GOLD Pocket 2010Mar31

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POCKET GUIDETO COPD DIAGNOSIS, MANAGEMENT,

AND PREVENTION

A Guide for Health Care ProfessionalsUPDATED 2010

Global Initiative for ChronicObstructiveLung

Disease

Global Initiative for ChronicObstructiveLungDisease


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GOLD Ex ecu tive Commi t t ee

Roberto Rodriguez-Roisin, MD, Spain,Chair Antonio Anzueto, MD, US (representing ATS) Jean Bourbeau, MD, CanadaTeresita S. DeGuia, MD, Philippines

David Hui, MD, Hong Kong, ROCChristine Jenkins, MD, AustraliaFernando Martinez, MD, US

Mara Montes de Oca, MD, PhD (representing ALAT)

Chris van Weel, MD, Netherlands (representing WONCA) Jorgen Vestbo, MD, Denmark

Observer: Jadwiga Wedzicha, MD, UK (Representing ERS)

GOLD Nation al Lead ers

Representatives from many countries serve as a network for the dissemination andimplementation of programs for diagnosis, management, and prevention of COPD.The GOLD Executive Committee is grateful to the many GOLD National Leaders whoparticipated in discussions of concepts that appear in GOLD reports, and for theircomments during the review of the 2006Global Strategy for the Diagnosis,Management, and Prevention of COPD .

Global Initiative for ChronicObstructiveLungDisease

Pocket Guide to COPD Diagnosis, Management,

and Prevention

2010 Global Initiative for Chronic Obstructive Lung Disease, Inc.

Michiaki Mishima, MD, Japan (representing APSR)

Robert Stockley, MD, UK


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TABLE OF CONTENTS

PREFACE

KEY P OINTSWHAT IS CHRONIC OBSTRUCTIVE

P ULMONARY DISEASE (COPD)?RISK FACTORS: WHAT CAU SES COPD?DIAGNOSING COPD

Figure 1: Key Indicators for Considering aCOPD Diagnosis Figure 2: Normal Spirogram and Spirogram Typical of Patients with Mild to Moderate COPD Figure 3: Differential Diagnosis of COPD

COMPONENTS OF CARE:A COPD MANAGEMENT PROGRAMCom ponen t 1: Assess an d Monitor DiseaseCom ponen t 2: R edu ce R isk Factor s

Figure 4: Strategy to Help a Patient Quit Smoking Com pon en t 3: Man age Stable COP D

Patient EducationPharmacologic TreatmentFigure 5: Commonly Used Formulations of Drugs for COPD Non-Pharmacologic TreatmentFigure 6: Therapy at Each Stage of COPD

Com ponen t 4: Mana ge Ex acerbat ionsHow to Assess the Severity of an ExacerbationHome ManagementHospital ManagementFigure 7: Indications for Hospital Admissionfor Exacerbations

APPENDIXI: SPIR OMETRY FOR DIAGNOSIS OF COP D

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Chronic Obstructive Pulmonary Disease (COPD) is a major cause ofchronic morbidity and mortality throughout the world. TheGlobalInitiative for Chro nic Obst ru ctiv e Lu n g Diseas ewas created toincrease awareness of COPD among health professionals, public healthauthorities, and the general public, and to improve prevention andmanagement through a concerted worldwide effort. The Initiativeprepares scientific reports on COPD, encourages dissemination andadoption of the reports, and promotes international collaboration onCOPD research.

While COPD has been recognized for many years, public health officialsare concerned about continuing increases in its prevalence and mortality,which are due in large part to the increasing use of tobacco productsworldwide and the changing age structure of populations in developingcountries. TheGlobal Initiative for Chronic Obstructiv e Lun gDisease offers a framework for management of COPD that can beadapted to local health care systems and resources. Educational tools,such as laminated cards or computer-based learning programs, can beprepared that are tailored to these systems and resources.

TheGlobal Initiative for Chronic Obstructive Lu ng Diseaseprogram includes the following publications:

Global Strategy for the Diagnosis, Management, and Prevention of COPD . Scientific information and recommendations for COPDprograms. (Updated 2010)

Executive Summary , Global Strategy for the Diagnosis, Management,and Prevention of COPD . (Updated 2010)

Pocket Guide to COPD Diagnosis , Management, and Prevention.Summary of patient care information for primary health care

professionals. (Updated 2010) What You and Your Family Can Do About COPD . Information booklet

for patients and their families.

PREFACE


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These publications are available on the Internet atwww.goldcopd.org .This site provides links to other websites with information about COPD.

This Pocket Guide has been developed from theGlobal Strategy for the Diagnosis, Management, and Prevention of COPD (2010). Technicaldiscussions of COPD and COPD management, evidence levels, and specificcitations from the scientific literature are included in that source document.

Acknowledgements : Grateful acknowledgement is given for the educationalgrants from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, Dey, ForestLaboratories, GlaxoSmithKline, Novartis, Nycomed, Pfizer, Philips Respironics, andSchering-Plough. The generous contributions of these companies assured that theparticipants could meet together and publications could be printed for wide distribu-tion. The participants, however, are solely responsible for the statements and con-clusions in the publications.


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KEY POINTS Chr onic Obstr uctiv e P ulm onar y Disease (COP D) is a

preventable and treatable disease with some significant extra-pulmonary effects that may contribute to the severity in individualpatients. Its pulmonary component is characterized by airflow limitationthat is not fully reversible. The airflow limitation is usually progressiveand associated with an abnormal inflammatory response of the lungto noxious particles or gases.

Worldwide, the most commonly encounteredrisk factor for COPDis cigaret te sm ok ing. At every possible opportu nityindividuals w ho sm ok e shou ld be encouraged to qui t. Inmany countries, air pollution resulting from the burning of wood andother biomass fuels has also been identified as a COPD risk factor.

A diagnosis of COPD should be considered in any patient who hasdyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should beconfirmed by spirometry.

A COPD m anagem ent program includes four components:assess and monitor disease, reduce risk factors, manage stableCOPD, and manage exacerbations.

Pharmacologic treatmentcan prevent and control symptoms,

reduce the frequency and severity of exacerbations, improve healthstatus, and improve exercise tolerance.

Patient education can help improve skills, ability to cope withillness, and health status. It is an effective way to accomplish smokingcessation, initiate discussions and understanding of advance directivesand end-of-life issues, and improve responses to acute exacerbations.

COPD is often associated with exacerbations of symptoms.


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WHAT IS CHRONIC

OBSTRUCTIVEPULMONARY DISEASE(COPD)?Ch ronic Obstr u ctive P u lm ona ry Disease (COP D)is a preventableand treatable disease with some significant extrapulmonary effects that maycontribute to the severity in individual patients. Its pulmonary componentis characterized by airflow limitation that is not fully reversible. The air-flow limitation is usually progressive and associated with an abnormalinflammatory response of the lung to noxious particles or gases.

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

Sym ptom s of COP D includ e:

Cough Sputum production Dyspnea on exertion

Episodes of acute worsening of these symptoms often occur.

*Chronic bronchitis , defined as the presence of cough and sputum production for at least 3months in each of 2 consecutive years, is not necessarily associated with airflow limitation.Emphysema , defined as destruction of the alveoli, is a pathological term that is sometimes(incorrectly) used clinically and describes only one of several structural abnormalities presentin patients with COPD.

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Chron ic cou gh an d spu tum produ ction often pr ecede thedevelopm ent of a ir f low l im ita t ion by m any years , a lthoughnot al l individu als w ith cough and spu tu m production go onto dev elop COP D.


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RISK FACTORS:

WHAT CAUSES COPD?Worldw ide, cigaret te sm ok ing is the m ost com m onlyencou nt ered risk factor for COP D.

The genetic risk factor that is best documented is a severe hereditarydeficiency of alpha-1 antitrypsin. It provides a model for how othergenetic risk factors are thought to contribute to COPD.

COPD risk is related to the total burden of inhaled particles a personencounters over their lifetime:

Tobacco sm ok e, including cigarette, pipe, cigar, and other typesof tobacco smoking popular in many countries, as well asenvironmental tobacco smoke (ETS)

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

Indoor a ir pollut ionfrom biomass fuel used for cooking andheating in poorly vented dwellings, a risk factor that particularlyaffects women in developing countries

Out door air pollution also contributes to the lungs total burdenof inhaled particles, although it appears to have a relatively smalleffect in causing COPD

In addition, any factor that affects lung growth during gestation and

childhood (low birth weight, respiratory infections, etc.) has the potentialfor increasing an individuals risk of developing COPD.


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When performing spirometry, measure:

Forced Vital Capacity (FV C) and Forced Expiratory Volume in one second (FEV1).

Calculate the FEV1/FVC ratio.

Spirometric results are expressed as% P redicted usingappropriate normal values for the persons sex, age, and height.

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P atients w ith COP D typ ically sh ow a decrease in both FEV1

and FEV1 /FVC. The degree of spirom etr ic abn orm alitygen erally reflects the severity of COP D. How ev er, bothsym ptom s and sp irom etry s hould be cons idered w hendeveloping an individu alized m anagem ent s trategy foreach patient.

Figu re 2: Norm al Spirogra m an d Spirogra m Ty pical of

P atients w ith Mild to Moderate COP D*

*Postbronchodilator FEV 1 is recommended for the diagnosis and assessment of severity of COPD.


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Stages of COP D

St age I: Mild C OP D - Mild airflow limitation (FEV1 /FVC < 70%;

FEV1 80% predicted) and sometimes, but not always, chronic coughand sputum production. At this stage, the individual may not be aware that his or her lung

function is abnormal.

Stage II: Moderate C OP D - Worsening airflow limitation(FEV1 /FVC < 70%; 50% FEV1 < 80% predicted), with shortnessof breath typically developing on exertion.

This is the stage at which patients typically seek medical attentionbecause of chronic respiratory symptoms or an exacerbation of theirdisease.

Stage III: Sev ere C OPD - Further worsening of airflow limitation(FEV1 /FVC < 70%; 30% FEV1 < 50% predicted), greater shortness ofbreath, reduced exercise capacity, and repeated exacerbations whichhave an impact on patients quality of life.Stage IV: Very Sev ere C OP D - Severe airflow limitation(FEV1 /FVC < 70%; FEV1 < 30% predicted) or FEV1 < 50% predictedplus chronic respiratory failure. Patients may haveVery Severe (Stage IV) COPD even if the FEV1 is > 30% predicted, whenever this complicationis present.

At this stage, quality of life is very appreciably impaired andexacerbations may be life-threatening.

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At Risk fo r COPD

A major objective of GOLD is to increase awareness among health care providers and thegeneral public of the significance of COPD symptoms. The classification of severity of COPDnow includes four stages classified by spirometryStage I: Mild COPD; Stage II: Moderate COPD; Stage III: Severe COPD; Stage IV: Very Severe COPD . A fifth categoryStage 0: At

Risk that appeared in the 2001 report is no longer included as a stage of COPD, as thereis incomplete evidence that the individuals who meet the definition of At Risk (chronic coughand sputum production, normal spirometry) necessarily progress on toStage I: Mild COPD .Nevertheless, the importance of the public health message that chronic cough and sputum arenot normal is unchanged and their presence should trigger a search for underlying cause(s).


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Diffe ren tial Diagnosis:A major differential diagnosis is asthma. Insome patients with chronic asthma, a clear distinction from COPD is notpossible using current imaging and physiological testing techniques. In these

patients, current management is similar to that of asthma. Other potentialdiagnoses are usually easier to distinguish from COPD (Figu re 3).

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Diagnosis Suggestive Features*COPD Onset in mid-life.

Symptoms slowly progressive.Long smoking history.Dyspnea during exercise.Largely irreversible airflow limitation.

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

Congestive Heart Failure Fine basilar crackles on auscultation.Chest X-ray shows dilated heart, pulmonary edema.Pulmonary function tests indicate volume restriction, not airflowlimitation.

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

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

Obliterative Bronchiolitis Onset in younger age, nonsmokers.May have history of rheumatoid arthritis or fume exposure.CT on expiration shows hypodense areas.

Diffuse Panbronchiolitis Most patients are male and nonsmokers.Almost all have chronic sinusitis.Chest X-ray and HRCT show diffuse small centrilobularnodular opacities and hyperinflation.

Figu re 3: Diff eren t ial Diagn osis of COP D

*These features tend to be characteristic of the respective diseases, but do not occur inevery case. For example, a person who has never smoked may develop COPD (especiallyin the developing world, where other risk factors may be more important than cigarettesmoking); asthma may develop in adult and even elderly patients.


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COMPONENTS OF CARE:

A COPD MANAGEMENTPROGRAM

The goals of COPD management include:

Relieve symptoms Prevent disease progression Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment

Cessation of cigarette smoking should be included as a goal throughoutthe management program.

THESE GOALS CAN BE ACHIEVED THROUGHIMP LEMENTATION OF A COP D MANAGEMENT P ROGRAMWITH FOUR COMPONENTS:

1. Assess and Monitor Disease

2. Redu ce Risk Factor s

3. Man age Stab le COPD

4. Manage Ex acerbations


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Component 1: Assess and Monitor Disease

A detailed m edical histor yof a new patient known or thought tohave COPD should assess:

Exposure to risk factors, including intensity and duration.

Past medical history, including asthma, allergy, sinusitis or nasalpolyps, respiratory infections in childhood, and other respiratorydiseases.

Family history of COPD or other chronic respiratory disease.

Pattern of symptom development.

History of exacerbations or previous hospitalizations forrespiratory disorder.

Presence of comorbidities, such as heart disease, malignancies,osteoporosis, and musculoskeletal disorders, which may alsocontribute to restriction of activity.

Appropriateness of current medical treatments.

Impact of disease on patients life, including limitation of activity;missed work and economic impact; effect on family routines; andfeelings of depression or anxiety.

Social and family support available to the patient.

Possibilities for reducing risk factors, especially smoking cessation.


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In addition to spirometry, the followingother testsmay be consideredfor the assessment of a patient withModerate (Stage II), Severe (Stage III),and Very Severe (Stage IV) COPD .

Bronchod ilator rev ersibility testing:To rule out a diagnosis ofasthma, particularly in patients with an atypical history (e.g., asthmain childhood and regular night waking with cough and wheeze).

Ches t X - ray : Seldom diagnostic in COPD but valuable to excludealternative diagnoses such as pulmonary tuberculosis, and identifycomorbidities such as cardiac failure.

Art erial blood gas m easurem ent: Perform in patients withFEV1 < 50% predicted or with clinical signs suggestive of respiratoryfailure or right heart failure. The major clinical sign of respiratoryfailure is cyanosis. Clinical signs of right heart failure include ankleedema and an increase in the jugular venous pressure. Respiratoryfailure is indicated by PaO2 < 8.0 kPa (60 mm Hg), with or withoutPaCO2 > 6.7 kPa (50 mm Hg) while breathing air at sea level.

Alpha- 1 ant itr y psin deficiency screening: Perform whenCOPD develops in patients of Caucasian descent under 45 years orwith a strong family history of COPD.

COP D is usu ally a progressive disease. Lu ng fu nctioncan b e ex pected to w orsen ov er t im e, even w ith the bestavai lable care . Sy m ptom s and lung funct ion sh ould bem onitored to fo l low the developm ent of complications, toguide treatm ent , and t o facili tate discussion of m anagem entopt ions w ith pat ients. Com orbidit ies are com m on in COP Dand should be actively identified.


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Component 2: Reduce Risk Factors

Sm ok ing cessat ion is t he single m ost ef fect iv eand cost-

ef fect iveint erv ention to r educe th e r isk of dev elopingCOP D and slow its progress ion.

Even a brief, 3-minute period of counseling to urge a smoker toquit can be effective, and at a minimum this should be done forevery smoker at every health care provider visit. More intensivestrategies increase the likelihood of sustained quitting (Figur e 4).

Pharmacotherapy (nicotine replacement, buproprion/nortryptiline,and/or varenicline) is recommended when counseling is not sufficientto help patients stop smoking. Special consideration should begiven before using pharmacotherapy in people smoking fewer than10 cigarettes per day, pregnant women, adolescents, and thosewith medical contraindications (unstable coronary artery disease,untreated peptic ulcer, and recent myocardial infarction or strokefor nicotine replacement; and history of seizures for buproprion).

Figure 4: Strategy to Help a Pa tient Quit Sm ok ing

1. ASK:Systematically identify all tobacco users at every visit.Implement an office-wide system that ensures that, for EVERY patientat EVERY clinic visit, tobacco-use status is queried and documented.

2. AD VISE: Strongly urge all tobacco users to quit.In a clear, strong, and personalized manner, urge every tobacco user to quit.

3. ASSESS:Determine willingness to make a quit attempt.Ask every tobacco user if he or she is willing to make a quit attempt at this time (e.g., within the next 30 days).

4. ASSIST:Aid the patient in quitting.Help the patient with a quit plan; provide practical counseling;provide intra-treatment social support; help the patient obtainextra-treatment social support; recommend use of approvedpharmacotherapy if appropriate; provide supplementary materials.

5. ARRANGE:Schedule follow-up contact.Schedule follow-up contact, either in person or via telephone.


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Sm ok ing P revent ion: Encourage comprehensive tobacco-controlpolicies and programs with clear, consistent, and repeated nonsmokingmessages. Work with government officials to pass legislation to establish

smoke-free schools, public facilities, and work environments andencourage patients to keep smoke-free homes.

Occupa tional Ex posu res: Emphasize primary prevention, whichis best achieved by elimination or reduction of exposures to varioussubstances in the workplace. Secondary prevention, achieved throughsurveillance and early detection, is also important.

Indoor an d Out door Air P ollut ion:Implement measures to reduceor avoid indoor air pollution from biomass fuel, burned for cooking andheating in poorly ventilated dwellings. Advise patients to monitor publicannouncements of air quality and, depending on the severity of theirdisease, avoid vigorous exercise outdoors or stay indoors altogetherduring pollution episodes.


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Component 3: Manage Stable COPD

Managem ent of s table COPD sho uld be guided by th e

follow ing gen eral pr inciples: Determine disease severity on an individual basis by taking into

account the patients symptoms, airflow limitation, frequency andseverity of exacerbations, complications, respiratory failure,comorbidities, and general health status.

Implement a stepwise treatment plan that reflects this assessment of disease severity.

Choose treatments according to national and cultural preferences,the patients skills and preferences, and the local availability ofmedications.

P atient education can help improve skills, ability to cope with illness,and health status. It is an effective way to accomplish smoking cessation,initiate discussions and understanding of advance directives and end-of-life issues, and improve responses to acute exacerbations.

Pharmacologic treatment(Figu re 5) can control and preventsymptoms, reduce the frequency and severity of exacerbations, improvehealth status, and improve exercise tolerance.

Bronchodilators: These medications are central to symptommanagement in COPD.

Inhaled therapy is preferred.

Give as needed to relieve intermittent or worsening symptoms, andon a regular basis to prevent or reduce persistent symptoms. The choice between 2-agonists, anticholinergics, methylxanthines,

and combination therapy depends on the availability of medicationsand each patients individual response in terms of both symptomrelief and side effects.

Regular treatment with long-acting bronchodilators, including nebu-lized formulations, is more effective and convenient than treatment

with short-acting bronchodilators. Combining bronchodilators of different pharmacologic classes mayimprove efficacy and decrease the risk of side effects compared toincreasing the dose of a single bronchodilator.


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Figure 5. Formulations and Typical Doses of COPD Medications*Drug Inhaler

(g)Solution forNebulizer(mg/ml)

Oral Vials forInjection

(mg)

Duration ofAction (hours)

2-agonists Short-acting

Fenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8Salbutamol (albuterol) 100, 200 (MDI & DPI) 5 5mg (Pill), 0.024%(Syrup) 0.1, 0.5 4Terbutaline 400, 500 (DPI) 2.5, 5 (Pill) 4-6

Long-actingFormoterol 4.5-12 (MDI & DPI) 0.01 12+

Arformoterol 0.0075 12+Indacaterol 150-300 (DPI) 24Salmeterol 25-50 (MDI & DPI) 12+

Anticholinergics Short-acting

Ipratropium bromide 20, 40 (MDI) 0.25-0.5 6-8Oxitropium bromide 100 (MDI) 1.5 7-9

Long-acting Tiotropium 18 (DPI), 5 (SMI) 24+

Combination short-acting 2-agonists plus anticholinergic in one inhalerFenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 6-8

MethylxanthinesAminophylline 200-600 mg (Pill) 240 mg Variable, up toTheophylline (SR) 100-600 mg (Pill) Variable, up to

Inhaled glucocorticosteroidsBeclomethasone 50-400 (MDI & DPI) 0.2-0.4

Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5Fluticasone propionate50-500 (MDI & DPI)

Combination long-acting 2-agonists plus glucocorticosteroids in one inhalerFormoterol/Budesonide 4.5/160, 9/320 (DPI)Salmeterol/Fluticasone propionate

50/100, 250. 500 (DPI)25/50, 125, 250 (MDI)

Systemic glucocorticosteroidsPrednisone 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*Not all formulations are available in all countries; in some countries, other formulations may be avaiFormoterol nebulized solution is based on the unit dose vial containing 20 gm in a volume of 2.0m


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Inhaled Glucocorticosteroids: Regular treatment with inhaledglucocorticosteroids does not modify the long-term decline in FEV1 buthas been shown to reduce the frequency of exacerbations and thusimprove health status for symptomatic patients with an FEV1 < 50%

predicted and repeated exacerbations (for example, 3 in the last threeyears). The dose-response relationships and long-term safety of inhaledglucocorticosteroids in COPD are not known. Treatment with inhaled glu-cocorticosteroids increases the likelihood of pneumonia and does notreduce overall mortality.

An inhaled glucocorticosteroid combined with a long-acting2-agonist ismore effective than the individual components in reducing exacerbationsand improving lung function and health status. Combination therapy

increases the likelihood of pneumonia and has no significant effects onmortality. In patients with an FEV1 less than 60%, pharmacotherapy withlong-acting2-agonist, inhaled glucocorticosteroid and its combinationdecreases the rate of decline of lung function. Addition of a long-acting2-agonist/inhaled glucocorticosteroid to an anticholinergic (tiotropium)appears to provide additional benefits.Oral Glucocorticosteroids: Long-term treatment with oral glucocorticosteroidsis not recommended.

Vaccines: Influenza vaccines reduce serious illness and death in COPD patients by 50%. Vaccines containing killed or live, inactivated virusesare recommended, and should be given once each year. Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years andolder, and has been shown to reduce community-acquired pneumonia inthose under age 65 with FEV1 < 40% predicted.

Ant ib io t ic s : Not recommended except for treatment of infectiousexacerbations and other bacterial infections.

Mu coly t ic (Mucok inetic, Muc oregulator) Agents: Patients withviscous sputum may benefit from mucolytics, but overall benefits are verysmall. Use is not recommended.

Ant it u ssiv es: Regular use contraindicated in stable COPD.

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Phosphodiesterase-4 inhibitors: In patients withStage III: Severe COPD orStage IV: Very Severe COPD and a history of exacerbations and chronicbronchitis, the phosphodiesterase-4 inhibitor, roflumilast, reduces exacerba-tions treated with oral glucocorticosteroids. These effects are also seenwhen roflumilast is added to long-acting bronchodilators; there are nocomparison studies with inhaled glucocorticosteroids.


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Ox y gen Therapy : The long-term administration of oxygen (>15 hoursper day) to patients with chronic respiratory failure increases survival andhas a beneficial impact on pulmonary hemodynamics, hematologiccharacteristics, exercise capacity, lung mechanics, and mental state.

Initiate oxygen therapy for patients withStage IV: Very Severe COPD if:

PaO2 is at or below 7.3 kPa (55 mm Hg) or SaO2 is at or below88%, with or without hypercapnia; or

PO2 is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg)or SaO2 is 88%, if there is evidence of pulmonary hypertension,peripheral edema suggesting congestive heart failure, orpolycythemia (hematocrit > 55%).

Surgical Treatm ents : Bullectomy and lung transplantation may beconsidered in carefully selected patients withStage IV: Very Severe COPD . There is currently no sufficient evidence that would support thewidespread use of lung volume reduction surgery (LVRS).

There is no c onvinc ing evidence that m echan ic al v entilatory suppor t has a role in the routine m anagem ent of stable C OPD.

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The goal of long-ter m ox y gen therapy is to increase the base-l ine P aO2 at rest to a t least 8.0 k Pa (60 m m Hg) at sea level ,and/or produce SaO 2 at least 90% , w hich w il l preserv e vi ta lo rgan fun ct ion by ensu ring an adequate del iv ery of ox y gen.

Non- P harm acologic Treatm entincludes rehabilitation, oxygentherapy, and surgical interventions.

Patients at all stages of disease benefit from exercise training programs,

The goals of pulm onary rehabi lita t ion are to reduce sym ptom s,

im prove qua lity of l ife, an d increase pa rt icipation in ever y dayactivities.

Rehabilitation: Patients at all stages of disease benefit from exercisetraining programs improvements in exercise tolerance and symptoms ofdyspnea and fatigue. Benefits can be sustained even after a single pulmo-nary rehabilitation program. The minimum length of an effective rehabili-tation program is 6 weeks; the longer the program continues, the moreeffective the results. Benefit does wane after a rehabilitation programends, but if exercise training is maintained at home the patient's healthstatus remains above pre-rehabilitation levels.


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A summary of characteristics and recommended treatment at each stageof COPD is shown inFigur e 6.

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Figure 6: Therapy at Each Stage of COPD*

*Postbronchodilator FEV 1 is recommended for the diagnosis and assessment of severity of COPD.

FEV 1 /FVC < 0.70

FEV 1 8 0% predicted

FEV 1 /FVC < 0.70

50% FEV 1 < 80%predicted

Active reduction of risk factor(s); influenza vaccination

Add short-acting bronchodilator (when needed)

Add regular treatment with one or more long-acting bronchodilators(when needed); Add rehabilitation

Add inhaled glucocorticosteroids ifrepeated exacerbations

Add long term oxygen ifchronic respiratoryfailure

Consider surgicaltreatments

FEV 1 /FVC < 0.70

30% FEV 1 < 50%predicted

FEV 1 /FVC < 0.70

FEV 1 < 30% predictedor FEV 1 < 50%predicted plus chronicrespiratory failure

I: Mild II: Moderate III: Severe IV: Very Severe


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Component 4: Manage Exacerbations

An exacerbation of COPD is defined asan event in the natural

cou rse of th e disease cha racterized by a chan ge in th e patient s baselin e dyspn ea, cou gh, an d/or spu tu m th at is beyon d norm al day - to- day v ariat ions, is acute in onset ,and m ay w arran t a chan ge in regular m edicat ion in a pat ient w ith un derlying COPD.

The most common causes of an exacerbation are infection of thetracheobronchial tree and air pollution, but the cause of about one-third

of severe exacerbations cannot be identified.

How to Assess th e Severi ty of an Ex acerbation

Arterial blood gas measurements (in hospital):

PaO 2 < 8.0 kPa (60 mm Hg) and/or SaO 2 < 90% with or without

PaCO2 > 6.7 kPa, (50 mmHg) when breathing room air indicatesrespiratory failure.

Moderate-to-severe acidosis (pH < 7.36) plus hypercapnia (PaCO2> 6-8 kPa, 45-60 mm Hg) in a patient with respiratory failure is anindication for mechanical ventilation.

Chest X-ray: Chest radiographs (posterior/anterior plus lateral) identifyalternative diagnoses that can mimic the symptoms of an exacerbation.

ECG: Aids in the diagnosis of right ventricular hypertrophy, arrhythmias,and ischemic episodes.

Other laboratory tests:

Sputum culture and antibiogram to identify infection if there isno response to initial antibiotic treatment.

Biochemical tests to detect electrolyte disturbances, diabetes,and poor nutrition.

Whole blood count can identify polycythemia or bleeding.

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Hom e Managem entBronchodi l a to r s : Increase dose and/or frequency of existing short-acting bronchodilator therapy, preferably with 2-agonists. If not alreadyused, add anticholinergics until symptoms improve.Glu cocor t ic os t e ro ids : If baseline FEV1 < 50% predicted, add 30-40mg oral prednisolone per day for 7-10 days to the bronchodilator regimen.Budesonide alone may be an alternative to oral glucocorticosteroids in thetreatment of exacerbations and is associated with significant reduction

of complications.Hospital Managem entPatients with the characteristics listed inFigu re 7 should be hospitalized.Indications for referral and the management of exacerbations of COPDin the hospital depend on local resources and the facilities of the localhospital.

An t ib io t ics : Antibiotics should be given to patients: With the following three cardinal symptoms: increased dyspnea,

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

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Hom e Care or Hospital Care for End- Stage COPD P atient s?The r isk of dying from an ex acerbat ion of COP D is closely relat edto the dev elopm ent of res pirat ory acidosis, th e presence of

serious com orbidit ies, and the need for vent i la tory suppor t .Pat ients lack ing th ese features ar e not a t high r isk of dying, butthose w ith severe under ly ing COP D often requ ire h ospitalizationin any case. Attem pts a t m anaging such pat ients ent i re ly in thecom m uni ty have m e t w ith l im ited success, bu t re turn ing themto their hom es w ith increased social support and a s uperv isedmedical care program after an init ia l em ergency room assessm enthas been m uch m ore su ccessfu l. How ever, detailed cost - benefitanalys es of these approaches h ave n ot been report ed.

Figur e 7: In dications for Hospital Adm ission for Ex acerbat ions Marked increase in intensity of

symptoms, such as sudden develop-ment of resting dyspnea

Severe underlying COPD Onset of new physical signs (e.g.,

cyanosis, peripheral edema)

Failure of exacerbation to respondto initial medical management

Significant comorbidities Frequent exacerbations Newly occurring arrhythmias Diagnostic uncertainty Older age Insufficient home support


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APPENDIX I:SPIROMETRY FORDIAGNOSIS OF COPDSpirometry is as important for the diagnosis of COPD as bloodpressure measurements are for the diagnosis of hypertension.Spirometry should be available to all health care professionals.

Wha t is Spirom etry ?Spirometry is a simple test to measure the amount of air aperson can breathe out, and the amount of time taken to do so.A spirometer is a device used to measure how effectively, andhow quickly, the lungs can be emptied.A spirogram is a volume-time curve.

Spirometry measurements used for diagnosis of COPD include(see Figure 2, page 9):

FVC(Forced Vital Capacity): maximum volume of air thatcan be exhaled during a forced maneuver.

FEV1 (Forced Expired Volume in one second): volume expired inthe first second of maximal expiration after a maximal inspiration.This is a measure of how quickly the lungs can be emptied.

FEV1/FVC: FEV1 expressed as a percentage of the FVC,gives a clinically useful index of airflow limitation.

The ratio FEV1/FVC is between 70% and 80% in normal adults; avalue less than 70% indicates airflow limitation and the possibilityof COPD.

FEV1 is influenced by the age, sex, height and ethnicity, and isbest considered as a percentage of the predicted normal value.There is a vast literature on normal values; those appropriate forlocal populations should be used1,2,3 .

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Where to f ind m ore detailed info rm ation onspi rometry

1. Am erican Thoracic Societyhttp://www.thoracic.org/adobe/statements/spirometry1-30.pdf

2. Au st ralian/New Zea land Th ora cic Societyhttp://www.nationalasthma.org.au/publications/spiro/index.htm

3. British Thor acic Societyhttp://www.brit-thoracic.org.uk/copd/consortium.html

4. GOLDA spirometry guide for general practitioners and a teaching slideset is available:http://www.goldcopd.org

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The Global Initiative for Chronic Obstructive Lung Diseaseis supported by unrestricted educational grants from:

GOLD Pocket 2010Mar31

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