COPD GOLD_pocket Guide 2013(1)

7/29/2019 COPD GOLD_pocket Guide 2013(1)

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Global Initiative for ChronicObstructive

Lung

Disease

Global Initiative for Chronic

Obstructive

Lung

Disease

POCKET GUIDE TO

COPD DIAGNOSIS, MANAGEMENT,

AND PREVENTION

A Guide or Health Care ProessionalsUPDATED 2013


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Global Initiative for ChronicObstructive

LungDisease

Pocket Guide to COPD Diagnosis, Management,

And Prevention, 2013GOLD Board o DirectorsMarc Decramer, MD, Chair Jean Bourbeau, MD

Katholieke Universiteit Leuven McGill University Health CentreLeuven, Belgium Montreal, Quebec, Canada

Jorgen Vestbo, MD, Vice Chair Bartolome R. Celli, MDOdense University Hospital Brigham and Womens HospitalOdense C, Denmark (and) Boston, Massachusetts USAUniversity o ManchesterManchester, UK M.Victorina Lpez Varela, MD

Universidad de la RepblicDavid S.C. Hui, MD Montevideo, UruguayThe Chinese University o Hong Kong

Hong Kong, ROC Roberto Rodriguez Roisin, MDHospital Clnic, University o Barcelona

Masaharu Nishimura, MD Barcelona, SpainHokkaido University School o MedicineSapporo, Japan Claus Vogelmeier, MD University o Gieen and MarburgRobert A. Stockley Marburg, GermanyUniversity Hospitals BirminghamBirmingham, UK

GOLD Science CommitteeJrgen Vestbo, MD, Denmark, UK, Chair Fernando Martinez, MD, USAAlvar Agusti, MD, Spain Masaharu Nishimura, MD,JapanAntonio Anzueto, MD, USA Nicolas Roche, MD, FrancePeter J. Barnes, MD, UK Roberto Rodriguez Roisin, MD, SpainMarc Decramer, MD, Belgium Donald Sin, MD, CanadaLeonardo M. Fabbri, MD, Italy Robert A. Stockley, MD, UKPaul Jones, MD, UK Claus Vogelmeier, MD, GermanyGOLD Science DirectorSuzanne Hurd, PhD, USA

GOLD National LeadersRepresentatives rom many countries serve as a network or the dissemination andimplementation o programs or diagnosis, management, and prevention o COPD. TheGOLD Board o Directors is grateul to the many GOLD National Leaders who participated indiscussions o concepts that appear in GOLD reports.

2013 Global Initiative or Chronic Obstructive Lung Disease, Inc.


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TABLE OF CONTENTS

3 INTRODUCTION

4 KEY POINTS

5 WHAT IS CHRONIC OBSTRUCTIVEPULMONARY DISEASE (COPD)?

6 WHAT CAUSES COPD?

7 DIAGNOSIS OF COPD7 Table 1: Key Indicators or Considering a

Diagnosis o COPD8 Table 2: COPD and its Dierential Diagnoses

9 ASSESSMENT OF COPD9 Table 3: Classication o Severity o Airfow

Limitation in COPD

10 Table 4: Combined Assessment o COPD

11 THERAPEUTIC OPTIONS14 Table 5: Formulations and Typical Doses o

COPD Medications

17 MANAGEMENT OF STABLE COPD17 Table 6: Non-Pharmacologic Management o COPD19 Table 7: Pharmacologic Therapy or Stable COPD

20 MANAGEMENT OF EXACERBATIONS21 Table 8: Indications or Hospital Assessment

or Admission

22 COPD AND COMORBIDITIES

23 APPENDIX I: SPIROMETRY FOR DIAGNOSIS OF AIRLOW LIMITATION

IN COPD24 Figure 1A: Normal Spirogram24 Figure 1B: Spirogram Typical o Patients with

Mild to Moderate COPD


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3

INTRODUCTIONChronic Obstructive Pulmonary Disease (COPD) is a major cause o morbidity

and mortality throughout the world. Much has been learned about COPDsince the Global Initiative or Chronic Obstructive Lung Disease issued its rstreport, Global Strategy or the Diagnosis, Management, and Prevention oCOPD, in 2001. Treatment o COPD is now aimed at immediately relievingand reducing the impact o symptoms, as well as reducing the risk o utureadverse health events such as exacerbations. These dual goals emphasizethe need or clinicians to maintain a ocus on both the short-term and long-term impact o COPD on their patients. A ramework or COPD managementthat matches individualized assessment o the disease to these treatment

objectives will better meet each patients needs.

Several educational tools and publications oriented around this approach toCOPD are available at http://www.goldcopd.org and can be adapted tolocal health care systems and resources:

Global Strategy or the Diagnosis, Management, and Preventiono COPD. Scientic inormation and recommendations or COPDprograms. (Updated 2013)

Executive Summary, Global Strategy or the Diagnosis, Management,and Prevention o COPD. American Journal o Respiratory and CriticalCare Medicine(in press).

Pocket Guide to COPD Diagnosis, Management, and Prevention.Summary o patient care inormation or primary health careproessionals. (Updated 2013)

What You and Your Family Can Do About COPD. Inormation bookletor patients and their amilies.

This Pocket Guide has been developed rom the Global Strategy or theDiagnosis, Management, and Prevention o COPD(Updated 2013). Technicaldiscussions o COPD and COPD management, evidence levels, and speciccitations rom the scientic literature are included in that source document.

Acknowledgements: Unconditional educational grants have been providedby Almirall, AstraZeneca, Boehringer-Ingelheim, Chiesi, Forest Laboratories,GlaxoSmithKline, Groupo Ferrer, Merck Sharp & Dohme, Mylan, NoninMedical, Novartis, Pearl Therapeutics, Pzer, Quintiles, and Takeda. The

participants o the GOLD committees, however, are solely responsible or thestatements and conclusions in the publications.


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KEY POINTS

Chronic Obstructive Pulmonary Disease (COPD), a common preventableand treatable disease, is characterized by persistent airfow limitationthat is usually progressive and associated with an enhanced chronicinfammatory response in the airways and the lung to noxious particlesor gases. Exacerbations and comorbidities contribute to the overallseverity in individual patients.

Worldwide, the most commonly encountered risk actor or COPD istobacco smoking. In many countries, outdoor, occupational, and indoor

air pollution the latter resulting rom the burning o biomass uels arealso major COPD risk actors.

A clinical diagnosis o COPD should be considered in any patient whohas dyspnea, chronic cough or sputum production, and a history oexposure to risk actors or the disease. Spirometry is required to makethe diagnosis in this clinical context.

Assessment o COPD is based on the patients symptoms, risk oexacerbations, the severity o the spirometric abnormality, and theidentication o comorbidities.

Appropriate pharmacologic therapy can reduce COPD symptoms,reduce the requency and severity o exacerbations, and improve healthstatus and exercise tolerance.

All COPD patients with breathlessness when walking at their own pace

on level ground appear to benet rom rehabilitation and maintenanceophysical activity.

An exacerbation o COPD is an acute event characterized by aworsening o the patients respiratory symptoms that is beyond normalday-to-day variations and leads to a change in medication.

COPD oten coexists with other diseases (comorbidities) that may havea signicant impact on prognosis.


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5

WHAT IS CHRONIC

OBSTRUCTIVEPULMONARY DISEASE (COPD)?

Chronic Obstructive Pulmonary Disease (COPD), a common preventable andtreatable disease, is characterized by persistent airfow limitation that is usually

progressive and associated with an enhanced chronic infammatory responsein the airways and the lung to noxious particles or gases. Exacerbations andcomorbidities contribute to the overall severity in individual patients.

This denition does not use the terms chronic bronchitis and emphysema*and excludes asthma (reversible airfow limitation).

Symptoms o COPD include:

Dyspnea

Chronic cough

Chronic sputum production

Episodes o acute worsening o these symptoms (exacerbations) oten occur.

Spirometry is required to make a clinical diagnosis o COPD; the presence oa post-bronchodilator FEV1/FVC < 0.70 conrms the presence o persistent

airfow limitation and thus o COPD.

*Chronic bronchitis, dened as the presence o cough and sputum production or at least 3months in each o 2 consecutive years, is not necessarily associated with airfow limitation.Emphysema, dened as destruction o the alveoli, is a pathological term that is sometimes(incorrectly) used clinically and describes only one o several structural abnormalities presentin patients with COPD but can also be ound in subjects with normal lung unction.


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WHAT CAUSES COPD?Worldwide, the most commonly encountered risk actor or COPD istobacco smoking. Outdoor, occupational, and indoor air pollution thelatter resulting rom the burning o biomass uels are other major COPDrisk actors. Nonsmokers may also develop COPD.

The genetic risk actor that is best documented is a severe hereditarydeciency o alpha-1 antitrypsin. It provides a model or how other geneticrisk actors are thought to contribute to COPD.

COPD risk is related to the total burden o inhaled particles a personencounters over their lietime:

Tobacco smoke, including cigarette, pipe, cigar, and othertypes o tobacco smoking popular in many countries, as well asenvironmental tobacco smoke (ETS)

Indoor air pollution rom biomass uel used or cooking and heating

in poorly vented dwellings, a risk actor that particularly aectswomen in developing countries

Occupational dusts and chemicals (vapors, irritants, and umes)when the exposures are suciently intense or prolonged

Outdoor air pollution also contributes to the lungs total burden oinhaled particles, although it appears to have a relatively smalleect in causing COPD

In addition, any actor that aects lung growth during gestation andchildhood (low birth weight, respiratory inections, etc.) has the potential toincrease an individuals risk o developing COPD.


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DIAGNOSIS OF COPDA clinical diagnosis o COPD should be considered in any patient who hasdyspnea, chronic cough or sputum production, and a history o exposure torisk actors or the disease (Table 1).

Spirometry is required to make a clinical diagnosis o COPD; the presence oa postbronchodilator FEV

1/FVC < 0.70 conrms the presence o persistent

airfow limitation and thus o COPD. All health care workers who care orCOPD patients should have access to spirometry. Appendix I: Spirometry

or Diagnosis o Airow Limitation in COPD summarizes the lung unctionmeasurements that are key to making a spirometry diagnosis and detailssome o the actors needed to achieve accurate test results.

Table 1. Key Indicators or Considering a Diagnosis o COPD

Consider COPD, and perorm spirometry, i any o these indicators arepresent in an individual over age 40. These indicators are not diagnostic

themselves, but the presence o multiple key indicators increases theprobability o a diagnosis o COPD. Spirometry is required to establish adiagnosis o COPD.

Dyspnea that is: Progressive (worsens over time).Characteristically worse with exercise.Persistent.

Chronic cough: May be intermittent and may be unproductive.

Chronic sputum production:

Any pattern o chronic sputum production mayindicate COPD.

History o exposure to risk actors:Tobacco smoke (including popular local preparations).Smoke rom home cooking and heating uels.Occupational dusts and chemicals.

Family history o COPD


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Dierential Diagnosis: A major dierential diagnosis is asthma. In somepatients with chronic asthma, a clear distinction rom COPD is not possibleusing current imaging and physiological testing techniques. In these patients,

current management is similar to that o asthma. Other potential diagnosesare usually easier to distinguish rom COPD (Table 2).

Table 2. COPD and its Dierential Diagnoses

Diagnosis Suggestive Features

COPD Onset in mid-life.

Symptoms slowly progressive.History of tobacco smoking or exposure to other types of smoke.

Asthma Onset early in life (often childhood).Symptoms vary widely from day to day.Symptoms worse at night/early morning.Allergy, rhinitis, and/or eczema also present.Family history of asthma.

Congestive HeartFailure

Chest X-ray shows dilated heart, pulmonary edema.Pulmonary function tests indicate volume restriction,

not airflow limitation.

Bronchiectasis Large volumes of purulent sputum.Commonly associated with bacterial infection.Chest X-ray/CT shows bronchial dilation, bronchial wall thickening.

Tuberculosis Onset all ages.Chest X-ray shows lung infiltrate.Microbiological confirmation.High local prevalence of tuberculosis.

Obliterative

Bronchiolitis

Onset at younger age, nonsmokers.May have history of rheumatoid arthritis or acute fume exposure.Seen after lung or bone marrow transplantation.CT on expiration shows hypodense areas.

Diuse Panbronchiolitis Predominantly seen in patients of Asian descent.Most patients are male and nonsmokers.Almost all have chronic sinusitis.Chest X-ray and HRCT show diffuse small centrilobular nodular

opacities and hyperinflation.

These eatures tend to be characteristic o the respective diseases, but are notmandatory. For example, a person who has never smoked may develop COPD

(especially in the developing world where other risk actors may be more importantthan cigarette smoking); asthma may develop in adult and even in elderly patients.


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ASSESSMENT OF COPDThe goals o COPD assessment are to determine the severity o the disease, itsimpact on patients health status, and the risk o uture events (exacerbations,hospital admissions, death) in order to guide therapy. Assess the ollowingaspects o the disease separately:

Symptoms Degree o airfow limitation (using spirometry) Risk o exacerbations Comorbidities

Assess Symptoms: Validated questionnaires such as the COPD Assessment Test(CAT), the Modied British Medical Research Council (mMRC) breathlessnessscale, or the Clinical COPD Questionnaire (CCQ) should be used to assesssymptoms.

Assess Degree o Airow Limitation Using Spirometry: Table 3 provides theclassication o airfow limitation severity in COPD.

Assess Risk o Exacerbations: An exacerbation o COPD is dened as an acuteevent characterized by a worsening o the patients respiratory symptoms thatis beyond normal day-to-day variations and leads to a change in medication.The best predictor o having requent exacerbations (2 or more per year) is a

history o previous treated events; the risk o exacerbations also increases asairfow limitation worsens.

Assess Comorbidities: Cardiovascular diseases, osteoporosis, depression and

Table 3. Classifcation o Severity o Airow Limitation in COPD(Based on Post-Bronchodilator FEV

1)

In patients with FEV1/FVC < 0.70:

GOLD 1: Mild FEV1

80% predicted

GOLD 2: Moderate 50% FEV1

< 80% predicted

GOLD 3: Severe 30% FEV1 < 50% predicted

GOLD 4: Very Severe FEV1

< 30% predicted


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anxiety, skeletal muscle dysunction, metabolic syndrome, and lung canceramong other diseases occur requently in COPD patients. These comorbidconditions may infuence mortality and hospitalizations, and should be looked

or routinely and treated appropriately.Combined Assessement o COPD: Table 4 provides a rubric or combiningthese assessments to improve management o COPD.

Symptoms:Less Symptoms (mMRC 0-1 or CAT < 10): patient is (A) or (C)More Symptoms (mMRC 2 or CAT 10): patient is (B) or (D)

Airow Limitation:

Low Risk (GOLD 1 or 2): patient is (A) or (B)High Risk (GOLD 3 or 4): patient is (C) or (D)

Exacerbations:Low Risk ( 1 per year): patient is (A) or (B)High Risk ( 2 per year): patient is (C) or (D)

Table 4. Combined Assessment o COPDWhen assessing risk, choose thehighest riskaccording to GOLD grade or exacerbation history.

(One or more hospitalizations or COPD exacerbations should be considered high risk.)

Patient CharacteristicSpirometric

ClassificationExacerbations per

yearmMRC CAT

ALow Risk

Less SymptomsGOLD 1-2 1 0-1 < 10

BLow Risk

More Symptoms

GOLD 1-2 1 2 10

CHigh Risk

Less SymptomsGOLD 3-4 2 0-1 < 10

DHigh Risk

More SymptomsGOLD 3-4 2 2 10


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THERAPEUTIC OPTIONS

Smoking cessationhas the greatest capacity to infuence the natural history oCOPD. Health care providers should encourage all patients who smoke to quit.

Counseling delivered by physicians and other healthproessionals signicantly increases quit rates over sel-initiatedstrategies. Even a brie (3-minute) period o counseling tourge a smoker to quit results in smoking quit rates o 5-10%.

Nicotine replacement therapy (nicotine gum, inhaler, nasal

spray, transdermal patch, sublingual tablet, or lozenge) aswell as pharmacotherapy with varenicline, bupropion, ornortriptyline reliably increases long-term smoking abstinencerates and these treatments are signicantly more eectivethan placebo.

Smoking Prevention:Encourage comprehensive tobacco-control policies and

programs with clear, consistent, and repeated nonsmoking messages. Workwith government ocials to pass legislation to establish smoke-ree schools,public acilities, and work environments and encourage patients to keep smoke-ree homes.

Occupational Exposure:Emphasize primary prevention, which is best achievedby elimination or reduction o exposures to various substances in the workplace.Secondary prevention, achieved through surveillance and early detection, isalso important.

Indoor and Outdoor Air Pollution: Implement measures to reduce or avoidindoor air pollution rom burning biomass uel or cooking and heating inpoorly ventilated dwellings. Advise patients to monitor public announcementso air quality and, depending on the severity o their disease, avoid vigorousexercise outdoors or stay indoors during pollution episodes.

Physical Activity:All COPD patients benet rom regular physical activity and

should repeatedly be encouraged to remain active.


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PHARMACOLOGIC THERAPIES FOR STABLE COPD

Pharmacologic therapy is used to reduce symptoms, reduce the requency andseverity o exacerbations, and improve health status and exercise tolerance.Each treatment regimen needs to be patient-specic as the relationship betweenthe severity o symptoms and the severity o airfow limitation is infuenced byother actors, such as the requency and severity o exacerbations, the presenceo respiratory ailure, comorbidities (cardiovascular disease, osteoporosis,etc.), and general health status. The classes o medications commonly used intreating COPD are shown in Table 5. The choice within each class depends onthe availability o medication and the patients response.

Bronchodilators:These medications are central to symptom management inCOPD.

Inhaled therapy is preerred. The choice between beta

2-agonists, anticholinergics, theophylline,

or combination therapy depends on the availability o medicationsand each patients individual response in terms o symptom relie

and side eects. Bronchodilators are prescribed on an as-needed or on a regular

basis to prevent or reduce symptoms. Long-acting inhaled bronchodilators are convenient and more

eective at producing maintained symptom relie than short-actingbronchodilators.

Long-acting inhaled bronchodilators reduce exacerbations andrelated hospitalizations and improve symptoms and health status,

and tiotropium improves the eectiveness o pulmonary rehabilitation. Combining bronchodilators o dierent pharmacological classes

may improve ecacy and decrease the risk o side eects comparedto increasing the dose o a single bronchodilator.

Inhaled Corticosteroids:In COPD patients with FEV1

< 60% predicted, regulartreatment with inhaled corticosteroids improves symptoms, lung unction, andquality o lie, and reduces the requency o exacerbations. Inhaled corticosteroid

therapy is associated with an increased risk o pneumonia. Withdrawalrom treatment with inhaled corticosteroids may lead to exacerbations insome patients. Long-term monotherapy with inhaled corticosteroids is notrecommended.


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Combination Inhaled Corticosteroid/Bronchodilator Therapy: An inhaledcorticosteroid combined with a long-acting beta

2-agonist is more eective

than either individual component in improving lung unction and health statusand reducing exacerbations in patients with moderate to very severe COPD.Combination therapy is associated with an increased risk o pneumonia.Addition o a long-acting beta

2-agonist/inhaled glucocorticosteroid to tiotropium

appears to provide additional benets.

Oral Corticosteroids: Long-term treatment with oral corticosteroids is notrecommended.

Phosphodiesterase-4 inhibitors:In GOLD 3 and GOLD 4 patients with a historyo exacerbations and chronic bronchitis, the phosphodiesterase-4 inhibitorrofumilast reduces exacerbations treated with oral corticosteroids. These eectsare also seen when rofumilast is added to long-acting bronchodilators; thereare no comparison studies with inhaled corticosteroids.

Methylxanthines. Methylxanthines are less eective and less well tolerated thaninhaled long-acting bronchodilators and are not recommended i those drugs

are available and aordable. There is evidence or a modest bronchodilatoreect and some symptomatic benet o these medications compared withplacebo in stable COPD. Addition o theophylline to salmeterol produces agreater increase in FEV

1and relie o breathlessness than salmeterol alone.

Low-dose theophylline reduces exacerbations but does not improve post-bronchodilator lung unction.

Other Pharmacologic Treatments

Vaccines: Infuenza vaccines can reduce serious illness and death in COPDpatients. Vaccines containing killed or live, inactivated viruses are recommended,and should be given once each year. Pneumococcal polysaccharide vaccine isrecommended or COPD patients 65 years and older, and has been shown toreduce community-acquired pneumonia in those under age 65 with FEV

1

< 40% predicted.

Alpha-1 Antitrypsin Augmentation Therapy: Not recommended or patientswith COPD that is unrelated to alpha-1 antitrypsin deciency.

Antibiotics:Not recommended except or treatment o inectious exacerbationsand other bacterial inections.


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Table 5. Formulations and Typical Doses o COPD Medications*

DrugInhaler

(mcg)

Solution forNebulizer(mg/ml)

OralVials forInjection

(mg)

Durationof Action(hours)

Beta2-agonists

Short-actingFenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8

Salbutamol (albuterol) 100, 200(MDI & DPI)

5 5 mg (Pill),0.024%(Syrup)

0.1, 0.5 4-6

Terbutaline 400, 500 (DPI) 2.5, 5 mg (Pill) 4-6 Long-actingFormoterol 4.5-12 (MDI & DPI) 0.01 12

Arformoterol 0.0075 12Indacaterol 75-300 (DPI) 24Salmeterol 25-50 (MDI & DPI) 12Tulobuterol 2 mg (transdermal) 24

AnticholinergicsShort-acting

Ipratropium bromide 20, 40 (MDI) 0.25-0.5 6-8Oxitropium bromide 100 (MDI) 1.5 7-9 Long-actingAclidinium bromide 322 (DPI) 12

Glycopyrronium bromide 44 (DPI) 24Tiotropium 18 (DPI), 5 (SMI) 24Combination short-acting beta

2-agonists plus anticholinergic in one inhaler

Fenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 12 6-8Methylxanthines

Aminophylline 200-600 mg (Pill) 240Variable,up to 24

Theophylline (SR) 100-600 mg (Pill) Variable,up to 24Inhaled corticosteroids

Beclomethasone 50-400 (MDI & DPI) 0.2-0.4Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5Fluticasone 50-500 (MDI & DPI)Combination long-acting beta

2-agonists plus corticosteroids in one inhaler

Formoterol/Budesonide 4.5/160 (MDI)9/320 (DPI)Formoterol/mometasone 10/200, 10/400 (MDI)

Salmeterol/Fluticasone 50/100, 250, 500 (DPI)25/50, 125, 250 (MDI)Systemic corticosteroidsPrednisone 5-60 mg (Pill)Methyl-prednisolone 4, 8, 16 mg (Pill)Phosphodiesterase-4 inhibitorsRoflumilast 500 mcg (Pill) 24

MDI=metered dose inhaler; DPI=dry powder inhaler; SMI=sot mist inhaler*Not all ormulations are available in all countries; in some countries, other ormulations may be available.Formoterol nebulized solution is based on the unit dose vial containing 20 mcg in a volume o 2.0 ml


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Mucolytic Agents: Patients with viscous sputum may benet rom mucolytics(e.g. carbocysteine), but overall benets are very small.

Antitussives:Use is not recommended.

Vasodilators: Nitric oxide is contraindicated in stable COPD. The use oendothelium-modulating agents or the treatment o pulmonary hypertensionassociated with COPD is not recommended.

OTHER TREATMENTS

Rehabilitation:Patients at all stages o disease benet rom exercise trainingprograms with improvements in exercise tolerance and symptoms o dyspneaand atigue. Benets can be sustained even ater a single pulmonaryrehabilitation program. The minimum length o an eective rehabilitationprogram is 6 weeks; the longer the program continues, the more eective theresults. Benet does wane ater a rehabilitation program ends, but i exercisetraining is maintained at home the patients health status remains above pre-rehabilitation levels.

Oxygen Therapy: The long-term administration o oxygen (> 15 hours perday) to patients with chronic respiratory ailure has been shown to increasesurvival in patients with severe, resting hypoxemia. Long-term oxygen therapyis indicated or patients who have:

PaO2at or below 7.3 kPa (55 mmHg) or SaO

2at or below 88%, with

or without hypercapnia conrmed twice over a three-week period; or

PaO2between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO

2

o 88%, i there is evidence o pulmonary hypertension, peripheraledema suggesting congestive cardiac ailure, or polycythemia(hematocrit > 55%).

Ventilatory Support: The combination o non-invasive ventilation with long-termoxygen therapy may be o some use in a selected subset o patients, particularlyin those with pronounced daytime hypercapnia. It may improve survival butdoes not improve quality o lie. There are clear benets o continuous positiveairway pressure (CPAP) on both survival and risk o hospital admission.


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Surgical Treatments:The advantage o lung volume reduction surgery (LVRS)over medical therapy is more signicant among patients with upper-lobepredominant emphysema and low exercise capacity prior to treatment,

although LVRS is costly relative to health-care programs not including surgery.In appropriately selected patients with very severe COPD, lung transplantationhas been shown to improve quality o lie and unctional capacity.

Palliative Care, End-o-lie Care, and Hospice Care: The disease trajectory inCOPD is usually marked by a gradual decline in health status and increasingsymptoms, punctuated by acute exacerbations that are associated with anincreased risk o dying. Progressive respiratory ailure, cardiovascular diseases,malignancies and other diseases are the primary cause o death in patients withCOPD hospitalized or an exacerbation. Thus palliative care, end-o-lie care,and hospice care are important components o the management o patientswith advanced COPD.


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MANAGEMENT OF STABLE COPDOnce COPD has been diagnosed, eective management should be basedon an individualized assessment o current symptoms and uture risks:

Relieve symptoms Improve exercise tolerance Improve health status

and Prevent disease progression Prevent and treat exacerbations Reduce mortality

These goals should be reached with minimal side eects rom treatment,a particular challenge in COPD patients because they commonly havecomorbidities that also need to be careully identied and treated.

NON-PHARMACOLOGIC TREATMENT

Non-pharmacologic management o COPD according to the individualizedassessment o symptoms and exacerbation risk is shown in Table 6.

REDUCE SYMPTOMS

REDUCE RISK

Table 6. Non-Pharmacologic Management o COPD

Patient Group Essential RecommendedDepending on

Local Guidelines

A

Smokingcessation

(can includepharmacologic

treatment)

Physical activityFlu vaccinationPneumococcalvaccination

B, C, D

Smokingcessation

(can includepharmacologic

treatment)Pulmonary

rehabilitation

Physical activityFlu vaccinationPneumococcalvaccination


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PHARMACOLOGIC TREATMENT

A proposed model or initial pharmacological management o COPD

according to the assessment o symptoms and risk (Table 3) is shown inTable 7.

Bronchodilators Recommendations:

For both beta2-agonists and anticholinergics, long-acting

ormulations are preerred over short-acting ormulations. The combined use o short- or long-acting beta

2-agonists and

anticholinergics may be considered i symptoms are not improvedwith single agents.

Based on ecacy and side eects, inhaled bronchodilators arepreerred over oral bronchodilators.

Based on evidence o relatively low ecacy and greater sideeects, treatment with theophylline is not recommended unlessother bronchodilators are not available or unaordable or long-term treatment.

Corticosteroids and Phosphodiesterase-4 Inhibitors Recommendations

There is no evidence to recommend a short-term therapeutic trialwith oral corticosteroids in patients with COPD to identiy thosewho will respond to inhaled corticosteroids or other medications.

Long-term treatment with inhaled corticosteroids is recommendedor patients with severe and very severe airfow limitation andor patients with requent exacerbations that are not adequately

controlled by long-acting bronchodilators. Long-term monotherapy with oral corticosteroids is not recommendedin COPD.

Long-term monotherapy with inhaled corticosteroids is not recommendedin COPD because it is less eective than the combination o inhaledcorticosteroids with long-acting beta

2-agonists.

Long-term treatment containing inhaled corticosteroids should notbe prescribed outside their indications, due to the risk o pneumoniaand the possibility o a slightly increased risk o ractures ollowinglong-term exposure.

The phosphodiesterase-4 inhibitor rofumilast may also be used toreduce exacerbations or patients with chronic bronchitis, severeand very severe airfow limitation, and requent exacerbations thatare not adequately controlled by long-acting bronchodilators.


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*Medicationsineach

boxarementione

din

alphabeticalorderand

thereforenotnecessarilyin

orderofpreferen

ce.

**Medicationsin

this

columncanbeusedalone

orincombination

with

otheroptionsintheFirst

andAlternativeC

hoice

columns

Glossary:

SA:short-acting

LA:long-acting

ICS:inhaledcorticosteroid

PDE-4:phosphodiesterase-4

prn:whennecess

ary

Table7:PharmacologicTherapyforStableCOPD*

Patient

Group

RECOMMENDED

FIRSTCHOICE

ALTERNATIVECHOICE

OTHERPOSSIBLE

TREATMENTS**

A

SAanticholinergicprn

or

SAbeta2-agonistprn

LAanticholinergic

or

LAbeta2-agonist

or

SAbeta2-agonistand

SAanticholinergic

Theophylline

B

LAanticholinergic

or

LAbeta2-agonist

LAanticholinergicand

LAbeta2-agonist

SAbeta2-agonistand/

or

SAanticholinergic

Theophylline

C

ICS+

LAbeta2-agonist

or

LAanticholinergic


LAbeta2-agonist

or


PDE-4

Inhibitor

or

LAbeta2-agonistand

PDE-4

Inhibitor

SAbeta2-agonistand/

or

SAanticholinergic

Theophylline

D

ICS+

LAbeta2-agonist

and/or

LAanticholinergic

ICS+LA

beta2-agonistand

LA

anticholinergic

or

ICS+LA

beta2-agonistand

PDE-4inhibitor

or

LA

anticholinergicand

LA

beta2-agonist

or

LA

anticholinergicand

PDE-4inhibitor

Carbocysteine

SAbeta2-agonistand/

or

SAanticholinergic

Theophylline


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MANAGEMENT OF

EXACERBATIONSAn exacerbation o COPD is dened as an acute event characterized by aworsening o the patients respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication.

The most common causes appear to be respiratory tract inections (viral orbacterial).

How to Assess the Severity o an Exacerbation

Arterial blood gas measurements (in hospital): PaO2

< 8.0 kPa(60 mmHg) with or without PaCO

2> 6.7 kPa, (50 mmHg) when

breathing room air indicates respiratory ailure. Chest radiographs are useul in excluding alternative diagnoses. An ECG may aid in the diagnosis o coexisting cardiac problems.

Other laboratory tests:

Whole blood countcan identiy polycythemia or bleeding. The presence opurulent sputum during an exacerbation can be

sucient indication or starting empirical antibiotic treatment. Biochemical tests can help detect electrolyte disturbances, diabetes,

and poor nutrition.

Spirometric tests are not recommended during an exacerbation because theycan be dicult to perorm and measurements are not accurate enough.

Treatment Options

Oxygen:Supplemental oxygen should be titrated to improve the patientshypoxemia with a target saturation o 88-92%.

Bronchodilators:Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are the preerred bronchodilators or treatment o anexacerbation.


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Systemic Corticosteroids: Systemic corticosteroids shorten recovery time,improve lung unction (FEV

1) and arterial hypoxemia (PaO

2), and reduce

the risks o early relapse, treatment ailure, and length o hospital stay. A

dose o 30-40 mg prednisolone per day or 10-14 days is recommended.

Antibiotics:Antibiotics should be given to patients:

With the ollowing three cardinal symptoms: increased dyspnea,increased sputum volume, increased sputum purulence;

With increased sputum purulence and one other cardinal symptom; Who require mechanical ventilation

Adjunct Therapies: Depending on the clinical condition o the patient, anappropriate fuid balance with special attention to the administration odiuretics, anticoagulants, treatment o comorbidities, and nutritional aspectsshould be considered. At any time, health care providers should stronglyenorce stringent measures against active cigarette smoking.

Patients with characteristics o a severe exacerbation should be hospitalized(Table 8). Indications or reerral and the management o exacerbations o

COPD in the hospital depend on local resources and the acilities o thelocal hospital.

Table 8. Indications or Hospital Assessment or Admission

Marked increase in intensity o symptoms

Severe underlying COPD Onset o new physical signs

Failure o an exacerbation to respond to initial medical management

Presence o serious comorbidities

Frequent exacerbations

Older age

Insucient home support


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COPD AND COMORBIDITIESCOPD oten coexists with other diseases (comorbidities) that may have asignicant impact on prognosis. In general, the presence o comorbiditiesshould not alter COPD treatment and comorbidities should be treated as ithe patient did not have COPD.

Cardiovascular disease (including ischemic heart disease, heart ailure,atrial brillation, and hypertension) is a major comorbidity in COPD andprobably both the most requent and most important disease coexisting withCOPD. Cardioselective beta-blockers are not contraindicated in COPD.

Osteoporosisand anxiety/depression, major comorbidities in COPD, areoten under-diagnosed and are associated with poor health status andprognosis.

Lung canceris requently seen in patients with COPD and has been ound tobe the most requent cause o death in patients with mild COPD.

Serious inections, especially respiratory inections, are requently seen inpatients with COPD.

The presence o metabolic syndrome and maniest diabetes are morerequent in COPD and the latter is likely to impact on prognosis.


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APPENDIX I: SPIROMETRY

FOR DIAGNOSIS OF AIRFLOWLIMITATION IN COPDSpirometry is required to make a clinical diagnosis o COPD and shouldbe available to all health care proessionals who work with COPD patients.

What is Spirometry?

Spirometryis a simple test to measure the amount o air aperson can breathe out, and the amount o time taken to do so.

A spirometer is a device used to measure how eectively, andhow quickly, the lungs can be emptied.

A spirogram is a volume-time curve.

Spirometry measurements used or diagnosis o COPD include(see Figures 1A and 1B):

FVC (Forced Vital Capacity): maximum volume o air that can beexhaled during a orced maneuver.

FEV1

(Forced Expired Volume in one second): volume expired in therst second o maximal expiration ater a maximal inspiration. This

is a measure o how quickly the lungs can be emptied.

FEV1/FVC: FEV

1expressed as a proportion o the FVC, gives a

clinically useul index o airfow limitation.

The ratio FEV1/FVC is between 0.70 and 0.80 in normal adults; a

value less than 0.70 indicates airfow limitation and thus o COPD.

FEV1

is infuenced by the age, sex, height, and ethnicity, and is

best considered as a percentage o the predicted normal value.There is a vast literature on normal values; those appropriate orlocal populations should be used1,2,3,4.


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Why do Spirometry or COPD?

Spirometry is needed to make a clinical diagnosis o COPD.

Together with the presence o symptoms, spirometry helps gaugeCOPD severity and can be a guide to specic treatment steps.

A normal value or spirometry eectively excludes the diagnosis oclinically relevant COPD.

The lower the percentage predicted FEV1, the worse the subsequent

prognosis.

Figure 1A: Normal Spirogram

1 2 3 4 5 6

1

2

3

4

Volume,

liters

Time, seconds

5

1

FEV1 = 4L

FVC = 5L

FEV1/FVC = 0.8

Figure 1B: Spirogram Typical o Patients with Mild to Moderate COPD*

Vo

lume,

liter

s

Time, seconds

5

4

3

2

1

1 2 3 4 5 6

FEV1 = 1.8L

FVC = 3.2L

FEV1/FVC = 0.56

Obstructive


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FEV1

declines over time and usually aster in COPD than in healthysubjects. Spirometry can be used to monitor disease progression,but to be reliable the intervals between measurements must be at

least 12 months.

What You Need to Perorm Spirometry

Several types o spirometers are available. Relatively large bellows orrolling-seal spirometers are usually only available in pulmonary unctionlaboratories. Calibration should be checked against a known volume (e.g.,rom a 3-litre syringe) on a regular basis. There are several smaller hand-held devices, oten with electronic calibration systems.

A hard copy o the volume-time plot is very useul to checkoptimalperormance and interpretation, and to exclude errors.

Most spirometers require electrical power to permit operation o the motorand/or sensors. Some battery-operated versions are available that candock with a computer to provide hard copy.

It is essential to learn how your machine is calibrated and when and howto clean it.

How to Perorm Spirometry

Spirometry is best perormed with the patient seated. Patients may beanxious about perorming the tests properly, and should be reassured.Careul explanation o the test, accompanied by a demonstration, is very

useul. The patient should:

Breathe in ully.

Seal their lips around the mouthpiece.

Force the air out o the chest as hard and ast as they can until theirlungs are completely empty.

Breathe in again and relax.

Exhalation must continue until no more air can be exhaled, must be at least6 seconds, and can take up to 15 seconds or more.


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Like any test, spirometry results will only be o value i the expirations areperormed satisactorily and consistently. Both FVC and FEV

1should be the

largest value obtained rom any o 3 technically satisactory curves and the

FVC and FEV1 values in these three curves should vary by no more than5% or 150 ml, whichever is greater. The FEV1/FVC is calculated using the

maximum FEV1

and FVC rom technically acceptable (not necessarily thesame) curves.

Those with chest pain or requent cough may be unable to perorm asatisactory test and this should be noted.

Where to nd more detailed inormation on spirometry:

1. GOLD: A spirometry guide or general practitioners and a teachingslide set is available: http://www.goldcopd.org

2. American Thoracic Societyhttp://www.thoracic.org/adobe/statements/spirometry1-30.pd

3. Australian/New Zealand Thoracic Society

http://www.nationalasthma.org.au/publications/spiro/index.htm

4. British Thoracic Societyhttp://www.brit-thoracic.org.uk/copd/consortium.html


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NOTES


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NOTES


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The Global Initiative or Chronic Obstructive Lung Diseaseis supported by unrestricted educational grants rom:

2013 Global Initiative or Chronic Obstructive Lung Disease Inc

Almirall

AstraZeneca

Boehringer Ingelheim

ChiesiForest Laboratories

GlaxoSmithKline

Grupo Ferrer

Merck Sharp and DohmeMylan

Nonin Medical

Novartis

Pearl Therapeutics

Pzer

Quintiles

Takeda

Documents

COPD GOLD_pocket Guide 2013(1)