysema

The airow obstruction in COPD may be due to chronic bronchitis or emphysema. Chronic bronchitis

is dened as the presence of a chronic productive cough for three months in each of two successive

years in a patient in whom other causes of chronic cough have been excluded.

Emphysema is dened as an abnormal permanent enlargement of the air spaces distal to the terminalbronchioles, accompanied by destruction of their walls and without obvious brosis. Radiographically,

bullae may be visible on a chest computerized tomography scan or occasionally on a chest radiograph.Clinically, emphysema typically presents with a non-productive or minimally productive cough and

progressive dyspnea. Since both chronic bronchitis and emphysema result in airow limitation, manage-

ment goals are similar.

Differential Diagnosis

In addition to asthma, possible differential diagnoses for COPD include bronchiectasis, cystic brosis,

obliterative bronchiolitis, congestive heart failure and upper airway lesions.

For more information on diagnosis and treatment of asthma, please refer to the ICSI Diagnosis and

Treatment of Asthma guideline.

Denition of COPD from Other Guidelines:

The Global Initiative for Chronic Obstructive Lung Disease (Global Initiative for Chronic Obstructive Lung

Disease) denes COPD as follows:

A preventable and treatable disease characterized by chronic airow limitation that is not fully

reversible. Airow limitation is usually progressive and associated with an abnormal inammatory

response of the lungs.

(Global Initiative for Chronic Obstructive Lung Disease, 2006)

The British Thoracic Society (BTS) denes COPD as follows:

A chronic, slowly progressive disorder characterized by airow obstruction that does not changemarkedly over several months. Most of the lung function impairment is xed, although some

reversibility can be produced by bronchodilator.

The diagnosis requires a history of chronic progressive symptoms (cough and/or wheeze and/or

breathlessness), objective evidence of airway obstruction ideally by spirometric testing that

does not return to normal with treatment.

The presence of chronic cough and sputum production for at least three months of two consecutive

years in the absence of other diseases is used as a denition of chronic bronchitis, but does not

necessarily signify the presence of airway obstruction or a diagnosis of COPD.

(British Thoracic Society, 1997)

The European Respiratory Society (ERS) denes COPD as follows:

A disorder characterized by reduced maximum expiratory ows and slow, forced emptying of the

lungs; features do not change markedly over several months

Airow limitation due to varying combinations of airway disease and emphysema

Patients exhibit minimal reversibility of airow limitation with bronchodilators

(European Respiratory Society, 1995)


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Recommended Tools for the Diagnosis of COPD from Other Guidelines

Spirometry is recommended by ATS, BTS, ERS and GOLD

Pre- and post-bronchodilator recommended by ATS, BTS, ERS and GOLD

Chest radiograph recommended by ATS, ERS and GOLD. BTS recommends chest radiograph ifdisease is severe

Resting oxygen saturation measurement suggested by ERS in moderate or severe disease, and BTS

in severe disease

ABG recommended by ERS in moderate or severe disease or if oxygen saturation is less than 92%,

by ATS in moderate or severe disease, and by BTS and GOLD in severe disease

Screening for alpha1-antitrypsin concentration recommended by ERS, GOLD and ATS in patients

who develop COPD at a young age

Reversibility Testing (measurement of pre- and post-bronchial dilator)

NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (Global Initiative for ChronicObstructive Lung Disease):

- Generally performed only once at time of diagnosis, this test is useful to help rule out asthma, to

establish a patient's best attainable lung function, to gauge a patient's prognosis, and to guide treat-

ment decisions.

- Even patients who do not show a signicant FEV1

response to a short-acting bronchodilator test

can benet symptomatically from long-term bronchodilator treatment.

British Thoracic Society, COPD Guidelines Group of the Standards of Care Committee:

- A positive bronchodilator response (FEV1greater than 200 mL and 15% over baseline value) suggests

asthma.

- More than 20% variability in absolute measurement of serial PEF may suggest asthma.

European Respiratory Society (ERS):

- Atopy and marked improvement of spirometry with administration of bronchodilators or glucocor-

ticosteroids favor the diagnosis of asthma.

- Testing of bronchoconstrictor response is of doubtful clinical value in patients with established

airow limitation.

American Thoracic Society (ATS):

- Signicant reversibility is indicated by an increase of over 12% and 200 mL after inhaling a short-

acting bronchodilator.

4. Acute Exacerbation?Signs and symptoms of an acute exacerbation of COPD may include any of the following:

Increased dyspnea

Increased heart rate

Increased cough


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Increased sputum production

Change in sputum color or character


Peripheral edema

Development or increase in wheeze

Change in mental status

Fatigue

Fever

Increased respiratory rate

Decrease in FEV1

or peak expiratory ow

Hypoxemia

Chest tightness

Change in mental status or a combination of two or more of the following new symptoms indicates a severeacute exacerbation:

Dyspnea at rest

Respiratory rate of greater than 25 breaths per minute

Heart rate of greater than 110 beats per minute


5. Evaluation

When a patient with known COPD presents with a moderate to severe acute exacerbation, the following keyelements of the history, physical examination and laboratory/radiology evaluation should be considered:

History

Baseline respiratory status

Present treatment regimen and recent medication use

Signs of airway infection, e.g., fever and/or change in volume and/or color of sputum

Duration of worsening symptoms

Limitation of activities

History of previous exacerbations

Increased cough

Decrease in exercise tolerance

Chest tightness

Change in alertness

Other non-specic symptoms including malaise, difculty sleeping, and fatigue


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Symptoms associated with comorbid acute and chronic conditions

Although rarely used, non-selective beta-blockers may contribute to bronchospasms

Physical Examination

Measurement of heart rate and blood pressure

Measurement of respiratory rate

Measurement of pulse oximetry

Measurement of temperature

Respiratory distress

Accessory respiratory muscle use

Increased pulmonary ndings (e.g., wheezing, decreased air entry, prolonged expiratory phase

etc.)

Peripheral edema

Somnolence and/or hyperactivity Acute comorbid conditions

Laboratory/Radiology

Chest x-ray (in patients with suspected pneumonia)

ABG (if O2

saturation less than 88%, positive history of hypercapnia, questionable accuracy of

oximetry, somnolence, or other evidence of impending respiratory failure [e.g., respiratory rate

greater than 40 breaths per minute])

Theophylline level (if theophylline is being utilized)

WBC (in patients with suspected severe respiratory infection)

A sputum culture and an antibiogram, if available, should be performed when an infectious exac-erbation does not respond to initial antibiotic treatment (Global Initiative for Chronic Obstructive

Lung Disease, 2006). It is important that the sputum specimen is of good quality.

Brain Natriuretic Peptide (BNP), a simple blood lab test, can be of some use in evaluating a patient

presenting with dyspnea, although its interpretation needs to be carefully applied along with clinical

and other lab data such as chest x-ray and echocardiogram. Its sensitivity and specicity in this

setting increase at levels above 400 but do not differentiate between acute left ventricular (LV)

failure, cor pulmonale or pulmonary embolism (McCullough, 2002). It is of particular value if the

level is very low. The probability of LV failure as a cause of dyspnea is less than 10% if the BNP

is less than 100 (Maisel, 2002).

In patients with an acute COPD exacerbation, spirometry is of little value. For that reason, oximetry and/or

arterial blood gases should be monitored.

There is little evidence regarding the contribution of additional laboratory testing or the usefulness of electro-cardiography or echocardiography in an acute exacerbation of COPD. They may be a useful consideration

if the diagnosis is unclear, in order to evaluate other comorbid conditions.

(McCrory, 2001)

Supporting evidence is of classes: B, M, R


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6. Treatment

Key Points:

Albuterol is the preferred bronchodilator in the setting of an acute exacerba-

tion of COPD because of its rapid onset of action. Ipratropium may be added to produce additive bronchodilation and allow the

use of lower doses of albuterol.

Steroids should be used in acute exacerbations.

It is mandatory to check oxygen saturation or ABG measurement.

Bronchodilators

Albuterol is the preferred bronchodilator in the setting of an acute exacerbation of COPD because of its

rapid onset of action. Serial administration is indicated until either relief of symptoms and improvement

in signs of respiratory failure is achieved, or side effects of tachycardia and/or tremor develop. If clinical

improvement does not occur before side effects develop, ipratropium may be added to produce additivebronchodilation and allow the use of lower doses of albuterol, thus diminishing dose-dependent toxicity.

However, no study has examined the benet of using both agents concurrently. Administration of either

agent by MDI with a spacer or by nebulization is acceptable, though the patient may be too dyspneic to retain

a MDI puff effectively or severe coughing may prevent effective employment. In such cases, nebulization

is necessary and arrangement for home use should be made (Moayyedi, 1995; O'Driscoll, 1989; Patrick,

1990; Turner, 1997).

Supporting evidence is of classes: A, M

Role of Levalbuterol (Xopenex) in COPD

There are many theoretical advantages of levalbuterol over albuterol in the treatment of bronchospasm.

Albuterol is a racemic combination of two isomers: the "R" isomer (levalbuterol) that is a potent broncho-dilator, and the "S" isomer that has been shown in animal studies to counteract bronchodilation and can

promote inammation. Unfortunately, clinical studies in human subjects with bronchospasm have not

consistently shown greater bronchodilation, or fewer side effects of levalbuterol over equivalent doses of a

racemic agent such as albuterol. In individual patients with COPD and acute bronchospasm, who demon-

strate excessive tachycardia and/or tremor, ipratropium is the next bronchodilator of choice. Levalbuterol

may be an acceptable alternative as a trial agent, especially in patients whose bronchospasm worsens or

shows no improvement on ipratropium (Costello, 1999; Nelson, 1999; Scott, 2003).

Supporting evidence is of classes: C, R

Steroids

Studies have shown benets of systemic steroids in the outpatient management of COPD exacerbation.Doses of oral prednisone 30-60 mg per day should be used for 10 to 14 days. If longer durations are needed,

consider a tapering schedule. There is no need to discontinue inhaled steroids while the patient is taking oral

prednisone. In fact, the inhaled steroid may serve as a "systemic-steroid-sparing-agent" and the concomitant

use may minimize the dose of systemic steroids needed to diminish airway inammation (Davies, 1999;

McEvoy, 2000; Niewoehner, 1999).



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Antibiotics

If the acute exacerbation of COPD is clearly post-viral, antibiotics may not be necessary. In the presence of amore prolonged illness, especially with purulent sputum, an antibiotic is warranted. The choice of antibiotic

is controversial and needs to be tailored to the individual situation. "First-line agents," such as amoxicillin,

TMP/SMX and doxycycline are often effective. If the incidence of resistant organisms is 25% or higher

in the community, the use of a "second-line agent" may be preferable. These second-line agents include

second-generation cephalosporins, azithromycin, clarithromycin and amoxicillin/clavulanate (Anthonisen,

1987; Amsden, 2003; Chodosh, 1998).

Oxygen saturation/ABG measurement

Oxymetric evaluation of patients with COPD exacerbations is mandatory. Patients with O2

satura-

tions of 80%-90% on room air can be titrated with supplemental O2

to a saturation level of 90% with

little concern of signicant hypercarbia, unless such intervention results in somnolence. In such cases,

or if the O2

saturation is less than 80% upon presentation, an ABG should be obtained. If the pH is

less than 7.32, admission to the hospital should be arranged because of the risk of acute respiratory

failure. If outpatient management has been decided upon, the patient should be ambulated to determine

what O2 ow is needed to maintain O2 saturations at 90% while walking. Home O2 then needs to bearranged (Bone, 1978).

Supporting evidence is of class: D

7. Positive Response to Treatment?The following criteria may be used as evidence of improvement in COPD exacerbation:

Decrease in cough, sputum production, fever or dyspnea

Decrease in respiratory rate

Decrease in heart rate

Decrease in accessory muscle use

Increase in function and endurance

8. Arrange for Follow-UpA follow-up appointment between the primary care clinician and the patient should occur within one to four

weeks to reassess management strategies and supplemental oxygen needs.

9. Admit to Hospital Out of GuidelineThe following may be indications to consider hospital admission for an acute exacerbation of COPD:

Marked increase in intensity of symptoms, such as sudden development of resting dyspnea

History of severe COPD, especially if mechanical ventilation was required

Onset of new physical signs (e.g., cyanosis, peripheral edema)

Failure of exacerbation to respond to initial outpatient medical management

High risk comorbidities, pulmonary (e.g., pneumonia requiring hospitalization) or cardiac symp-

toms

Increasing hypoxemia despite supplemental oxygen


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New or worsening CO2

retention or Ph less than 7.32

Marked decrease in ability to ambulate, eat or sleep due to dyspnea

History of prolonged, progressive symptoms

Newly occurring arrhythmias

Diagnostic uncertainty

Older age

Insufcient home support

Decrease in alertness

(McCrory, 2001)

Supporting evidence is of class: M

10. Establish Severity of Stable COPD

Key Points: Both spirometry and/or signs and symptoms are used to establish severity.

The signs, symptoms and airow limitation in COPD vary with the severity of the disease. The severity of

COPD may be categorized according to the following table.

Table I

Category of COPD FEV1 (% predicted) Typical Symptoms and Signs

Mild 80 or greater No abnormal signs

Cough ( sputum)

Little or no dyspnea

Moderate Between 80 and 50 Breathlessness

( wheeze on moderate exertion)

Cough ( sputum)

Variable abnormal signs (general reduction in

breath sounds, presence of wheezes)

Hypoxemia may be present

Severe 30 to 50 Dyspnea with any exertion or at rest

Wheeze and cough often prominent

Very severe Less than 30 Lung hyperinflation usual; cyanosis,

peripheral edema and polycythemia in

advanced disease

Hypoxemia and hypercapnia are common

Adapted from NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD)

workshop summary.

The best correlation with morbidity and mortality is decrease in FEV1. With FEV

1greater than 1.0 L, there

is a slight increase in mortality at 10 years. With FEV1

less than 0.75 L, the approximate mortality rate at

one year is 30%, and at 10 years is 95%. Because of the relationship of prognosis and FEV1, the severity


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of COPD is staged on the basis of this spirometry measurement. Patients are categorized as mild, moderate

or severe. The COPD work group selected the COPD severity categories recommended by GOLD because

they are straightforward and correlate with clinical experience. However, it is clear that there are wide-

spread differences relative to disease severity classication among published guidelines (Hodgkin, 1990;

Pauwels, 2001).

Supporting evidence is of class: R

11. Step-Care Pharmacologic Approach for Managing Stable COPD

Key Points:

Drug therapy is determined by severity of symptoms.

Each step in Table II represents an intervention that should be considered only if the previous course

of action fails to improve symptoms of COPD. Step 1 is an intervention that is generally associated with

mild COPD. Step 2 is associated with moderate COPD. Steps 3 and 4 are associated with severe and verysevere COPD.

A table of estimated comparative daily dosages for inhaled corticosteroids is attached in Appendix A, "Esti-mated Comparative Daily Dosage for Inhaled Corticosteroids."


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Table II

STEP PHARMACEUTICAL INTERVENTION DOSING INFORMATION ANDCOMMENTS

1

Consider Step 2 ifsymptoms persist

Inhaled short-acting bronchodilator Short-acting beta agonist (albuterol ispreferred)

2-4 puffs as needed (every 4-6 hours)See Annotation #11

2 Continue PRN inhaled short-actingbronchodilator PLUS scheduled dosing ofone of the following:

Tiotropium (Spiriva)

Salmeterol* (Serevent Discus)

one capsule (inhaled) daily

1 puff twice daily

Formoterol* (Foradil) 1 puff (12 mcg) twice daily

Albuterol (Proventil, Ventolin) 2-4 puffs 4 times a day

Ipratropium (Atrovent) 2-4 puffs 4 times a day

Albuterol + Ipratropium(Combivent)

2-4 puffs 4 times a day

Levalbuterol (Xopenex) 0.63-1.25 mg every 6-8 hours vianebulizer2 puffs every 4-6 hours

Consider Step 3 ifsymptoms persist

3

Consider Step 4 if

symptoms persist

Continue therapy specified in Step 2 andperform corticosteroid trial.

Assess symptoms before and after trialperiod, especially cough and sputumproduction. Also measure post-

bronchodilator FEV1, 6-minute walk beforeand after trial.

Prednisone oral 30-40 mg/day for 2-4weeks or inhaled corticosteroid (seeAppendix A) at less than 2000 mcg for 6-8 weeks/day or dose equivalent ofanother inhaled steroid for 6-8 weeks

(Approximately 15% of patients whoundergo a corticosteroid trial will haveimproved symptoms and post-

bronchodilator FEV1)

* Tiotropium is the preferred scheduled bronchodilator.

POSITIVE RESPONSE: greater than or equal to 15%improvement in post-bronchodilator FEV1, symptoms,improvement in 6-minute walk

PHARMACEUTICAL INTERVENTIONTaper off or discontinue oral corticosteroids andprescribe or continue inhaled corticosteroids.

NEGATIVE RESPONSE: less than 15% improvement inpost-bronchodilator FEV1 or no improvement in symptoms

PHARMACEUTICAL INTERVENTIONDiscontinue corticosteroids and consider theophylline asadjunctive therapy with inhaled bronchodilators (2agonists and/or anticholinergic)

Step 4: Response AfterStep 3

negativepositive


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Bronchodilator Medications

Albuterol or Ipratropium

Albuterol and ipratropium are equipotent as bronchodilators, improving dyspnea and exercise tolerance

equally well. No dramatic evidence showing an advantage of either albuterol or ipratropium as a sched-

uled rst-step therapy for COPD symptoms or improved quality of life has been shown in the medicalliterature.

Albuterol is recommended as the rst-line treatment for patients with symptoms of mild COPD because the

onset of bronchodilator effect (15 minutes) is more rapid than ipratropium (30-90 minutes). The dose-response

curve of albuterol for improvement in FEV1

continues to increase to at least eight puffs. Ipratropium is to

be used on a regularly scheduled basis rather than as needed (PRN) because its' dose-response time is too

long to titrate its use to control symptoms.

Ipratropium bronchodilator duration (two puffs for four hours) is greater than albuterol (two puffs for two or

three hours). The dose-response curve for ipratroprium levels off above six puffs, whereas therapeutic efcacy

for albuterol continues to increase at higher doses, although side effects such as tremor can develop. Studies

were small and may not have been of a statistical power to detect differences between bronchodilators.

(Blosser, 1995; Easton, 1986; Rennard, 1996)

Clinicians should consider replacing ipratropuim with tiotropium as a scheduled bronchodilator because it

provides improved benets and only requires once-a-day dosing (Oostenbrink, 2004).

Supporting evidence is of classes: A, M

Combination Albuterol and Ipratropium

Many studies show that the combination of ipratropium 0.5 mg and albuterol 2.5 mg provides greater bron-

chodilator effect compared to each alone; however, the same effect could probably be achieved by doublingthe dose of either agent. This is reective of the additive bronchodilator effect of both, as expected. No study

compares the combination of ipratropium and albuterol to an equivalent dose of albuterol or ipratropium

(e.g., four puffs of combination to four puffs of albuterol or ipratropium).

One study also showed that patients randomized to albuterol two puffs four times/day had 18% more COPD

exacerbations than those randomized to ipratropium two puffs four times/day (therefore "more expensive"

p

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If a patient with COPD has unacceptable symptoms while on tiotropium, a long-acting beta-agonist can be

added (van Noord, 2006).

No studies have compared the additive effects of tiotropium with steroids as a single agent in effectiveness

of COPD management.

Supporting evidence is of class: A

Long-Acting Beta-Agonists (LABAs)

Formoterol

Twice-daily dosing of formoterol offers advantages similar to those of salmeterol. Data also show that

formoterol has quicker onset of action than salmeterol (Dahl, 2001; Kottakis, 2002).

Salmeterol

Glaxo-Wellcome, Inc., maker of salmeterol, funded a study that showed salmeterol gave greater increase

in FEV1

and FVC than albuterol or ipratropium, much longer duration of BD and, therefore, greater "area

under the curve." Improvements in dyspnea and exercise tolerance were similar to those using ipratropium.

Sixteen weeks of salmeterol therapy provided an increased baseline FEV1 of 7%. Salmeterol at doses ofeight puffs produced no signicant cardiovascular effects in patients with COPD (heart rate or PVCs).

However, tremor developed after four puffs. Quality of life indicators increased with salmeterol compared

to PRN use of albuterol. Signicant evidence exists for salmeterol to be used as a scheduled treatment for

COPD. When compared to other beta-agonists, its benets include a higher and more prolonged BD effect.

In addition, salmeterol's twice-daily dosing compared to four times/day dosing required by albuterol and

ipratropium may improve compliance (Matera, 1995; Matera, 1996; Patakas, 1998).

Supporting evidence is of class: A

Summary

Albuterol is the preferred agent for as-needed control of symptoms in patients with mild COPD and as an

additive as needed agent to a scheduled bronchodilator in patients with more severe COPD because the onsetof bronchodilator effect (15 minutes) is more rapid than ipratropium (30-90 minutes).

Tiotropium has been shown to be a superior scheduled bronchodilator to salmeterol and ipratropium.

As a scheduled bronchodilator, salmeterol has the main advantage of requiring only twice-daily dosing, and

therefore may improve compliance.

Albuterol and ipratropium are equipotent as bronchodilators, improving dyspnea and exercise tolerance

equally well. Salmeterol is a long-acting bronchodilator that is a suitable agent for scheduled administra-

tion. [Conclusion Grade II: See Conclusion Grading Worksheet A Annotation #11 (Pharmacological

Management)]

(Brusasco, 2003; Donohue, 2002; Hvizdos, 2002)


Systemic Corticosteroid Trials

Prednisone up to 40 mg/day for 10-14 days (ATS, 1995)

Prednisone 30 mg/day for two weeks or inhaled corticosteroid for six weeks (BTS, 1997)

A trial of prednisone (0.4-0.6 mg/kg for two to four weeks or inhaled corticosteroids at less than 2,000

mcg/day for six to eight weeks) may be used to test reversibility of airow (ERS, 1995).


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Every-other-day dosing of oral corticosteroids may minimize side effects yet still provide anti-inammatory

benets. The value of oral corticosteroids in treating stable COPD is controversial. While oral cortico-

steroids are useful in treating acute exacerbations, their long-term use in stable COPD is benecial in only

10%-15% of cases.


Inhaled Corticosteroids

Airway inammation is a prominent feature in some patients with COPD. Although the benets of inhaled

corticosteroids are well established in asthma, their utility for the chronic management of COPD is contro-

versial. Previous studies have shown that inhaled corticosteroids do not decelerate the rate of decline inexpiratory ow volumes over time in patients with COPD. A recent meta-analysis showed that high doses (but

not medium or low doses) of inhaled corticosteroids did slow the rate of decline in forced expiratory volume

in one second (FEV1) in patients with COPD. Another study suggested that inhaled corticosteroids may

reduce airway hyperreactivity and decrease clinical symptoms of COPD, including dyspnea and cough.

The effects of inhaled corticosteroids on clinical outcomes such as COPD exacerbation rates, hospital

readmission rates, and mortality have been evaluated. A systematic review of all placebo-controlled,

randomized trials of inhaled corticosteroids given for at least six months for stable COPD demonstrated abenecial effect in reducing rates of COPD exacerbation. In this review, the use of inhaled corticosteroid

therapy reduced the rate of exacerbations with similar benets in those who were and were not pretreated

with systemic steroids. Inhaled corticosteroid therapy was also associated with increased rates of oropha-

ryngeal candidiasis and skin bruising over placebo. The effects on bone mineral density and mean cortisol

concentrations were variable. No effects on mortality were seen.

In contrast, in a population-based cohort study, patients who received inhaled corticosteroid therapy after

hospitalization discharge for COPD had a relative risk reduction for all-cause mortality of 29% and for

repeat hospitalization of 24%.

(Alsaeedi, 2002; Burge, 2000; Lung Health Study Research Group, 2000; Paggiaro, 1998; Sin, 2001; van

Grunsven, 1999; Vestbo, 1999; Weir, 1993)

Two recent large studies compared the effects of combined uticasone and salmeterol to placebo in patients

with severe but stable COPD. Those randomized to combination therapy had signicant improvement in

symptoms, spirometry, quality of life, and exacerbations. However, 50% of patients were current smokers.

Subgroup analysis was not published in these papers, leaving questions regarding whether these benecial

effects are expected in non-smoking patients without evidence of airway inammation (Hannania, 2003;

Calverley, 2003).

There is evidence that a trial of oral prednisone may not accurately predict which patients will respond to

inhaled steroids (Senderovitz, 1999; Boothman-Burrell, 1997; Shim, 1985).

Supporting evidence is of classes: A, B, M

Methods of Drug Delivery

Metered Dose Inhaler (MDI) with Spacer

Some studies support the use of spacers to obtain effective MDI drug delivery. The increased distance slows

the velocity of the ne particles, increasing their chances of reaching the bronchial tree. It is of utmost

importance to train and retrain patients, nurses, physicians and pharmacists in proper inhaler technique for

optimal drug delivery. Evidence of the effectiveness of one type of spacer over another is variable and

controversial.


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Chlorouorocarbons (CFCs) are freon compounds commonly used as propellants in commercial aerosols

including MDIs. Concerns have been raised about the toxicity of freon and its role in depleting the ozone

layer. The production of ozone-depleting substances is being phased out worldwide under terms of an

international agreement. Since most MDIs in the U.S. contain CFCs as propellants, they will eventually

need to be reformulated (UN Environment Programme, 2000).

MDIs that use CFCs as a propellant will not be removed until sufcient alternatives exist to serve patient

needs. The FDA is developing strategies to ensure that patients in the U.S. who rely on MDIs to maintain

their health will have continued access to an array of safe and effective treatment options.

Non-freon alternatives include hydrouorocarbons (HFAs). These non-freon formations are well-tolerated

and equally efcacious when compared with compounds containing freon.

Dry Powder Inhaler (DPI)

DPIs are an alternative to MDIs that are strongly supported by study data. DPIs deliver drugs in dry-powderform without the use of propellants. In addition, DPIs are breath-activated, eliminating the need to synchro-

nize inhalation with actuation.

DPIs have been developed as a response to concerns about freon toxicity. Newer DPI products deliver pure

drug from self-enclosed, multiple-dose devices that help avoid the potential adverse effects of additivesused in MDIs.

Table II contrasts features of conventional pressurized MDIs and DPIs.

Table III: Contrasting Features of Conventional Pressurized Metered-Dose Inhaler and

Dry Powder Inhaler

MDI DPI

1. Aerosol generation dependent on propellants. 1. Aerosol generation does not require any

propellants.

2. Requires coordination of actuation with

inhalation.

2. Relatively easy to administer, since it is

breath-activated.

3. With correct technique, the lung deposition of

the drug is 10%-15%.

3. Lung deposition of the drug is similar to

properly used MDI (in some studies

deposition is greater in DPI than MDI).

4. With add-on spacer device, may be improved

drug deposition into the lungs and

oropharyngeal side effects may be reduced.

4. No add-on spacer device needed.

5. Because of propellants and other additives,

patients feel the drug delivered.

5. Patient may not feel the drug delivered and

may be uncertain of the drug dosing.

6. No dose indicators. Risk of continued use of

empty inhaler.

6. Newer multidose DPIs have a window with

dose indicator.

Adapted from Vaswani, 1998.

Nebulizers

Aerosol particle diameters range from 1-5 mcg in SVN (small volume nebulizer), which are comparable

with MDI or DPI. Studies have shown no difference in the efcacy of the delivery methods. Reports suggest

that between 47% and 89% of adults may have unacceptable inhaler technique. Clinical situations in which

nebulized therapy is preferable to either MDI or DPI include:


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Patients incapable of performing MDI or DPI maneuver

Adults who have a vital capacity less than 1.5 times their predicted tidal volume (7mL/kg)

Aerosol therapy via nebulizer is generally considered expensive, inconvenient and inefcient. Nebulizer

therapy should be considered a second choice when compared with other modes of aerosol delivery, e.g.,

MDIs and DPIs.

The following is a comparison of the advantages and disadvantages of aerosol delivery via nebulizer.

Table IV: Comparison of Nebulizers and MDIs

Nebulizers

Advantages Disadvantages

Pneumatic small volume nebulizers (SVN)

Limited patient coordination Expensive compressed gas source required

High dose levels possible Greater time required (expense)

Continuous therapy available Some medications not readily available

No chlorofluorocarbon (CFC) release

Covered by Medicare

Ultrasonic small volume nebulizers (USN)

Less patient coordination Expensive initial purchase

Fast delivery Contamination possible

No CFC release or compressed gas source Electrical or mechanical malfunction

required Not portable

Some medications not available

Adapted from Ward, 1997.

Theophylline

Theophylline has a narrow therapeutic index with potentially signicant adverse effects and drug interac-

tions that must be carefully considered and closely monitored during therapy.

The use of theophylline for COPD has decreased over the past decade for various reasons. Newer inha-

lational therapies have potentially equal or greater efcacy. There is concern about adverse reaction and

drug-interaction proles of theophylline. Based upon a retrospective valuation of 3,720 patients with COPD

enrolled in 10 bronchodilator clinical trials from 1987 to 1995, the percentage of patients receiving oral

theophylline decreased signicantly from 63% to 29% related to changing prescribing and COPD manage-ment practices (Van Andel, 1999).

The mechanisms of action of theophylline in COPD remain unclear. The assumption that theophylline relaxes

bronchial smooth muscle by inhibiting phosphodiesterase, subsequently leading to an increase of cAMP, is

no longer generally accepted as the predominant mode producing efcacy. Newer proposed mechanisms of

action include antagonism of the effects of prostaglandins and adenosine; alternation of calcium metabolism

by cells; inhibition of mediator release, membrane phospholipid methylation, and calcium ion inux in mast

cells; and the inhibition of specic phosphodiesterase enzymes, leading to smooth muscle relaxation and

inhibition of inammatory cell function (Vaz Fragoso, 1993).


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A table of drug interactions with theophylline has been published (Michalets, 1998).

There is general agreement among previously published consensus guidelines for the management of COPD

that theophylline has a role after inhaled bronchodilators prove inadequate; however, there is disagreement

as to whether theophylline should be considered before or after corticosteroid use. There is considerable

evidence that theophylline provides signicant improvement in spirometry and/or symptoms such as

dyspnea of patients with COPD and particularly chronic stable disease and in combination with otherbronchodilator therapies. Theophylline may also improve mucociliary clearance, diaphragmatic strength,

cardiovascular function, central respiratory drive and exercise capacity. The degree of efcacy of theoph-

ylline in patients with COPD, however, may be inuenced by the chronicity and severity of obstruction,

duration of therapy, and extent of follow-up evaluation, and the use must be individualized to the patient

and clinical situation.

Potential adverse effects with theophylline are gastrointestinal irritation (nausea, dyspepsia and GERD) due

to increased gastric acid secretion, irritability, tremor and sleep disturbance.

Theophylline has a narrow therapeutic index: seizures and tachyarrhythmias correlate positively withhigher serum concentrations. Theophylline is extensively hepatically metabolized primarily by cytochrome

P4501A2. As a result, several drugs, cigarette smoking and hepatic insufciency, in addition to cardiac

decompensation and age, may alter theophylline's clearance.

Supporting evidence is of classes: D, R

12. Other Pharmacologic Treatment

Antibiotics

The routine use of antibiotics is not recommended except for treatment of bacterial exacerbations ofCOPD.

Antitussives

Regular use of antitussives is not recommended in COPD since cough can have a signicant protectiveeffect.

Antiviral Agents

Treatments other than vaccination are available to treat inuenza but are not a substitute for vaccination

unless it is contraindicated. Amantadine (Symmetrel) and rimantadine (Flumadine) are indicated for

symptomatic treatment and prophylaxis of inuenza A, which is more prevalent and more severe than

inuenza B. If started within the rst 48 hours of symptom onset, amantadine and rimantadine may reduce

the duration and symptoms by 50%.

Zanamivir (Relenza) and oseltamivir (Tamiu) are also available. Zanamivir must be inhaled whereas

oseltamivir is available orally. Zanamivir and oseltamivir may be considered for treatment if there is anoutbreak of inuenza B. These medications are, however, very costly relative to their benets.

A consumer information report from the FDA regarding Relenza and chronic lung disease issued in October

2000 included a caution that "some patients have had bronchospasm (wheezing) or serious breathing problems

when they used Relenza. Many, but not all, of these patients had previous asthma or chronic obstructive

pulmonary disease. Relenza has not been shown to shorten the duration of inuenza in people with these

diseases. Because of the risk of side effects, and because it has not been shown to help them, Relenza is

not generally recommended for people with chronic respiratory disease such as asthma or chronic obstruc-tive pulmonary disease" (U.S. Food and Drug Administration, 2000).

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Dosage and Cost

a. Amantadine: 100 mg twice daily x 7 days $

b. Rimantadine: 100 mg twice daily x 7 days $$

c. Zanamivir 10 mg (2 inhalations) every 12 hr for 5 days $$$

d. Oseltamivir 75 mg by mouth twice daily for 5 days $$$$

Leukotriene Modiers

This drug class has not been adequately tested in COPD patients and its use cannot be recommended until

additional evidence relative to its efcacy is available.

Mucolytics

In theory, reducing mucus viscosity and enhancing cough clearance or mucociliary clearance of mucus

could improve pulmonary function and reduce the incidence of respiratory infections in individuals with

COPD. Ideally, treatment would result in both objective (increase in FEV1) and subjective (better sense of

well-being) improvement for those individuals.

To date, there has been no conclusive evidence for signicant improvement in pulmonary function with any

of the agents studied so far. Guaifenesin is widely used as an over-the-counter expectorant but documented

objective or even subjective improvement has not been consistently demonstrated. Iodinated glycerol was

once thought to promote a decrease in symptoms and overall improvement in subjects with COPD, but this

result could not be conrmed in subsequent investigations.

Some evidence for improvement in subjects with chronic bronchitis is present using other agents, including

inhaled surfactant, amiloride, hypertonic saline, N-acetylcysteine and acetylcysteine, but for now is notsubstantial enough to be conclusive. Albuterol may have some effect in improving mucociliary clearance,

which may add to its utility as a bronchodilator.

(Houtmeyers, 1999; Parvez, 1996; Petty, 1990; Rubin, 1999; Rubin, 1996)

Supporting evidence is of classes: A, C, R

Oral Beta-Agonists

Inhaled bronchodilator therapy is preferred.

Vaccines

Inuenza and pneumococcal pneumonia together are the sixth leading cause of death in the U.S. among

persons 65 years of age or older. Immunization with pneumococcal and inuenza vaccines are recom-

mended by the U.S. Public Health Service's Advisory Committee on Immunization Practices to reduce

infectious complications involving the respiratory tract (Centers for Disease Control,1999; Centers for

Disease Control, 1997; Murphy, 1992).

Pneumococcal

The American Thoracic Society and the U.S. Public Health Service's Advisory Committee on Immu-nization Practices (ACIP) recommends pneumococcal vaccine for all COPD patients. Pneumococcal

vaccination is generally good for life, but revaccination may provide additional protection in certain

groups. The risks of revaccination are minimal, and the ACIP recommends revaccination once for COPD

patients if at least ve years have passed since receipt of the previous dose. Immunize at age 65 if not

done previously. See the ICSI Immunizations guideline for Adults.


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Inuenza

Inuenza vaccine should be provided on an annual basis because of new antigens and waning immu-

nity from the previous year. The optimal time for inuenza vaccination is usually from early October

through mid-November. To avoid a missed opportunity, vaccination can be done as soon as vaccine

is available, but not prior to September. Vaccine may be given even after u activity is known to be

occurring in the community (Couch, 2000).


13. Non-Pharmacologic Treatment Applicable to All Levels of

Severity

Key Points:

Treatment of COPD should also include an education plan suited to the patient's

specic needs, along with encouragement of exercise.

Pulmonary rehabilitation programs are effective in improving exercisecapacity, quality of life and perception of symptoms.

Encourage Exercise

Regular exercise has been shown to reduce symptoms of COPD and improve the quality of life in

patients with COPD. See "Pulmonary Rehabilitation Program for Moderate to Severe Disease" later inthis annotation. For patients who do not have access to a pulmonary rehab program, it is reasonable to

prescribe a regular exercise schedule.

Education

Considerations

Patient education for those with COPD may be complex. Education methods aimed at continuousimprovement should be incorporated into educational strategies that take the long-term relationships

between patients and health care professionals into account.

Patient Education Model

The following model presents core learning-needs and objectives, along with some examples of tools to

assist individual clinicians in designing a patient education plan. This model is based on the Transtheo-

retical Change Model (Prochaska Model), which emphasizes recognition of patients' stages of readiness

to incorporate educational messages into long-term behavior change.

Patient education should be tailored based on learning-needs assessments. It is important to develop a

plan that includes the educator, patient and family. Learning assessment and feedback tools should:

incorporate COPD needs and interventions within a conceptual behavior change model,

be exible enough to t the various ofce practice models (step-care model with stages of

change), and

be exible enough to match the cultural and learning styles of the intended target population.


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Core Learning Needs/Objectives

Knowledge of Basic Facts about COPD

- What is COPD?

- What symptoms are related to COPD?

- What causes COPD? (emphasis on tobacco use)

- What diagnostic testing is usually necessary?

- Role of medications and modes of delivery

- Importance of appropriate immunizations

Skills

(with or without a return visit by the patient to demonstrate skill improvement)

- Recognize symptoms of infections and exacerbations

- Breathing and physical exercise (at least lower extremity)

- Medication use and proper technique for inhalers (MDI/DPI), spacers, nebulizers,

oxygen

- Environmental modication energy conservation, irritants

Attitude

- Smoking cessation and dangers of continued use (from ICSI Tobacco Cessation guide-

line)

- Nutrition and exercise

- Quality of life factors dyspnea, fatigue, fear and depression

- Coping skills relaxation techniques, stress management and understandingof need to have COPD under control

Partnership in Care

- Written plan (with and without symptoms), exercise and medication diary

- When to call the clinic or seek emergency help

- Other educational support resources (e.g., pulmonary rehabilitation, tobacco

cessation)

Comprehensive programs, e.g., formal pulmonary rehabilitation, may expand on the above learningneeds, as well as phase in additional health-related behavioral advice based on severity, resources and

learning capacity of individual patients.

How Does the Practitioner Know That Patient Education Is Making a Difference?

In developing this patient education model, the ICSI COPD guideline work group identied a number

of individual outcomes to be achieved through guided self-management that incorporate a process of

education with objective monitoring and an explicit action plan. Individual outcomes to help practitio-

ners know if education is making a difference include the following:

Initiation of treatment for acute exacerbation is quicker


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Decreased missed work days

Improved self-efcacy and ability to perform ADLs

Increased adherence to and use of medications (psychomotor skills)

Variable impact on general quality of life measures

Barriers to Patient Education

Barriers to successful implementation of patient education and subsequent long-term behavior change

include individual educator and organizational factors such as:

lack of education due to insufcient time, resources or nances of patient;

inconsistent messages from health care team/sites;

ineffective communication of goals/planning change;

patient's fear of change and/or of not meeting expectations/lack of condence in ability to

understand and manage illness (self-efcacy);

non-adherence; and

insufcient time or resources for response or feedback on illness from practitioner.

Educational Framework/Themes for COPD

Denitions

In general, health education is concerned with a person's learning to live life in the healthiest way

possible. Patient (health) education can be dened as: (Bartlett, 1985; Stewart, 1966)

A process that is intended to improve the patient's level of knowledge, skill and attitudeto effectively adopt or reinforce healthy behaviors.

The process involving a planned learning experience using a combination of methodssuch as teaching, counseling and behavior modication techniques that inuence an

individual's knowledge and health behavior. The intent would be to prevent, promote,

maintain or modify a jointly developed set of health-related behaviors for a given patient

with COPD.

Self-efcacy is dened as a person's belief in his/her own capacity to perform a specic task. These

expectations about personal success determine a patient's motivation to participate in behavior

changes. For providers of care interacting with patients, outcome expectancy (conviction that certain

behaviors will lead to certain outcomes) are inuenced by efcacy expectancy (conviction that one

can successfully execute the behavior required to produce the outcome). Personal experience is

the most dependable source of self-efcacy, which in turn may inuence health belief and need for

further self-change (Celli, 1996; Scherer, 1996).

Conceptual Models

There are many theoretical frameworks for patient education that may be useful for various aspects ofCOPD care. Two frameworks that have been extensively studied and may be applicable to the COPD

population include the Transtheoretical Change Model and the Precede-Proceed Model. Two areas

where these have been applied include smoking cessation and physical activity.


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General Goals

In order to be effective, patient education needs to be developed as an integral part of a disease manage-

ment strategy with the goals of:

increasing awareness and understanding of basic disease pathophysiology,

facilitating long-term change toward health-preserving or enhancing attitudes and behaviors

(improved self-efcacy and quality of life), and

minimizing adverse effects from inappropriate use of therapeutic alternatives or interactions

with recommended treatments by the care team.

A key theme in overall health education is consistency of educational messages between access points

and along a time continuum tailored to meet the patient's learning needs and readiness to change.

Critical Components

The critical components of educator training and integration of the educator's role into the care process

are: 1) communication skills, 2) interpersonal interactions and 3) ability to empathize with patient's

needs and prioritize/evaluate desired reality-based behavior change(s). The interactive process betweeneducator and patient occurs in the context of a created environment or learning space arising from each

individual's internal state and his/her local external environment, and involves ve interrelated domains:

physiologic, psychologic, sociocultural, developmental and spiritual (Clark, 1994; Narsavage, 1997).

The literature review related to impact and cost effectiveness of educational interventions in COPD is

minimal and of variable quality for denitive recommendation.

Educational programs should be of graded intensity and should be consistent with emphasis on tailoring

to three levels:

1. Core messages to all patients as one-on-one ofce sessions

2. Add facilitator or peer-led support groups and other community resources

3. Add comprehensive rehab components (with or without specialty referral)

Three chronic conditions that may be useful to benchmark for program design and implementationprocess include asthma, diabetes and osteoarthritis.

How Does the Practitioner Know That Education Is Making a Difference?

There are several conclusions reached in the research reviewed.

There is no evidence to indicate that education alone can improve pulmonary function. Educa-

tion is most effective when coupled with exercise programs and timely access to supportive

care teams.

There may be improvement in quality of life for patients receiving education about COPD, but

the data is subjective and not consistently demonstrated. The meta-analysis conducted on 65studies concluded that education alone had signicant benecial effect only on psychomotor

skills (inhaler technique). There were only three relevant studies to review the effects of educa-

tion alone, making conclusions on other outcomes unreliable.

Education alone may reduce patients' use of short-acting 2-agonists by as much as one-half.

Self-management studies did demonstrate statistical differences in response to changes in symp-

toms; one study showed patient initiation of prednisone 27% greater than control and antibiotic


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therapy 37% greater than control. Other studies showed improvement in self-efcacy but no

changes in overall quality of life.

Progressive muscle relaxation has been shown to reduce psychological distress and dyspnea.

(Bauldoff, 1997; Devine, 1996; Folgering, 1994; Gibson, 1999; Ketelaars, 1994; Scherer, 1998; Watson,

1997)

Supporting evidence is of classes: A, C, D, M, R, X

Pulmonary Rehabilitation Program for Moderate to Severe Disease

The primary goal of pulmonary rehabilitation is to decrease respiratory symptoms and improve quality of

life. Pulmonary rehabilitation, with a multidisciplinary approach including education and exercise training,

should be considered for COPD patients who have functional limitations that affect their quality of life,have maximized on standard medical therapy, and are not limited by other serious or unstable medical

conditions. For willing patients who are able to learn about their disease and are motivated to participate

in a comprehensive rehabilitation program, selecting a program that emphasizes regular in-home exercise

veried by an exercise log is strongly recommended. Long-term benets from programs after completion

have not been demonstrated except for home-based exercise programs. A summary of structures and servicesin pulmonary rehabilitation is attached in Appendix C, "Summary of Structure and Services - Pulmonary

Rehabilitation Program."

Studies of pulmonary rehabilitation programs for patients with COPD, including an ICSI Technology

Assessment, found the following:

Pulmonary rehabilitation programs standardly available in the United States are effective in improving

exercise capacity, quality of life and perception of symptoms but only for the duration of the program, typi-

cally 8-12 weeks. Deterioration toward baseline after completion of the program can be routinely expected,

unless the patient continues to participate in an exercise program. Pulmonary function measurements are

not benecially affected.

Pulmonary rehabilitation programs are generally safe for COPD patients.

There is evidence that a long-term, structured exercise program can provide benet for up to 18

months (Berry, 2003).

Supervised follow-up may be helpful in maintaining improvements, although more studies are needed.

A multidisciplinary approach, including exercise, maximizes the benets of a pulmonary rehabilitation

program when compared to a limited program focusing on education alone.

There is a need for additional research to clarify questions related to patient selection, program components

(including contents, duration, intensity and site) and long-term effects. In addition, there is a need to validate

and standardize the outcome variables used to assess change.

Please refer to the ICSI Technology Assessment Report, "Pulmonary Rehabilitation for Chronic Obstructive

Pulmonary Disease, #32" for full discussion.

(American Thoracic Society [ATS], 1995; American Thoracic Society, 1999; Cambach, 1999; Donado,

1998; GOLD, 2006; Grosbois, 1999; Institute for Clinical Systems Improvement, 1997; Lacasse, 1997;

Man, 2004; Resnikoff, 1998)

Supporting evidence is of classes: A, C, M, R


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14. Assess for Hypoxemia and Hypercapnia and Treat If Indicated

Key Points:

Assess for hypoxemia and consider assessment for hypercapnia.

Hypoxemia

Progressive hypoxemia is commonly associated with COPD patients. Hypoxemia can rapidly lead to clinical

deterioration. By preventing or correcting cellular hypoxia, the treatment of hypoxemia can be life-preserving.

Long-term oxygen supplementation has been demonstrated to improve survival in hypoxemic patients withCOPD. However, tissue hypoxia may not always be adequately prevented or treated by simply addressing

the hypoxemia. Rather, the physician must carefully evaluate the full scope of the oxygen transport and

delivery (Medical Research Council Working Party, The, 1981; Weitzenblum, 1985).

The evaluation of gas exchange status by arterial blood gas (ABG) measurement is recommended for initia-

tion of oxygen therapy, as well as to determine PCO2and acid-base status. Assessment for long-term oxygen

needs by arterial blood gas analysis should be considered for stable outpatients with:

1. severe airow obstruction;2. symptomatic dyspnea with polycythemia, pulmonary hypertension (by ECG or echo), or altered

mental status;

3. problematic heart failure; and

4. severe symptoms out of proportion to the degree of airway obstruction.

Pulse oximetry cannot determine acid-base status and is not considered sufciently accurate to replace ABG

(available) measurement in an initial assessment. ABG measurement can be used to conrm the accuracy

of pulse oximetry at rest and with exercise when oximetry is less reliable.

Supporting evidence is of classes: A, C

Nocturnal HypoxiaDuring sleep, even in individuals without COPD, minute ventilation decreases. In patients with COPD whose

O2

saturation is already low or borderline, this hypoventilation results in hypoxia, which can exacerbate

or precipitate pulmonary hypertension. Sleep disruption from hypoxia or sleep apnea can induce daytime

hypersomnolence and may worsen symptoms of COPD.

Risk factors for hypoxia during sleep:

Severe COPD, especially with resting oxygen saturation less than 88% or exercise-induced

hypoxia

Evidence of cor pulmonale

Daytime hypersomnolence in the absence of sleep deprivation

Polycythemia

(Carskadon, 1981; Gimeno, 1986; Little, 1999; Nocturnal Oxygen Therapy Trial Group, 1980)

Supporting evidence is of classes: A, C, D


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Screening for Nocturnal Hypoxia

Screening for nocturnal hypoxia can be done easily and inexpensively with overnight pulse oximetry in thehome. The oximeter is returned to the clinic, where the overnight oximetry and heart rate data are down-

loaded. If a signicant portion of the night's data indicates oxygen saturations below 88%, supplemental

oxygen should be provided empirically at 1-2 L/min. Home oximetry can be repeated at that level to verify

correction of hypoxia (Hoch, 1990; Knight, 1987).

The patient should be referred to a sleep specialist to rule out sleep-related disordered breathing if additional

abnormalities are present.

Support evidence is of class: C

Hypercapnia

In an ambulatory, stable patient with COPD, assessment for hypercapnia by arterial blood gases (ABGs)

should be considered in the following circumstances:

Clinical suspicion of hypercapnia (asterixis, headache, hypersomnolence, altered mental status)

FEV1 less than 1.0

Upon initiation of oxygen

Morbid obesity

Excessive daytime somnolence

Problematic right heart failure/cor pulmonale

Severe airow obstruction

Carbon dioxide (CO2)

retention may pose a threat in patients with impaired CO

2ventilatory drive. Careful

titration of supplemental oxygen should be performed in these patients. A pH drop along with a rise in PaCO

2

with initiation of oxygen therapy or an increase in inspired oxygen concentration is usually well tolerated in

the ambulatory stable patient with COPD. If hypercapnia results in a decrease in mental status, the patientmay need admission to a hospital for more intensive respiratory care and monitoring.

In the unstable patient with resting hypercapnia, initiation of supplemental oxygen should be titrated upward,

as there is a small risk of worsening CO2retention. Reassessment by ABG and clinical status looking for

signs/symptoms of hypercapnia is suggested 30 minutes after initiation of oxygen.

Hypercapnia does not require specic therapy, but instead, therapeutic intervention should be directed at

correcting the hypoxemia. Nonetheless, a pH drop along with a rise in PaCO2

with initiation of oxygen

therapy, or an increase in inspired oxygen concentration is usually well tolerated in the ambulatory stable

COPD patient. If hypercapnia results in a decrease in mental status, the patient may need admission to ahospital for more intensive respiratory care.

These recommendations are further claried in the ICSI Diagnosis and Treatment of Obstructive Sleep

Apnea Hypopnea Syndrome guideline.

(American Thoracic Society [ATS], 1995; Dunn, 1991; Lopez-Majano, 1973)

Supporting evidence is of classes: C, R


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Oxygen Therapy

Important Points:

Long-term oxygen therapy (more than 15 hours per day) improves survival and quality of life in

hypoxemic patients.

ABG measurement is recommended for initiation of oxygen therapy, as well as to determine PCO2

and acid-base status.

Pulse oximetry is a good method for monitoring oxygen saturation and can be used in adjusting the

oxygen ow setting.

Indications for long-term oxygen therapy have been adopted by Medicare as reimbursement

criteria.*

Patients considered for long-term therapy may benet from assessment by a pulmonologist.

Supplemental long-term oxygen therapy should be provided at a ow rate sufcient to produce a

resting PaO

2of greater than 55 mm Hg, or S

aO

2greater than 89%.

Titrate liter-ow to goal at rest: add 1 L/min during exercise or sleep or titrate during exercise

to goal of SaO

2greater than 89%. Titrate sleep liter-ow to eight-hour sleep of S

aO

2greater than

89%.

Consider referral for sleep evaluation if patient experiences cyclic desaturation during sleep but is

normoxemic at rest.

Recheck Sa

O2

or PaO

2in one-three months if hypoxia developed during an acute exacerbation.

Rechecks should be performed annually if hypoxia is discovered in an outpatient with stable

COPD.

* Appendix B contains a summary of Medicare Oxygen Coverage Guidelines.

Oxygen Delivery MethodsThe dual-prong nasal cannula is the standard means of continuous ow oxygen delivery for the stable COPD

patient with hypoxemia. It is not only well tolerated, but is also simple and reliable. Care must be taken

when assigning an estimated FiO2

to patients as this low-ow system can have great uctuations (AARC,

1996).

Reservoir cannulas, demand pulse delivery devices, and transtracheal oxygen delivery are oxygen-conserving

devices that can improve the portability of oxygen therapy, reduce the overall costs of home oxygen therapy,especially in patients requiring higher ow rates, and can more effectively treat refractory hypoxemia. These

devices function by delivering all of the oxygen during early inhalation. They reduce oxygen requirements

by 25%-75% compared to continuous ow oxygen. Disadvantages of these devices are that they are bulky

on the face, mechanically more complicated, and require additional care as well as additional training of

the user.(Bower, 1988; Gibson, 1976; Kory, 1962; Soffer, 1985)

Supporting evidence is of classes: C, D, M

COPD and Air Travel

Airline travel is safe for most patients with COPD. Hypoxemic patients should be evaluated clinically,

and a decision should be made regarding oxygen requirements. Patients with COPD receiving continuous

oxygen at home will require supplementation during ight. A doctor's order is required for patients who


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need supplemental oxygen during air travel. Special arrangements with oxygen or equipment suppliers

and the airline must be made at least 48 hours