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    Gold pg 2010 Gold pg 2010 Document Transcript

    • Global Initiative for Chronic e ucObstructive odLung pr reDisease or er alt ot on -d ial ter ma POCKET GUIDE d hte TO COPD DIAGNOSIS, MANAGEMENT, rig AND PREVENTION py A Guide for Health Care ProfessionalsCo U P D AT ED 2 0 10
    • Global Initiative for Chronic Obstructive e L ung uc od Disease pr re Pocket Guide to COPD Diagnosis, Management, and Prevention or er GOLD Ex ecu t iv e Co m m it t ee Roberto Rodriguez-Roisin, MD, Spain, Chair alt Antonio Anzueto, MD, US (representing ATS) ot Jean Bourbeau, MD, Canada on Teresita S. DeGuia, MD, Philippines David Hui, MD, Hong Kong, ROC Christine Jenkins, MD, Australia -d Fernando Martinez, MD, US Michiaki Mishima, MD, Japan (representing APSR) ial María Montes de Oca, MD, PhD (representing ALAT) Robert Stockley, MD, UK ter Chris van Weel, MD, Netherlands (representing WONCA) Jorgen Vestbo, MD, Denmark ma Ob s er v er : Jadwiga Wedzicha, MD, UK (Representing ERS) d hte GOLD Nat io n al L ead er s Representatives from many countries serve as a network for the dissemination and rig implementation of programs for diagnosis, management, and prevention of COPD. The GOLD Executive Committee is grateful to the many GOLD National Leaders who py participated in discussions of concepts that appear in GOLD reports, and for their comments during the review of the 2006 Global Strategy for the Diagnosis,Co Management, and Prevention of COPD. © 2010 Global Initiative for Chronic Obstructive Lung Disease, Inc.
    • TA B L E O F CON T EN T S 3 P R EFA CE e uc 5 K EY P O I N T S 6 W H AT I S CH R O N I C OB S T R U CT I V E od P U L M ON A R Y D I S EA S E ( CO P D ) ? 7 R I S K FA CT OR S : WH AT CA U S ES CO P D ? pr 8 D I A GN O S I N G COP D re Figure 1: Key Indicators for Considering a COPD Diagnosis or Figure 2: Normal Spirogram and Spirogram Typical of Patients with Mild to Moderate COPD er Figure 3: Differential Diagnosis of COPD 12 13 CO M P ON EN T S OF CA R E: alt A COP D M A N A G EM EN T P R O GR A M Co m p o n e n t 1 : A s s e s s a n d M o n i t o r D i s e a s e ot 15 Co m p o n e n t 2 : R e d u ce R i s k F a ct o r s on Figure 4: Strategy to Help a Patient Quit Smoking 17 Co m p o n e n t 3 : M a n a g e S t a b l e COP D Patient Education -d Pharmacologic Treatment Figure 5: Commonly Used Formulations of Drugs for COPD ial Non-Pharmacologic Treatment Figure 6: Therapy at Each Stage of COPD ter 22 Co m p o n e n t 4 : M a n a g e Ex a ce r b a t i o n s How to Assess the Severity of an Exacerbation ma Home Management Hospital Management Figure 7: Indications for Hospital Admission d for Exacerbations hte 24 A P P EN D I X I : S P I R OM ET R Y F OR D I A G N OS I S OF COP D rig pyCo
    • PREFACE e uc Chronic Obstructive Pulmonary Disease (COPD) is a major cause of od chronic morbidity and mortality throughout the world. The Globa l In it iat iv e f or Ch ro n ic Ob s t r u ct iv e L u n g Dis eas e was created to pr increase awareness of COPD among health professionals, public health re authorities, and the general public, and to improve prevention and management through a concerted worldwide effort. The Initiative or prepares scientific reports on COPD, encourages dissemination and adoption of the reports, and promotes international collaboration on er COPD research. alt While COPD has been recognized for many years, public health officials are concerned about continuing increases in its prevalence and mortality, ot which are due in large part to the increasing use of tobacco products on worldwide and the changing age structure of populations in developing countries. The Global In it iat iv e f or Ch r on ic Obs t r u ct iv e L u n g Dis eas e offers a framework for management of COPD that can be -d adapted to local health care systems and resources. Educational tools, such as laminated cards or computer-based learning programs, can be ial prepared that are tailored to these systems and resources. ter The Glob al In it iat iv e f or Ch r on ic Ob s t r u ct iv e L u n g Dis eas e program includes the following publications: ma • Global Strategy for the Diagnosis, Management, and Prevention of COPD. Scientific information and recommendations for COPD d programs. (Updated 2010) hte • Executive Summary, Global Strategy for the Diagnosis, Management, and Prevention of COPD. (Updated 2010) rig • Pocket Guide to COPD Diagnosis, Management, and Prevention. Summary of patient care information for primary health care py professionals. (Updated 2010)Co • What You and Your Family Can Do About COPD. Information booklet for patients and their families. 3
    • These publications are available on the Internet at www.goldcopd.org. This site provides links to other websites with information about COPD. e This Pocket Guide has been developed from the Global Strategy for the uc Diagnosis, Management, and Prevention of COPD (2010). Technical discussions of COPD and COPD management, evidence levels, and specific od citations from the scientific literature are included in that source document. pr A ck n o w l e d g e m e n t s : Grateful acknowledgement is given for the educational re grants from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, Dey, Forest Laboratories, GlaxoSmithKline, Novartis, Nycomed, Pfizer, Philips Respironics, and or Schering-Plough. The generous contributions of these companies assured that the participants could meet together and publications could be printed for wide distribu- er tion. The participants, however, are solely responsible for the statements and con- clusions in the publications. alt ot on -d ial ter d ma hte rig pyCo 4
    • KEY POINTS e uc • Ch r o n i c O b s t r u ct i v e P u l m o n a r y D i s e a s e ( COP D ) is a preventable and treatable disease with some significant extra- od pulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation pr that is not fully reversible. The airflow limitation is usually progressive re and associated with an abnormal inflammatory response of the lung to noxious particles or gases. or • Worldwide, the most commonly encountered r i s k f a ct o r for COPD er is ci g a r e t t e s m o k i n g . A t e v e r y p o s s i b l e o p p o r t u n i t y i n d i v i d u a l s w h o s m o k e s h o u l d b e e n co u r a g e d t o q u i t . In alt many countries, air pollution resulting from the burning of wood and other biomass fuels has also been identified as a COPD risk factor. ot • A d i a g n o s i s of COPD should be considered in any patient who has on dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be -d confirmed by spirometry. • A CO P D m a n a g e m e n t p r o g r a m includes four components: ial assess and monitor disease, reduce risk factors, manage stable ter COPD, and manage exacerbations. ma • P h a r m a co l o g i c t r e a t m e n t can prevent and control symptoms, reduce the frequency and severity of exacerbations, improve health status, and improve exercise tolerance. d hte • P a t i e n t e d u ca t i o n 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 rig and end-of-life issues, and improve responses to acute exacerbations. py • COPD is often associated with e x a ce r b a t i o n s of symptoms.Co 5
    • WHAT IS CHRONIC OBSTRUCTIVE e uc PULMONARY DISEASE od (COPD)? pr re Ch r o n i c Ob s t r u ct i v e P u l m o n a r y D i s e a s e ( CO P D ) is a preventable or and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component er is characterized by airflow limitation that is not fully reversible. The air- flow limitation is usually progressive and associated with an abnormal alt inflammatory response of the lung to noxious particles or gases. ot This definition does not use the terms chronic bronchitis and emphysema* and excludes asthma (reversible airflow limitation). on S y m p t o m s o f CO P D i n cl u d e : -d • Cough ial • Sputum production • Dyspnea on exertion ter Episodes of acute worsening of these symptoms often occur. d ma Ch r o n i c co u g h a n d s p u t u m p r o d u ct i o n o f t e n p r e ce d e t h e hte d e v e l o p m e n t o f a i r f l o w l i m i t a t io n b y m a n y y e a r s , a l t h o u g h n o t a l l i n d i v i d u a l s w i t h co u g h a n d s p u t u m p r o d u ct i o n g o o n t o d e v e l o p COP D . rig pyCo *Chronic bronchitis, defined as the presence of cough and sputum production for at least 3 months 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 present in patients with COPD. 6
    • RISK FACTORS: WHAT CAUSES COPD? e uc Wo r l d w i d e , ci g a r e t t e s m o k i n g i s t h e m o s t co m m o n l y od e n co u n t e r e d r i s k f a ct o r f o r CO P D . pr The genetic risk factor that is best documented is a severe hereditary re deficiency of alpha-1 antitrypsin. It provides a model for how other genetic risk factors are thought to contribute to COPD. or COPD risk is related to the total burden of inhaled particles a person er encounters over their lifetime: alt • To b a cco s m o k e , including cigarette, pipe, cigar, and other types of tobacco smoking popular in many countries, as well as ot environmental tobacco smoke (ETS) • Occu p a t i o n a l d u s t s a n d ch e m i ca l s (vapors, irritants, and on fumes) when the exposures are sufficiently intense or prolonged • I n d o o r a i r p o l l u t i o n from biomass fuel used for cooking and -d heating in poorly vented dwellings, a risk factor that particularly affects women in developing countries • Ou t d o o r a i r p o l l u t i o n also contributes to the lungs’ total burden ial of inhaled particles, although it appears to have a relatively small ter effect in causing COPD ma In addition, any factor that affects lung growth during gestation and childhood (low birth weight, respiratory infections, etc.) has the potential for increasing an individual’s risk of developing COPD. d hte rig pyCo 7
    • DIAGNOSING COPD e uc A diagnosis of COPD should be considered in any patient who has dyspnea, od chronic cough or sputum production, and/or a history of exposure to risk factors for the disease, especially cigarette smoking (F i g u r e 1 ). F pr re F i g u r e 1 : K e y I n d i ca t o r s f o r Co n s id e r i n g a COP D D i a g n o s i s or Consider COPD, and perform spirometry, if any of these indicators er are present in an individual over age 40. These indicators are not diagnostic themselves, but the presence of multiple key indicators increases the probability of a diagnosis of COPD. alt • D y s p n e a that is: Progressive (worsens over time). ot Usually worse with exercise. Persistent (present every day). on Described by the patient as an “increased effort to breathe,” “heaviness,” “air hunger,” -d or “gasping.” • Ch r o n ic co u g h : May be intermittent and may be unproductive. • Ch r o n ic s p u t u m p r o d u ct i o n : ial Any pattern of chronic sputum production may indicate COPD. ter • H i s t o r y o f e x p o s u r e t o r i s k f a ct o r s : To b a cco s m o k e ( in cl u d in g p o p u l a r l o ca l ma p r e p a r a t io n s ) . Occupational dusts and chemicals. Smoke from home cooking and heating fuel. d hte T h e d i a g n o s i s s h o u l d b e co n f i r m e d b y s p i r o m e t r y * ( F i g u r e 2 , p a g e 9 a n d A p p e n d i x I, p a g e 2 4 ) . rig py *Where spirometry is unavailable, the diagnosis of COPD should be made using allCo available tools. Clinical symptoms and signs (abnormal shortness of breath and increased forced expiratory time) can be used to help with the diagnosis. A low peak flow is consistent with COPD but has poor specificity since it can be caused by other lung diseases and by poor performance. In the interest of improving the accuracy of a diagnosis of COPD, every effort should be made to provide access to standardized spirometry. 8
    • When performing spirometry, measure: • F orced V ital Capacity (F V C) and F e • F orced Expiratory V olume in one second (F EV 1 ). F uc Calculate the FEV1/FVC ratio. od Spirometric results are expressed as % P r e d i ct e d using pr appropriate normal values for the person’s sex, age, and height. re F i g u r e 2 : N o r m a l S p i r o g r a m a n d S p i r o g r a m Ty p i ca l o f or P a t i e n t s w i t h M i l d t o M o d e r a t e CO P D * er alt ot on -d ial ter d ma hte *Postbronchodilator FEV1 is recommended for the diagnosis and assessment of severity of COPD. rig py P a t i e n t s w i t h COP D t y p ica l l y s h o w a d e cr e a s e in b o t h F EV 1 a n d F EV 1 /F V C. T h e d e g r e e o f s p i r o m e t r ic a b n o r m a l i t y g e n e r a l l y r e f l e ct s t h e s e v e r i t y o f COP D . H o w e v e r, b o t hCo s y m p t o m s a n d s p ir o m e t r y s h o u l d b e c o n s i d e r e d w h e n d e v e l o p in g a n i n d i v id u a l i z e d m a n a g e m e n t s t r a t e g y f o r e a ch p a t i e n t . 9
    • St a g es o f COP D St a ge I: Mild COP D - Mild airflow limitation (FEV1/FVC < 70%; e FEV1 ≥ 80% predicted) and sometimes, but not always, chronic cough uc and sputum production. od • At this stage, the individual may not be aware that his or her lung function is abnormal. pr re St a ge II: Mo de r at e COP D - Worsening airflow limitation (FEV1/FVC < 70%; 50% ≤ FEV1 < 80% predicted), with shortness or of breath typically developing on exertion. • This is the stage at which patients typically seek medical attention er because of chronic respiratory symptoms or an exacerbation of their disease. alt St a ge III: Sev er e COP D - Further worsening of airflow limitation ot (FEV1/FVC < 70%; 30% ≤ FEV1 < 50% predicted), greater shortness of on breath, reduced exercise capacity, and repeated exacerbations which have an impact on patients’ quality of life. -d St a ge IV: Ver y Sev e r e COP D - Severe airflow limitation (FEV1/FVC < 70%; FEV1 < 30% predicted) or FEV1 < 50% predicted ial plus chronic respiratory failure. Patients may have Very Severe (Stage IV) ter COPD even if the FEV1 is > 30% predicted, whenever this complication is present. ma • At this stage, quality of life is very appreciably impaired and exacerbations may be life-threatening. d hte “ At R is k f or COP D” A major objective of GOLD is to increase awareness among health care providers and the rig general public of the significance of COPD symptoms. The classification of severity of COPD now includes four stages classified by spirometry—Stage I: Mild COPD; Stage II: Moderate py COPD; Stage III: Severe COPD; Stage IV: Very Severe COPD. A fifth category—“Stage 0: At Risk”—that appeared in the 2001 report is no longer included as a stage of COPD, as thereCo is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. Nevertheless, the importance of the public health message that chronic cough and sputum are not normal is unchanged and their presence should trigger a search for underlying cause(s). 10
    • D if f e r e n t ia l D i a g n o s i s : A major differential diagnosis is asthma. In some patients with chronic asthma, a clear distinction from COPD is not e possible using current imaging and physiological testing techniques. In these uc patients, current management is similar to that of asthma. Other potential diagnoses are usually easier to distinguish from COPD (F ig u r e 3 ).F od pr F i g u r e 3 : D i f f e r e n t i a l D i a g n o s i s o f CO P D re D ia g n o s is Su g g e s t iv e Fe a t u r e s * COPD Onset in mid-life. or Symptoms slowly progressive. Long smoking history. er Dyspnea during exercise. Largely irreversible airflow limitation. Asthma alt Onset early in life (often childhood). Symptoms vary from day to day. Symptoms at night/early morning. ot Allergy, rhinitis, and/or eczema also present. on Family history of asthma. Largely reversible airflow limitation. Congestive Heart Failure Fine basilar crackles on auscultation. -d Chest X-ray shows dilated heart, pulmonary edema. Pulmonary function tests indicate volume restriction, not airflow limitation. ial Bronchiectasis Large volumes of purulent sputum. Commonly associated with bacterial infection. ter Coarse crackles/clubbing on auscultation. Chest X-ray/CT shows bronchial dilation, bronchial wall thickening. ma Tuberculosis Onset all ages. Chest X-ray shows lung infiltrate or nodular lesions. Microbiological confirmation. d High local prevalence of tuberculosis. hte Obliterative Bronchiolitis Onset in younger age, nonsmokers. May have history of rheumatoid arthritis or fume exposure. CT on expiration shows hypodense areas. rig Diffuse Panbronchiolitis Most patients are male and nonsmokers. Almost all have chronic sinusitis. py Chest X-ray and HRCT show diffuse small centrilobular nodular opacities and hyperinflation.Co *These features tend to be characteristic of the respective diseases, but do not occur in every case. For example, a person who has never smoked may develop COPD (especially in the developing world, where other risk factors may be more important than cigarette smoking); asthma may develop in adult and even elderly patients. 11
    • COMPONENTS OF CARE: A COPD MANAGEMENT e uc PROGRAM od pr re The goals of COPD management include: or • Relieve symptoms • Prevent disease progression er • Improve exercise tolerance • Improve health status • • Prevent and treat complications Prevent and treat exacerbations alt ot • Reduce mortality • Prevent or minimize side effects from treatment on Cessation of cigarette smoking should be included as a goal throughout -d the management program. T H ES E GOA L S CA N B E A CH I EV ED T H R OU G H ial I M P L EM EN TAT I ON OF A COP D M A N A GEM EN T P R OG R A M ter WI T H F OU R COM P O N EN T S : 1 . A s s e s s a n d M o n it o r D is e a s e ma 2 . R e d u ce R i s k F a ct o r s d 3 . M a n a g e S t a b l e CO P D hte 4 . M a n a g e Ex a c e r b a t i o n s rig pyCo 12
    • Component 1: Assess and Monitor Disease e A d e t a i l e d m e d i ca l h i s t o r y of a new patient known or thought to uc have COPD should assess: od • Exposure to risk factors, including intensity and duration. pr • Past medical history, including asthma, allergy, sinusitis or nasal re polyps, respiratory infections in childhood, and other respiratory diseases. or • Family history of COPD or other chronic respiratory disease. er • Pattern of symptom development. alt • History of exacerbations or previous hospitalizations for ot respiratory disorder. on • Presence of comorbidities, such as heart disease, malignancies, osteoporosis, and musculoskeletal disorders, which may also -d contribute to restriction of activity. • Appropriateness of current medical treatments. ial ter • Impact of disease on patient’s life, including limitation of activity; missed work and economic impact; effect on family routines; and ma feelings of depression or anxiety. • Social and family support available to the patient. d hte • Possibilities for reducing risk factors, especially smoking cessation. rig pyCo 13
    • In addition to s piro m e t r y , the following ot h er t es t s may be considered for the assessment of a patient with Moderate (Stage II), Severe (Stage III), and Very Severe (Stage IV) COPD. e uc • B ro n ch od ilat o r r e v er s ibilit y t e s t in g: To rule out a diagnosis of asthma, particularly in patients with an atypical history (e.g., asthma od in childhood and regular night waking with cough and wheeze). pr • Ch es t X - r a y : Seldom diagnostic in COPD but valuable to exclude re alternative diagnoses such as pulmonary tuberculosis, and identify comorbidities such as cardiac failure. or • Ar t er ia l blo od ga s m ea s u r em e n t : Perform in patients with er FEV1 < 50% predicted or with clinical signs suggestive of respiratory alt failure or right heart failure. The major clinical sign of respiratory failure is cyanosis. Clinical signs of right heart failure include ankle edema and an increase in the jugular venous pressure. Respiratory ot failure is indicated by PaO2 < 8.0 kPa (60 mm Hg), with or without on PaCO2 > 6.7 kPa (50 mm Hg) while breathing air at sea level. -d • Alph a - 1 an t it r y p s in def icie n cy s cr een in g: Perform when COPD develops in patients of Caucasian descent under 45 years or with a strong family history of COPD. ial ter d ma COP D is u s u ally a p ro g r es s iv e dis ea s e. L u n g f u n ct io n hte ca n b e ex pect ed t o w o r s en o v er t im e, ev en w it h t h e b es t av aila ble car e. Sy m p t o m s a n d lu n g f u n ct io n s h o u ld be m o n it o r ed t o f o llo w t h e d ev elo p m en t o f co m plica t ion s , t o rig gu ide t r ea t m en t , an d t o f acilit a te d is cu s s io n o f m an a gem en t o pt io n s w it h pa t ien t s . Co m o r bidit ies a r e co m m o n in COP D py an d s h o u ld b e a ct iv ely id en t if ied .Co 14
    • Component 2: Reduce Risk Factors S m o k i n g ce s s a t i o n i s t h e s i n g l e m o s t e f f e ct i v e —a n d co s t - e e f f e ct i v e —i n t e r v e n t i o n t o r e d u ce t h e r i s k o f d e v e l o p i n g uc COP D a n d s l o w i t s p r o g r e s s i o n . od • Even a brief, 3-minute period of counseling to urge a smoker to quit can be effective, and at a minimum this should be done for pr every smoker at every health care provider visit. More intensive re strategies increase the likelihood of sustained quitting (F i g u r e 4 ). F or • Pharmacotherapy (nicotine replacement, buproprion/nortryptiline, and/or varenicline) is recommended when counseling is not sufficient er to help patients stop smoking. Special consideration should be given before using pharmacotherapy in people smoking fewer than alt 10 cigarettes per day, pregnant women, adolescents, and those with medical contraindications (unstable coronary artery disease, ot untreated peptic ulcer, and recent myocardial infarction or stroke for nicotine replacement; and history of seizures for buproprion). on -d F ig u r e 4 : S t r a t e g y t o H e l p a P a t ie n t Qu it Sm o k in g 1. A S K : Systematically identify all tobacco users at every visit. ial Implement an office-wide system that ensures that, for EVERY patient at EVERY clinic visit, tobacco-use status is queried and documented. ter 2. A D V I S E: Strongly urge all tobacco users to quit. In a clear, strong, and personalized manner, urge every tobacco user ma to quit. 3. A S S ES S : Determine willingness to make a quit attempt. Ask every tobacco user if he or she is willing to make a quit attempt d at this time (e.g., within the next 30 days). hte 4. A S S I S T: Aid the patient in quitting. Help the patient with a quit plan; provide practical counseling; rig provide intra-treatment social support; help the patient obtain extra-treatment social support; recommend use of approved py pharmacotherapy if appropriate; provide supplementary materials. 5. A R R A NG E: Schedule follow-up contact.Co Schedule follow-up contact, either in person or via telephone. 15
    • S m o k i n g P r e v e n t i o n : Encourage comprehensive tobacco-controlpolicies and programs with clear, consistent, and repeated nonsmokingmessages. Work with government officials to pass legislation to establish esmoke-free schools, public facilities, and work environments and ucencourage patients to keep smoke-free homes. odOccu p a t i o n a l Ex p o s u r e s : Emphasize primary prevention, whichis best achieved by elimination or reduction of exposures to various prsubstances in the workplace. Secondary prevention, achieved through resurveillance and early detection, is also important. orI n d o o r a n d O u t d o o r A i r P o l l u t i o n : Implement measures to reduceor avoid indoor air pollution from biomass fuel, burned for cooking and erheating in poorly ventilated dwellings. Advise patients to monitor publicannouncements of air quality and, depending on the severity of their altdisease, avoid vigorous exercise outdoors or stay indoors altogetherduring pollution episodes. ot on -d ial ter d ma hte rig pyCo16
    • Component 3: Manage Stable COPD M a n a g e m e n t o f s t a b l e CO P D s h o u l d b e g u i d e d b y t h e e f o l l o w i n g g e n e r a l p r i n ci p l e s : uc • Determine disease severity on an individual basis by taking into od account the patient’s symptoms, airflow limitation, frequency and severity of exacerbations, complications, respiratory failure, pr comorbidities, and general health status. re • Implement a stepwise treatment plan that reflects this assessment of disease severity. or • Choose treatments according to national and cultural preferences, the patient’s skills and preferences, and the local availability of er medications. alt P a t i e n t e d u ca t i o n can help improve skills, ability to cope with illness, and health status. It is an effective way to accomplish smoking cessation, ot initiate discussions and understanding of advance directives and end-of- life issues, and improve responses to acute exacerbations. on P h a r m a co l o g i c t r e a t m e n t (F i g u r e 5 ) can control and prevent F -d symptoms, reduce the frequency and severity of exacerbations, improve health status, and improve exercise tolerance. ial B r o n ch o d i l a t o r s : These medications are central to symptom ter management in COPD. ma • Inhaled therapy is preferred. • Give “as needed” to relieve intermittent or worsening symptoms, and on a regular basis to prevent or reduce persistent symptoms. d • The choice between 2-agonists, anticholinergics, methylxanthines, hte and combination therapy depends on the availability of medications and each patient’s individual response in terms of both symptom relief and side effects. rig • Regular treatment with long-acting bronchodilators, including nebu- lized formulations, is more effective and convenient than treatment py with short-acting bronchodilators. • Combining bronchodilators of different pharmacologic classes mayCo improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator. 17
    • Figure 5. Formulations and Typical Doses of COPD Medications* Drug Inhaler Solution for Oral Vials for Duration of (µg) Nebulizer Injection Action (hours) e (mg/ml) (mg) ucβ2-agonists Short-acting odFenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8 prSalbutamol (albuterol) 100, 200 (MDI & DPI) 5 5mg (Pill), 0.024%(Syrup) 0.1, 0.5 4-6Terbutaline 400, 500 (DPI) 2.5, 5 (Pill) 4-6 re Long-actingFormoterol 4.5-12 (MDI & DPI) 0.01± 12+ or Arformoterol 0.0075 12+Indacaterol 150-300 (DPI) 24 erSalmeterol 25-50 (MDI & DPI) 12+Anticholinergics Short-actingIpratropium bromide 20, 40 (MDI) 0.25-0.5 alt 6-8 otOxitropium bromide 100 (MDI) 1.5 7-9 Long-acting onTiotropium 18 (DPI), 5 (SMI) 24+Combination short-acting β2-agonists plus anticholinergic in one inhaler -dFenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 6-8Methylxanthines ialAminophylline 200-600 mg (Pill) 240 mg Variable, up to 24 terTheophylline (SR) 100-600 mg (Pill) Variable, up to 24Inhaled glucocorticosteroids maBeclomethasone 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 β2-agonists plus glucocorticosteroids in one inhaler d hteFormoterol/Budesonide 4.5/160, 9/320 (DPI)Salmeterol/Fluticasone 50/100, 250. 500 (DPI) 25/50, 125, 250 (MDI) rigSystemic glucocorticosteroidsPrednisone 5-60 mg (Pill) pyMethyl-prednisolone 4, 8, 16 mg (Pill)Phosphodiesterase-4 inhibitorsCoRoflumilast 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 available. ±Formoterol nebulized solution is based on the unit dose vial containing 20 µgm in a volume of 2.0ml 18
    • Inhaled Glucocorticosteroids: Regular treatment with inhaled glucocorticosteroids does not modify the long-term decline in FEV1 but has been shown to reduce the frequency of exacerbations and thus improve health status for symptomatic patients with an FEV1 < 50% e predicted and repeated exacerbations (for example, 3 in the last three uc years). The dose-response relationships and long-term safety of inhaled glucocorticosteroids in COPD are not known. Treatment with inhaled glu- od cocorticosteroids increases the likelihood of pneumonia and does not reduce overall mortality. pr An inhaled glucocorticosteroid combined with a long-acting β2-agonist is re more effective than the individual components in reducing exacerbations and improving lung function and health status. Combination therapy or increases the likelihood of pneumonia and has no significant effects on mortality. In patients with an FEV1 less than 60%, pharmacotherapy with er long-acting β2-agonist, inhaled glucocorticosteroid and its combination alt decreases the rate of decline of lung function. Addition of a long-acting β2-agonist/inhaled glucocorticosteroid to an anticholinergic (tiotropium) appears to provide additional benefits. ot Oral Glucocorticosteroids: Long-term treatment with oral glucocorticosteroids on is not recommended. Phosphodiesterase-4 inhibitors: In patients with Stage III: Severe COPD or -d Stage IV: Very Severe COPD and a history of exacerbations and chronic bronchitis, the phosphodiesterase-4 inhibitor, roflumilast, reduces exacerba- ial tions treated with oral glucocorticosteroids. These effects are also seen when roflumilast is added to long-acting bronchodilators; there are no ter comparison studies with inhaled glucocorticosteroids. ma Vaccines: Influenza vaccines reduce serious illness and death in COPD patients by 50%. Vaccines containing killed or live, inactivated viruses are recommended, and should be given once each year. Pneumococcal d polysaccharide vaccine is recommended for COPD patients 65 years and hte older, and has been shown to reduce community-acquired pneumonia in those under age 65 with FEV1 < 40% predicted. rig An t ibiot ics : Not recommended except for treatment of infectious exacerbations and other bacterial infections. py M u co ly t ic (Mu co k in et ic, Mu cor e gu lat or ) Agen t s: Patients withCo viscous sputum may benefit from mucolytics, but overall benefits are very small. Use is not recommended. An t it u s siv e s: Regular use contraindicated in stable COPD. 19
    • Non - P h ar m acolo gic Tr e at m en t includes rehabilitation, oxygen therapy, and surgical interventions. Rehabilitation: Patients at all stages of disease benefit from exercize e training programs improvements in exercise tolerance and symptoms of uc dyspnea and fatigue. Benefits can be sustained even after a single pulmo- nary rehabilitation program. The minimum length of an effective rehabili- od tation program is 6 weeks; the longer the program continues, the more effective the results. Benefit does wane after a rehabilitation program pr ends, but if exercise training is maintained at home the patients health re status remains above pre-rehabilitation levels. Th e go a ls of pu lm on a r y r eh ab ilit at io n a r e t o r ed u ce s y m pt o m s , or im pr o v e qu a lit y o f life, a n d in cr ea s e pa r t icipa t io n in ev er y da y Patients it ies . stages of disease benefit from exercise training programs, a ct iv at all er alt Ox y gen Th e r apy : The long-term administration of oxygen (>15 hours per day) to patients with chronic respiratory failure increases survival and has a beneficial impact on pulmonary hemodynamics, hematologic ot characteristics, exercise capacity, lung mechanics, and mental state. on Initiate oxygen therapy for patients with Stage IV: Very Severe COPD if: -d • PaO2 is at or below 7.3 kPa (55 mm Hg) or SaO2 is at or below 88%, with or without hypercapnia; or • PO2 is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg) ial or SaO2 is 88%, if there is evidence of pulmonary hypertension, ter peripheral edema suggesting congestive heart failure, or polycythemia (hematocrit > 55%). ma Th e go a l o f lo n g- t er m o x y gen t h er a py is t o in cr ea s e t h e ba s e- lin e P a O2 a t r es t t o a t lea s t 8.0 k P a (60 m m Hg) a t s ea lev el, d a n d/o r pr o du ce Sa O2 a t lea s t 90% , w h ich w ill p r es er v e v it al hte o r ga n f u n ct io n b y en s u r in g an ad equ at e d eliv er y of o x y gen . rig Su r gical Tr e at m en t s : Bullectomy and lung transplantation may be py considered in carefully selected patients with Stage IV: Very Severe COPD. There is currently no sufficient evidence that would support theCo widespread use of lung volume reduction surgery (LVRS). Th er e is n o con v in cin g ev iden ce t h at m ech an ical v en t ilat or y su ppor t h as a role in t h e rou tin e m an agem en t of stable COP D. 20
    • A summary of characteristics and recommended treatment at each stage of COPD is shown in F i g u r e 6 . e uc Figure 6: Therapy at Each Stage of COPD* od pr I: Mild II: Moderate III: Severe IV: Very Severe re • FEV1/FVC < 0.70 or • FEV1/FVC < 0.70 • FEV1 < 30% predicted or FEV1 < 50% • er FEV1/FVC < 0.70 predicted plus chronic respiratory failure • FEV1/FVC < 0.70 • 30% ≤ FEV < 50% 1 • alt 50% ≤ FEV < 80% predicted 1 • FEV1 ≥ 8 0% predicted predicted ot Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) on Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation -d Add inhaled glucocorticosteroids if repeated exacerbations ial Add long term oxygen if ter chronic respiratory failure Consider surgical ma treatments d hte *Postbronchodilator FEV1 is recommended for the diagnosis and assessment of severity of COPD. rig pyCo 21
    • Component 4: Manage Exacerbations An exacerbation of COPD is defined as a n e v e n t in t h e n a t u r a l e uc co u r s e o f t h e d i s e a s e ch a r a ct e r i z e d b y a ch a n g e i n t h e p a t i e n t ’s b a s e l i n e d y s p n e a , co u g h , a n d /o r s p u t u m t h a t i s od b e y o n d n o r m a l d a y - t o - d a y v a r i a t i o n s , i s a cu t e i n o n s e t , a n d m a y w a r r a n t a ch a n g e i n r e g u l a r m e d i ca t i o n i n a pr p a t i e n t w i t h u n d e r l y i n g CO P D . re The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third or of severe exacerbations cannot be identified. er alt H o w t o A s s e s s t h e S e v e r i t y o f a n Ex a ce r b a t i o n ot Arterial blood gas measurements (in hospital): on • PaO2 < 8.0 kPa (60 mm Hg) and/or SaO2 < 90% with or without PaCO2 > 6.7 kPa, (50 mmHg) when breathing room air indicates respiratory failure. -d • Moderate-to-severe acidosis (pH < 7.36) plus hypercapnia (PaCO2 ial > 6-8 kPa, 45-60 mm Hg) in a patient with respiratory failure is an indication for mechanical ventilation. ter Chest X-ray: Chest radiographs (posterior/anterior plus lateral) identify ma alternative diagnoses that can mimic the symptoms of an exacerbation. ECG: Aids in the diagnosis of right ventricular hypertrophy, arrhythmias, and ischemic episodes. d hte Other laboratory tests: • Sputum culture and antibiogram to identify infection if there is rig no response to initial antibiotic treatment. py • Biochemical tests to detect electrolyte disturbances, diabetes, and poor nutrition.Co • Whole blood count can identify polycythemia or bleeding. 22
    • Hom e Car e o r Ho s pit al Car e f o r En d - St a ge COP D P at ien t s ? Th e r is k of dy in g f ro m a n ex acer ba t io n o f COP D is clos ely r ela t ed t o t h e dev elo p m en t o f r es pir a t o r y acido s is , t h e p r es en ce o f e s er iou s com o r b idit ies , a n d t h e n eed f o r v en t ila t o r y s u pp o r t . uc P at ien t s lack in g t h es e f eat u r es a r e n o t at h igh r is k o f dy in g , bu t t h o s e w it h s ev er e u n der ly in g COP D o f ten r eq u ir e h o s p ita lizat io n od in a n y ca s e. At t em p t s at m a n ag in g s u ch p at ien t s en t ir ely in t h e co m m u n it y h av e m et w it h lim it ed s u cces s , b u t r et u r n in g t h em pr t o t h eir h om es w it h in cr ea s ed s o cia l s u p po r t an d a s u p er v is ed m edica l car e p ro g r am af t er an in it ia l em er gen cy r o om as s es s m en t re h as b een m u ch m o r e s u cces s f u l. Ho w ev er, d et ailed co s t - ben ef it a n a ly s es o f t h es e ap p ro a ch es h av e n o t b een r ep o r t ed . or H om e Ma n age m e n t B ron ch odila t o r s: Increase dose and/or frequency of existing short- er acting bronchodilator therapy, preferably with 2-agonists. If not already used, add anticholinergics until symptoms improve. alt Glu cocor t ico st er oids : If baseline FEV1 < 50% predicted, add 30-40 ot mg oral prednisolone per day for 7-10 days to the bronchodilator regimen. Budesonide alone may be an alternative to oral glucocorticosteroids in the on treatment of exacerbations and is associated with significant reduction of complications. -d H os pit a l Man agem en t Patients with the characteristics listed in Figu r e 7 should be hospitalized. ial Indications for referral and the management of exacerbations of COPD in the hospital depend on local resources and the facilities of the local ter hospital. ma Figu r e 7: In dica t io n s fo r Ho s pit al Adm is s ion fo r Ex acerb at ion s • Marked increase in intensity of • Failure of exacerbation to respond symptoms, such as sudden develop- to initial medical management d ment of resting dyspnea • Significant comorbidities hte • Severe underlying COPD • Frequent exacerbations • Onset of new physical signs (e.g., • Newly occurring arrhythmias cyanosis, peripheral edema) • Diagnostic uncertainty rig • Older age • Insufficient home support py An t ibio t ics: Antibiotics should be given to patients:Co • 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 23
    • APPENDIX I: e SPIROMETRY FOR uc DIAGNOSIS OF COPD od pr Spirometry is as important for the diagnosis of COPD as blood re pressure measurements are for the diagnosis of hypertension. Spirometry should be available to all health care professionals. or Wh a t is S p i r o m e t r y ? er S p i r o m e t r y is a simple test to measure the amount of air a alt person can breathe out, and the amount of time taken to do so. A s p i r o m e t e r is a device used to measure how effectively, and ot how quickly, the lungs can be emptied. on A s p i r o g r a m is a volume-time curve. Spirometry measurements used for diagnosis of COPD include -d (see Figure 2, page 9): ial • F V C (Forced Vital Capacity): maximum volume of air that ter can be exhaled during a forced maneuver. • F EV 1 (Forced Expired Volume in one second): volume expired in ma the first second of maximal expiration after a maximal inspiration. This is a measure of how quickly the lungs can be emptied. d • F EV 1/F V C: FEV1 expressed as a percentage of the FVC, hte gives a clinically useful index of airflow limitation. rig The ratio FEV1/FVC is between 70% and 80% in normal adults; a value less than 70% indicates airflow limitation and the possibility py of COPD.Co FEV1 is influenced by the age, sex, height and ethnicity, and is best considered as a percentage of the predicted normal value. There is a vast literature on normal values; those appropriate for local populations should be used1,2,3. 24
    • W h y d o S p i r o m e t r y f o r CO P D ? • Spirometry is needed to make a firm diagnosis of COPD. e uc • Together with the presence of symptoms, spirometry helps stage COPD severity and can be a guide to specific treatment steps. od • A normal value for spirometry effectively excludes the diagnosis of clinically relevant COPD. pr • The lower the percentage predicted FEV1, the worse the re subsequent prognosis. or • FEV1 declines over time and faster in COPD than in healthy subjects. Spirometry can be used to monitor disease progres- er sion, but to be reliable the intervals between measurements must be at least 12 months. alt ot W h a t Yo u N e e d t o P e r f o r m S p i r o m e t r y on Several types of spirometers are available: -d • relatively large bellows or rolling-seal spirometers (usually only available in pulmonary function laboratories). Calibration should be checked against a known volume e.g. from a 3-litre ial syringe on a regular basis. ter • smaller hand-held devices, often with electronic calibration systems. ma A hard copy of the volume time plot is very useful to check optimal performance and interpretation, and to exclude errors. d hte Most spirometers require electrical power to permit operation of the motor and/or sensors. Some battery operated versions are rig available that can dock with a computer to provide hard copy. pyCo 25
    • I t i s e s s e n t i a l t o l e a r n h o w y o u r m a ch i n e i s ca l i b r a t e d a n d w h e n a n d h o w t o cl e a n i t . e uc H o w t o P e r f o r m S p ir o m e t r y od Spirometry is best performed with the patient seated. Patients may be anxious about performing the tests properly, and should be pr reassured. Careful explanation of the test, accompanied by a demonstration, is very useful. The patient should: re • Breathe in fully. or • Seal their lips around the mouthpiece. er • Force the air out of the chest as hard and fast as they can until their lungs are completely “empty.” • Breathe in again and relax. alt ot Exhalation must continue until no more air can be exhaled, must on be at least 6 seconds, and can take up to 15 seconds or more. Like any test, spirometry results will only be of value if the -d expirations are performed satisfactorily and consistently. Both FVC and FEV1 should be the largest value obtained from any of ial 3 technically satisfactory curves and the FVC and FEV1 values in ter these three curves should vary by no more than 5% or 100 ml, whichever is greater. The FEV1/FVC is calculated using the maxi- ma mum FEV1 and FVC from technically acceptable (not necessarily the same) curves. d Those with chest pain or frequent cough may be unable to hte perform a satisfactory test and this should be noted. rig pyCo 26
    • Wh e r e t o f in d m o r e d e t a i l e d i n f o r m a t i o n o n s p ir o m e t r y e 1 . A m e r i ca n T h o r a ci c S o ci e t y uc http://www.thoracic.org/adobe/statements/spirometry1-30.pdf od 2. A u s t r a l i a n /N e w Z e a l a n d T h o r a ci c S o ci e t y http://www.nationalasthma.org.au/publications/spiro/index.htm pr re 3. B r i t i s h T h o r a ci c S o ci e t y http://www.brit-thoracic.org.uk/copd/consortium.html or 4. GO L D A spirometry guide for general practitioners and a teaching slide er set is available: http://www.goldcopd.org alt ot on -d ial ter d ma hte rig pyCo 27
    • 28 Co py rig hte d NOTES ma ter ial -d on ot alt er or re pr od uc e
    • The Global Initiative for Chronic Obstructive Lung Disease is supported by educational grants from: e uc od pr re or er alt ot on -d ial ter d ma hte rig pyCo Visit the GOLD website at www.goldcopd.org www.goldcopd.org/application.asp Copies of this document are available at www.us-health-network.com © 2009 Medical Communications Resources, Inc.