NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop Summary |
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CONTENTS
PREFACE
INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
FUTURE RESEARCH
Consultant Reviewers
REFERENCES
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Preface
Introduction
Definition and Classification of Severity
Definition
Classification of Severity
Pathogenesis
Pathology
Pathophysiology
Burden of COPD
Epidemiology
Economic and Social Burden of COPD
Risk Factors
The Four Components of COPD Management
Introduction
Component 1: Assess and Monitor Disease
Diagnosis
Ongoing Monitoring and Assessment
Component 2: Reduce Risk Factors
Smoking Prevention and Cessation
Occupational Exposures
Indoor/Outdoor Air Pollution
Component 3: Manage Stable COPD
Introduction
Education
Pharmacologic Treatment
Bronchodilators
Glucocorticosteroids
Other Pharmacologic Treatments
Nonpharmacologic Treatment
Rehabilitation
Oxygen Therapy
Ventilatory Support
Surgical Treatments
Component 4: Manage Exacerbations
Diagnosis and Assessment of Severity
Home Management
Hospital Management
Hospital Discharge and Follow-up
Future Research
References
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PREFACE |
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CONTENTS
PREFACE
INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
FUTURE RESEARCH
Consultant Reviewers
REFERENCES
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Chronic obstructive pulmonary disease (COPD) is a major public health problem. It is the fourth leading cause of chronic morbidity and mortality in the United States (1) and is projected to rank fifth in 2020 as a worldwide burden of disease according to a study published by the World Bank/World Health Organization (2). Yet, COPD fails to receive adequate attention from the health care community and government officials. With these concerns in mind, a committed group of scientists encouraged the U.S. National Heart, Lung, and Blood Institute and the World Health Organization to form the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Among GOLD's important objectives are to increase awareness of COPD and to help the thousands of people who suffer from this disease and die prematurely from COPD or its complications.
The first step in the GOLD program was to prepare a consensus Workshop Report, Global Strategy for the Diagnosis, Management, and Prevention of COPD. The GOLD Expert Panel, a distinguished group of health professionals from the fields of respiratory medicine, epidemiology, socioeconomics, public health, and health education, reviewed existing COPD guidelines, as well as new information on pathogenic mechanisms of COPD as they developed a consensus document. Many recommendations will require additional study and evaluation as the GOLD program is implemented.
A major problem is the incomplete information about the causes and prevalence of COPD, especially in developing countries. While cigarette smoking is a major known risk factor, much remains to be learned about other causes of this disease. The GOLD Initiative will bring COPD to the attention of governments, public health officials, health care workers, and the general public, but a concerted effort by all involved in health care will be necessary to control this major public health problem.
I would like to acknowledge the dedicated individuals who prepared the Workshop Report and the effective leadership of the Workshop Chair, Professor Romain Pauwels. It is a privilege for the National Heart, Lung, and Blood Institute to serve as one of the cosponsors. We look forward to working with the World Health Organization, and all other interested organizations and individuals, to meet the goals of the GOLD Initiative.
Development of the Workshop Report was supported through educational grants to the Department of Respiratory Diseases of the Ghent University Hospital, Belgium (WHO Collaborating Center for the Management of Asthma and COPD) from ASTA Medica, AstraZeneca, Aventis, Bayer, Boehringer-Ingelheim, Byk Gulden, Chiesi, Glaxo Wellcome, Merck, Sharp & Dohme, Mitsubishi-Tokyo, Nikken Chemicals, Novartis, Schering-Plough, SmithKline Beecham, Yamanouchi, and Zambon.
CLAUDE LENFANT, M.D.
Director
National Heart, Lung, and Blood Institute
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INTRODUCTION |
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CONTENTS
PREFACE
INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
FUTURE RESEARCH
Consultant Reviewers
REFERENCES
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Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality throughout the world. COPD is currently the fourth leading cause of death in the world (3), and further increases in the prevalence and mortality of the disease can be predicted in the coming decades. A unified international effort is required to reverse these trends.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) is a collaborative project of the U.S. National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO). Its goals are to increase awareness of COPD and decrease morbidity and mortality from this disease. GOLD aims to improve prevention and management of COPD through a concerted worldwide effort of people involved in all facets of health care and health care policy, and to encourage a renewed research interest in this extremely prevalent disease.
The GOLD Workshop Report, Global Strategy for the Diagnosis, Management, and Prevention of COPD, presents a COPD management plan with four components: (1) Assess and Monitor Disease; (2) Reduce Risk Factors; (3) Manage Stable COPD; (4) Manage Exacerbations. The Workshop Report is based on the best-validated current concepts of COPD pathogenesis and the available evidence on the most appropriate management and prevention strategies. It has been developed by individuals with expertise in COPD research and patient care and extensively reviewed by many experts and scientific societies. Before its release for publication, the Workshop Report was reviewed by the NHLBI and the WHO. This Executive Summary provides key information about COPD; the full Workshop Report provides more details.
In Section 3, Four Components of COPD Management, levels of evidence are assigned to statements, where appropriate, using a system developed by the NHLBI (Table 1). Levels of evidence are indicated in parentheses after the relevant statement, e.g., (Evidence A).
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DEFINITION AND CLASSIFICATION OF SEVERITY |
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INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
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REFERENCES
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Definition
COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
A diagnosis of COPD should be considered in any patient who has symptoms of cough, sputum production, or dyspnea, and/or a history of exposure to risk factors for the disease. The diagnosis is confirmed by spirometry. The presence of a postbronchodilator FEV1 < 80% of the predicted value in combination with an FEV1/FVC < 70% confirms the presence of airflow limitation that is not fully reversible. Where spirometry is unavailable, the diagnosis of COPD should be made using all available tools. Clinical symptoms and signs, such as 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 because it can be caused by other lung diseases and by poor performance. In the interest of improving the diagnosis of COPD, every effort should be made to provide access to standardized spirometry. Chronic cough and sputum production often precede the development of airflow limitation by many years, although not all individuals with cough and sputum production go on to develop COPD.
Classification of Severity
For educational reasons, a simple classification of disease severity into four stages is recommended (Table 2). The management of COPD is largely symptom-driven, and there is only an imperfect relationship between the degree of airflow limitation and the presence of symptoms. The staging, therefore, is a pragmatic approach aimed at practical implementation and should only be regarded as an educational tool, and a very general indication of the approach to management. All FEV1 values refer to postbronchodilator FEV1.
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Stage 0: At Risk. Characterized by chronic cough and sputum production. Lung function, as measured by spirometry, is still normal.
Stage I: Mild COPD. Characterized by mild airflow limitation (FEV1/FVC < 70% but FEV1 
80% predicted) and usually, but not always, by chronic cough and sputum production.
At this stage, the individual may not even be aware that his or
her lung function is abnormal.
Stage II: Moderate COPD. Characterized by worsening airflow limitation (30% 
FEV1 < 80% predicted) and usually
the progression of symptoms, with shortness of breath typically developing on exertion. This is the stage at which patients typically seek medical attention because of dyspnea or
an exacerbation of their disease. The division in Stages IIA
and IIB is based on the fact that exacerbations are especially
seen in patients with an FEV1 below 50% predicted. The presence of repeated exacerbations has an impact on the quality of
life of patients and requires appropriate management.
Stage III: Severe COPD. Characterized by severe airflow limitation (FEV1 < 30% predicted) or the presence of respiratory failure or clinical signs of right heart failure. Patients may have severe (Stage III) COPD even if the FEV1 is > 30% predicted, whenever these complications are present. At this stage, quality of life is appreciably impaired and exacerbations may be life-threatening.
Poorly reversible airflow limitation associated with bronchiectasis, cystic fibrosis, tuberculosis, or asthma is not included except insofar as these conditions overlap with COPD. In many developing countries both pulmonary tuberculosis and COPD are common. Therefore, in all subjects with symptoms of COPD, a possible diagnosis of tuberculosis should be considered, especially in areas where this disease is known to be prevalent. In countries in which the prevalence of tuberculosis is greatly diminished, the possible diagnosis of this disease is sometimes overlooked.
Pathogenesis
COPD is characterized by chronic inflammation throughout
the airways, parenchyma, and pulmonary vasculature. Macrophages, T lymphocytes (predominately CD8+), and neutrophils are increased in various parts of the lung. Activated inflammatory cells release a variety of mediators
including leukotriene B4 (LTB4) (4), interleukin-8 (IL-8) (5), tumor necrosis factor-
(TNF-) (5, 8), and otherscapable of damaging lung structures or sustaining neutrophilic inflammation. In addition to inflammation, two other processes thought to
be important in the pathogenesis of COPD are an imbalance
of proteinases and antiproteinases in the lung, and oxidative
stress. Inflammation of the lungs is caused by exposure to inhaled noxious particles and gases. Cigarette smoke can induce
inflammation and directly damage the lungs (9). Although
fewer data are available, it is likely that other COPD risk factors initiate a similar inflammatory process (15). It is believed that this inflammation can then lead to COPD.
Pathology
Pathologic changes characteristic of COPD are found in the
central airways, peripheral airways, lung parenchyma, and
pulmonary vasculature. In the central airwaysthe trachea,
bronchi, and bronchioles greater than 2 to 4 mm in internal diameterinflammatory cells infiltrate the surface epithelium
(9, 20, 21). Enlarged mucus-secreting glands and an increase in
the number of goblet cells are associated with mucus hypersecretion. In the peripheral airwayssmall bronchi and bronchioles that have an internal diameter of less than 2 mmchronic
inflammation leads to repeated cycles of injury and repair of
the airway wall (22). The repair process results in a structural
remodeling of the airway wall, with increasing collagen content and scar tissue formation, that narrows the lumen and
produces fixed airways obstruction (23).
Destruction of the lung parenchyma in patients with COPD typically occurs as centrilobular emphysema. This involves dilatation and destruction of the respiratory bronchioles (24). These lesions occur more frequently in the upper lung regions in milder cases, but in advanced disease they may appear diffusely throughout the entire lung and also involve destruction of the pulmonary capillary bed. An imbalance of endogenous proteinases and antiproteinases in the lung resulting from genetic factors or the action of inflammatory cells and mediators, is thought to be a major mechanism behind emphysematous lung destruction. Oxidative stress, another consequence of inflammation, may also contribute (25).
Pulmonary vascular changes in COPD are characterized by a thickening of the vessel wall that begins early in the natural history of the disease. Thickening of the intima is the first structural change (26), followed by an increase in smooth muscle and the infiltration of the vessel wall by inflammatory cells (27). As COPD worsens, greater amounts of smooth muscle, proteoglycans, and collagen (28) further thicken the vessel wall.
Pathophysiology
Pathologic changes in the lungs lead to corresponding physiologic changes characteristic of the disease, including mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, and cor pulmonale. They usually develop in this order over the course of the disease. Mucus hypersecretion and ciliary dysfunction lead to chronic cough and sputum production. These symptoms can be present for many years before other symptoms or physiologic abnormalities develop. Expiratory airflow limitation, best measured through spirometry, is the hallmark physiologic change of COPD and the key to diagnosis of the disease. It is primarily caused by fixed airway obstruction and the consequent increase in airway resistance. Destruction of alveolar attachments, which inhibits the ability of the small airways to maintain patency, plays a smaller role.
In advanced COPD, peripheral airways obstruction, parenchymal destruction, and pulmonary vascular abnormalities reduce the lung's capacity for gas exchange, producing hypoxemia and, later on, hypercapnia. Pulmonary hypertension, which develops late in the course of COPD (Stage III: Severe COPD), is the major cardiovascular complication of COPD and is associated with the development of cor pulmonale and a poor prognosis (29). The prevalence and natural history of cor pulmonale in COPD are not yet clear.
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BURDEN OF COPD |
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INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
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Epidemiology
Most of the information available on COPD prevalence, morbidity, and mortality comes from developed countries. Even in these countries, accurate epidemiologic data on COPD are difficult and expensive to collect. Prevalence and morbidity data greatly underestimate the total burden of COPD because the disease is usually not diagnosed until it is clinically apparent and moderately advanced. The imprecise and variable definitions of COPD have made it hard to quantify the morbidity and mortality of this disease in developed (30) and developing countries. Mortality data also underestimate COPD as a cause of death because the disease is more likely to be cited as a contributory than as an underlying cause of death, or may not be cited at all (31).
Prevalence. In the Global Burden of Disease Study conducted under the auspices of the WHO and the World Bank (2, 32), the worldwide prevalence of COPD in 1990 was estimated to be 9.34/1,000 in men and 7.33/1,000 in women. However, these estimates include all ages and underestimate the true prevalence of COPD in older adults. The prevalence of COPD is highest in countries where cigarette smoking has been, or still is, very common, whereas the prevalence is lowest in countries where smoking is less common, or total tobacco consumption per individual is low.
Morbidity. The limited data that are available indicate that morbidity due to COPD increases with age and is greater in men than women (1). COPD is responsible for a significant part of physician visits, emergency department visits, and hospitalizations.
Mortality. COPD is currently the fourth leading cause of death in the world (3), and further increases in the prevalence and mortality of the disease can be predicted in the coming decades (2, 32). In the United States, COPD death rates are very low among people younger than 45 yr of age but then increase with age, and COPD becomes the fourth or fifth leading cause of death among those over 45 (1).
Economic and Social Burden of COPD
Table 3 provides an understanding of the relative economic burden of COPD in four countries with Western styles of medical practice and social or private insurance structures. Similar data from developing countries are not available. The Global Burden of Disease Study (2, 32) estimated the fraction of mortality and disability attributable to major diseases and injuries using a composite measure of the burden of each health problem, the disability-adjusted life year (DALY = the sum of years lost because of premature mortality and years of life lived with disability, adjusted for the severity of disability). According to projections, COPD will be the fifth leading cause of DALYs lost worldwide in 2020 (in 1990 it ranked twelfth), behind ischemic heart disease, major depression, traffic accidents, and cerebrovascular disease (Table 4).
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Risk Factors
Risk factors for COPD include both host factors and environmental exposures, and the disease usually arises from an interaction between these two types of factors. The host factor that
is best documented is a rare hereditary deficiency of 1-antitrypsin. Other genes involved in the pathogenesis of COPD
have not yet been identified. The major environmental factors
are tobacco smoke; heavy exposure to occupational dusts and
chemicals (vapors, irritants, and fumes); and indoor/outdoor
air pollution. The role of sex as a risk factor for COPD remains unclear. In the past, most studies showed that COPD
prevalence and mortality were greater among men than women
(33). More recent studies (1, 37) from developed countries
show that the prevalence of the disease is almost equal in men
and women, which probably reflects changing patterns of tobacco smoking. Some studies have in fact suggested that
women are more susceptible to the effects of tobacco smoke
than men (35, 38). This is an important question given the increasing rate of smoking among women in both developed
and developing countries.
Host Factors
Genes. It is believed that many genetic factors increase (or decrease) a person's risk of developing COPD. The genetic risk factor that is best documented is a rare hereditary deficiency of 1-antitrypsin (39). Premature and accelerated development of panlobular emphysema and decline in lung function
occurs in many smokers and nonsmokers with the severe deficiency, although smoking increases the risk appreciably.
Other genes involved in the pathogenesis of COPD have not
yet been identified.
Airway hyperresponsiveness. Asthma and airway hyperresponsiveness, identified as risk factors that contribute to the development of COPD (42), are complex disorders related to a number of genetic and environmental factors. How they influence the development of COPD is unknown. Airway hyperresponsiveness may also develop after exposure to tobacco smoke or other environmental insults and thus may be a result of smoking-related airway disease.
Lung growth. Lung growth is related to processes occurring during gestation, birth weight, and exposures during childhood (43). Reduced maximal attained lung function (as measured by spirometry) may identify individuals who are at increased risk for the development of COPD (48).
Exposures
Tobacco smoke. Cigarette smokers have a higher prevalence of lung-function abnormalities and respiratory symptoms, a greater annual rate of decline in FEV1, and higher death rates for COPD than nonsmokers. Pipe and cigar smokers have higher COPD morbidity and mortality rates than nonsmokers, although their rates are lower than those for cigarette smokers (49). Not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual's risk. Passive exposure to cigarette smoke may also contribute to respiratory symptoms and COPD by increasing the lungs' total burden of inhaled particulates and gases (33, 50, 51). Smoking during pregnancy may also pose a risk for the fetus, by affecting lung growth and development in utero and possibly the priming of the immune system (47, 52).
Occupational dusts and chemicals. When the exposures are sufficiently intense or prolonged, occupational dusts and chemicals (vapors, irritants, fumes) can cause COPD independently of cigarette smoking and increase the risk of the disease in the presence of concurrent cigarette smoking (53). Exposure to particulate matter, irritants, organic dusts, and sensitizing agents can cause an increase in airway hyperresponsiveness (54), especially in airways already damaged by other occupational exposures, cigarette smoke, or asthma.
Outdoor and indoor air pollution. High levels of urban air pollution are harmful to persons with existing heart or lung disease. The role of outdoor air pollution in causing COPD is unclear, but appears to be small when compared with cigarette smoking. Indoor air pollution from biomass fuel, burned for cooking and heating in poorly vented dwellings, has been implicated as a risk factor for the development of COPD (55).
Infections. A history of severe childhood respiratory infection has been associated with reduced lung function and increased respiratory symptoms in adulthood (48). However, viral infections may be related to another factor, e.g., low birth weight, that itself is related to COPD.
Socioeconomic status. There is evidence that the risk of developing COPD is inversely related to socioeconomic status (65). It is not clear, however, whether this pattern reflects exposures to indoor and outdoor air pollutants, crowding, poor nutrition, or other factors that are related to socioeconomic status (64, 66).
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THE FOUR COMPONENTS OF COPD MANAGEMENT |
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CONTENTS
PREFACE
INTRODUCTION
DEFINITION AND CLASSIFICATION...
BURDEN OF COPD
THE FOUR COMPONENTS OF...
FUTURE RESEARCH
Consultant Reviewers
REFERENCES
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Introduction
An effective COPD management plan includes four components: (1) Assess and Monitor Disease; (2) Reduce Risk Factors; (3) Manage Stable COPD; (4) Manage Exacerbations.
The goals of effective COPD management are to:
- Prevent disease progression
- Relieve symptoms
- Improve exercise tolerance
- Improve health status
- Prevent and treat complications
- Prevent and treat exacerbations
- Reduce mortality
These goals should be reached with a minimum of side effects from treatment, a particular challenge in patients with COPD where comorbidities are common. The extent to which these goals can be realized varies with each individual, and some treatments will produce benefits in more than one area. In selecting a treatment plan, the benefits and risks to the individual and the costs, direct and indirect, to the community must be considered. Patients should be identified before the end stage of the illness, when disability is substantial. However, the benefits of spirometric screening, of either the general population or smokers, are still unclear. Educating patients and physicians to recognize that cough, sputum production, and especially breathlessness are not trivial symptoms is an essential aspect of the public health care of this disease.
Reduction of therapy once symptom control has been achieved is not normally possible in COPD. Further deterioration of lung function usually requires the progressive introduction of more treatments, both pharmacologic and nonpharmacologic, to attempt to limit the impact of these changes. Acute exacerbations of signs and symptoms, a hallmark of COPD, impair patients' quality of life and decrease their health status. Appropriate treatment and measures to prevent further exacerbations should be implemented as quickly as possible.
Component 1: Assess and Monitor Disease
Key Points
- Diagnosis of COPD is based on a history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, with or without the presence of symptoms.
- Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea.
- For the diagnosis and assessment of COPD, spirometry is the gold standard as it is the most reproducible, standardized, and objective way of measuring airflow limitation. FEV1/FVC < 70% and a postbronchodilator FEV1 < 80% predicted confirms the presence of airflow limitation that is not fully reversible.
- Health care workers involved in the diagnosis and management of patients with COPD should have access to spirometry.
- Measurement of arterial blood gas tensions should be considered in all patients with FEV1 < 40% predicted or clinical signs suggestive of respiratory failure or right heart failure.
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80% predicted). This approach to defining
airflow limitation is a pragmatic one in view of the fact that
universally applicable reference values for FEV1 and FVC are
not available.
Assessment of severity. Assessment of severity (Table 2) is
based on the level of symptoms, severity of the spirometric abnormality, and the presence of complications such as respiratory failure and right heart failure.
Additional investigations. For patients in Stage II: Moderate COPD and beyond, the following additional investigations
may be useful:
1. Bronchodilator reversibility testing. Generally performed
only once, at the time of diagnosis, this test is useful to help rule out a diagnosis of asthma, to establish a patient's best attainable lung function, to gauge a patient's prognosis, and to guide treatment decisions. However, even patients who
do not show a significant FEV1 response to a short-acting
bronchodilator test can benefit symptomatically from long-term bronchodilator treatment.
2. Glucocorticosteroid reversibility testing. The simplest, and
potentially safest, way to identify patients most likely to respond to long-term glucocorticosteroid treatment is with a
treatment trial of inhaled glucocorticosteroids for 6 wk to 3 mo, using as criteria for glucocorticosteroid reversibility an
FEV1 increase of 200 ml and 15% above baseline (70, 71).
The response to glucocorticosteroids should be evaluated
with respect to the postbronchodilator FEV1 (that is, the
effect of treatment with inhaled glucocorticosteroids should
be in addition to that of regular treatment with a bronchodilator).
3. Chest X-ray. A chest radiograph is seldom diagnostic in
COPD unless obvious bullous disease is present, but it is
valuable in excluding alternative diagnoses. Computed tomography (CT) of the chest is not routinely recommended.
However, when there is doubt about the diagnosis of
COPD, high-resolution CT (HRCT) might help in the differential diagnosis. In addition, if a surgical procedure such
as bullectomy or lung volume reduction is contemplated, chest CT is helpful.
4. Arterial blood gas measurement. In advanced COPD, measurement of arterial blood gases is important. This test
should be performed in patients with FEV1 < 40% predicted or with clinical signs suggestive of respiratory failure
or right heart failure. Clinical signs of respiratory failure or
right heart failure include central cyanosis, ankle swelling,
and an increase in the jugular venous pressure. Clinical
signs of hypercapnia are extremely nonspecific outside of
acute exacerbations. Respiratory failure is indicated by
PaO2 < 8.0 kPa (60 mm Hg) with or without PaCO2 > 6.0 kPa (45 mm Hg) while breathing air at sea level. Measurement of arterial blood gases should be obtained by arterial
puncture; finger or ear oximeters for assessing SaO2 are less reliable.
5. 1-Antitrypsin deficiency screening. In patients who develop COPD at a young age (< 45 yr) or who have a strong
family history of the disease, it may be valuable to identify
coexisting 1-antitrypsin deficiency. This could lead to family screening and appropriate counseling.
Differential diagnosis. A major differential diagnosis is
asthma. In some patients with chronic asthma, a clear distinction from COPD is not possible using current imaging and
physiologic testing techniques. In these cases, current management is similar to that of asthma. Other potential diagnoses
are usually easier to distinguish from COPD (Table 6).
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Ongoing Monitoring and Assessment
Monitor disease progression and development of complications. COPD is usually a progressive disease, and a patient's lung function can be expected to worsen over time, even with the best available care. Symptoms and objective measures of airflow limitation should be monitored for development of complications and to determine when to adjust therapy.
Follow-up visits should include a discussion of new or worsening symptoms. Spirometry should be performed if there is a substantial increase in symptoms or a complication. Measurement of arterial blood gas tensions should be performed in all patients with an FEV1 < 40% predicted or clinical signs of respiratory failure or right heart failure. Elevation of the jugular venous pressure and the presence of pitting ankle edema are often the most useful findings suggestive of right heart failure in clinical practice. Measurement of pulmonary arterial pressure is not recommended in clinical practice as it does not add practical information beyond that obtained from a knowledge of PaO2.
Monitor pharmacotherapy and other medical treatment. In order to adjust therapy appropriately as the disease progresses, each follow-up visit should include a discussion of the current therapeutic regimen. Dosages of various medications, adherence to the regimen, inhaler technique, effectiveness of the current regime at controlling symptoms, and side effects of treatment should be monitored.
Monitor exacerbation history. Frequency, severity, and likely causes of exacerbations should be evaluated. Increased sputum volume, acutely worsening dyspnea, and the presence of purulent sputum should be noted. Severity can be estimated by the increased need for bronchodilator medication or glucocorticosteroids and by the need for antibiotic treatment. Hospitalizations should be documented, including the facility, duration of stay, and any use of critical care or intubation.
Monitor comorbidities. In treating patients with COPD, it is important to consider the presence of concomitant conditions such as bronchial carcinoma, tuberculosis, sleep apnea, and left heart failure. The appropriate diagnostic tools (chest radiograph, electrocardiogram [ECG], etc.) should be used whenever symptoms (e.g., hemoptysis) suggest one of these conditions.
Component 2: Reduce Risk Factors
Key Points
- Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.
- Smoking cessation is the single most effectiveand cost-effectiveway to reduce the risk of developing COPD and
stop its progression (Evidence A).
- Brief tobacco dependence treatment is effective (Evidence A) and every tobacco user should be offered at least this treatment at every visit to a health care provider.
- Three types of counseling are especially effective: practical counseling, social support as part of treatment, and social support arranged outside of treatment (Evidence A).
- Several effective pharmacotherapies for tobacco dependence are available (Evidence A), and at least one of these medications should be added to counseling if necessary and in the absence of contraindications.
- Progression of many occupationally induced respiratory disorders can be reduced or controlled through a variety of strategies aimed at reducing the burden of inhaled particles and gases (Evidence B).
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cost-effectiveway to reduce the risk of developing COPD
and stop its progression. Even a brief, 3-min period of counseling to urge a smoker to quit can be effective, and at the very
least this should be done for every smoker at every visit (72,
73). Health education, public policy, and information dissemination programs are all vital components in a comprehensive
cessation effort.
Guidelines for smoking cessation. Guidelines for smoking
cessation were published by the U.S. Agency for Health Care
Policy and Research (AHCPR) in 1996 (74) and updated in
2000 by the U.S. Public Health Service in Treating Tobacco
Use and Dependence: A Clinical Practice Guideline (75).
Smoking cessation intervention process. The Public Health
Service Report recommends a five-step program for intervention
(Table 7), which provides a strategic framework helpful to health
care providers interested in helping their patients stop smoking.
Three types of counseling are especially effective: practical counseling, social support as part of treatment, and social support arranged outside of treatment (74) (Evidence A).
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Component 3: Manage Stable COPD
Key Points
- The overall approach to managing stable COPD should be characterized by a stepwise increase in treatment, depending on the severity of the disease.
- For patients with COPD, health education can play a role in improving skills, ability to cope with illness, and health status. It is effective in accomplishing certain goals, including smoking cessation (Evidence A).
- None of the existing medications for COPD has been shown to modify the long-term decline in lung function that is the hallmark of this disease (Evidence A). Therefore, pharmacotherapy for COPD is used to decrease symptoms and complications.
- Bronchodilator medications are central to the symptomatic management of COPD (Evidence A). They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms.
- The principal bronchodilator treatments are
2-agonists, anticholinergics, theophylline, and a combination of one or
more of these drugs (Evidence A).
- Regular treatment with inhaled glucocorticosteroids should only be prescribed for symptomatic patients with COPD with a documented spirometric response to glucocorticosteroids or for those with an FEV1 < 50% predicted and repeated exacerbations requiring treatment with antibiotics or oral glucocorticosteroids (Evidence B).
- Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio (Evidence A).
- All patients with COPD benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A).
- The long-term administration of oxygen (> 15 h per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A).
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2-agonists, anticholinergics, and methylxanthines,
are shown in Table 10. The choice depends on the availability
of the medication and the patient's response. All categories of
bronchodilators have been shown to increase exercise capacity
in COPD, without necessarily producing significant changes in
FEV1 (99) (Evidence A). Regular treatment with short-acting bronchodilators is cheaper but less convenient than
treatment with long-acting bronchodilators. The long-acting,
inhaled 2-agonist salmeterol has been shown to improve
health status significantly in doses of 50 µg twice daily (102)
(Evidence B). Similar data for short-acting 2-agonists are not
available. Use of inhaled ipratropium (an anticholinergic) four
times daily also improves health status (Evidence B) (103). Theophylline is effective in COPD, but because of its potential toxicity, inhaled bronchodilators are preferred when available. All studies that have shown efficacy of theophylline in COPD
were done with slow-release preparations.
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2-agonist and the anticholinergic drug ipratropium in stable COPD produces greater and more sustained improvements in FEV1 than either alone and does not produce
evidence of tachyphylaxis over 90 d of treatment (104)
(Evidence A). Combination of a 2-agonist, an anticholinergic, or theophylline may produce additional improvements
in lung function (104, 107) and health status (101, 104,
107, 110). Increasing the number of drugs usually increases
costs, and an equivalent benefit may occur by increasing the
dose of one bronchodilator when side effects are not a limiting
factor. Detailed assessments of this approach have not been
carried out.
Increasing the dose of either a 2-agonist or an anticholinergic, especially when given by a wet nebulizer, appears to
provide subjective benefit in acute episodes (111) (Evidence
B). Some patients may request regular treatment with high-dose, nebulized bronchodilators (112), especially if they have
experienced subjective benefit from this treatment during an
acute exacerbation. Clear scientific evidence for this approach
is lacking, but one option is to examine the improvement in
mean daily peak expiratory flow (PEF) recording during 2 wk
of treatment in the home and continue with nebulizer therapy
if a significant improvement occurs (112). In general, nebulized therapy for a stable patient is not appropriate unless it
has been shown to be better than conventional dose therapy.
Glucocorticosteroids. Prolonged treatment with inhaled
glucocorticosteroids does not modify the long-term decline in
FEV1 in patients with COPD (91). Regular treatment with
inhaled glucocorticosteroids is only appropriate for symptomatic COPD patients with a documented spirometric response
to inhaled glucocorticosteroids (see Component 1) or in those
with FEV1 < 50% predicted (Stage IIB: Moderate COPD and
Stage III: Severe COPD) and repeated exacerbations requiring treatment with antibiotics or oral glucocorticosteroids (91-
94) (Evidence B). The dose-response relationships and long-term safety of inhaled glucocorticosteroids in COPD are not
known. The present guidelines recommend a trial of 6 wk to
3 mo with inhaled glucocorticosteroids to identify COPD patients who may benefit from long-term inhaled glucocorticosteroid therapy. Many existing COPD guidelines recommend the use of a short course (2 wk) of oral glucocorticosteroids to
identify patients with COPD who might benefit from long-term treatment with oral or inhaled glucocorticosteroids.
There is mounting evidence, however, that a short course of
oral glucocorticosteroids is a poor predictor of the long-term
response to inhaled glucocorticosteroids in COPD (93, 113).
Long-term treatment with oral glucocorticosteroids is not
recommended in COPD (114) (Evidence A). There is no
evidence of long-term benefit from this treatment. Moreover,
a side effect of long-term treatment with systemic glucocorticosteroids is steroid myopathy (115, 116), which contributes to
muscle weakness, decreased functionality, and respiratory failure in patients with advanced COPD.
Other Pharmacologic Treatments
Vaccines. Influenza vaccines can reduce serious illness and death in patients with COPD by approximately 50% (117). Vaccines containing killed or live, inactivated viruses are recommended (118), and should be given once (in autumn) or twice (in autumn and winter) each year (Evidence A). A pneumococcal vaccine containing 23 virulent serotypes has been used but sufficient data to support its general use in COPD patients are lacking (119) (Evidence B).
1-Antitrypsin augmentation therapy. Young patients with
severe hereditary 1-antitrypsin deficiency and established emphysema may be candidates for 1-antitrypsin augmentation
therapy. However, this therapy is very expensive, is not available in most countries, and is not recommended for COPD
that is not related to 1-antitrypsin deficiency (Evidence C).
Antibiotics. The use of antibiotics, other than in treating infectious exacerbations of COPD and other bacterial infections, is not recommended (122, 123) (Evidence A).
Mucolytic (mucokinetic, mucoregulator) agents. (ambroxol, erdosteine, carbocysteine, iodinated glycerol): Although a few patients with viscous sputum may benefit from mucolytics (124, 125), the overall benefits seem to be very small. Therefore, the widespread use of these agents cannot be recommended on the basis of the present evidence (Evidence D).
Antioxidant agents. Antioxidants, in particular N-acetylcysteine, have been shown to reduce the frequency of exacerbations and could have a role in the treatment of patients with recurrent exacerbations (126) (Evidence B). However, before their routine use can be recommended, the results of ongoing trials will have to be carefully evaluated.
Immunoregulators (immunostimulators, immunomodulators). A study using an immunostimulator in COPD showed a decrease in the severity (though not in the frequency) of exacerbations (130), but these results have not been duplicated. Thus, the regular use of this therapy cannot be recommended based on the present evidence (131) (Evidence B).
Antitussives. Cough, although sometimes a troublesome symptom in COPD, has a significant protective role (132). Thus, the regular use of antitussives is contraindicated in stable COPD (Evidence D).
Vasodilators. In patients with stable COPD, inhaled nitric oxide can worsen gas exchange because of altered hypoxic regulation of ventilation-balance (133, 134) and thus is contraindicated.
Respiratory stimulants. The use of doxapram, a nonspecific respiratory stimulant available as an intravenous formulation, is not recommended in stable COPD (Evidence D). Almitrine bismesylate is not recommended for regular use in stable COPD patients (135) (Evidence B).
Narcotics. Narcotics are contraindicated in COPD because of their respiratory depressant effects and potential to worsen hypercapnia. Clinical studies suggest that morphine used to control dyspnea may have serious adverse effects and its benefits may be limited to a few sensitive subjects (138). Codeine and other narcotic analgesics should also be avoided.
Others. Nedocromil, leukotriene modifiers, and alternative healing methods (e.g., herbal medicine, acupuncture, homeopathy) have not been adequately tested in COPD patients and thus cannot be recommended at this time.
Nonpharmacologic Treatment
Rehabilitation. The principal goals of pulmonary rehabilitation are to reduce symptoms, improve quality of life, and increase physical and emotional participation in everyday activities. To accomplish these goals, pulmonary rehabilitation covers a range of nonpulmonary problems, including exercise deconditioning, relative social isolation, altered mood states (especially depression), muscle wasting, and weight loss. Patients with COPD at all stages of disease benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (143) (Evidence A). Data suggest that these benefits can be sustained even after a single pulmonary rehabilitation program (144). Benefits have been reported from rehabilitation programs conducted in inpatient, outpatient, and home settings (147).
Ideally, pulmonary rehabilitation should involve several types of health professionals. A comprehensive pulmonary rehabilitation program includes exercise training, nutrition counseling, and education. Baseline and outcome assessments of each participant in a pulmonary rehabilitation program should be made to quantify individual gains and target areas for improvement and should include:
1. Detailed medical history and physical examination.
2. Measurement of spirometry before and after a bronchodilator drug.
3. Assessment of exercise capacity.
4. Measurement of health status and the impact of breathlessness.
5. Assessment of inspiratory and expiratory muscle strength and lower limb strength (e.g., quadriceps) in patients who suffer from muscle wasting (optional).
The first two assessments are important for establishing entry suitability and baseline status but are not used in outcome assessment. The last three assessments are essential baseline and outcome measures.
Oxygen therapy. The long-term administration of oxygen (> 15 h per day) to patients with chronic respiratory failure has been shown to increase survival (123, 124, 150, 151) (Evidence A). It can also have a beneficial impact on hemodynamics, hematologic characteristics, exercise capacity, lung mechanics, and mental state (152). Long-term oxygen therapy is generally introduced in Stage III: Severe COPD for patients who have: (1) PaO2 at or below 7.3 kPa (55 mm Hg) or SaO2 at or below 88%, with or without hypercapnia; or (2) PaO2 between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg) or SaO2 at or below 89%, if there is evidence of pulmonary hypertension, peripheral edema suggesting congestive heart failure, or polycythemia (hematocrit > 55%).
The goal of long-term oxygen therapy is to increase the baseline PaO2 to at least 8.0 kPa (60 mm Hg) or to produce SaO2 at least 90%, which will preserve vital organ function by ensuring an adequate delivery of oxygen. A decision about the use of long-term oxygen should be based on the waking PaO2 values. The prescription should always include the source of supplemental oxygen (gas or liquid), the method of delivery, duration of use, and the flow rate at rest, during exercise, and during sleep.
Ventilatory support. To date there is no convincing evidence that mechanical ventilatory support has a role in the routine management of stable COPD.
Surgical Treatments
Bullectomy. In carefully selected patients, this procedure is effective in reducing dyspnea and improving lung function (152) (Evidence C). A thoracic CT scan, arterial blood gas measurement, and comprehensive respiratory function tests are essential before making a decision regarding a patient's suitability for resection of a bulla.
Lung volume reduction surgery (LVRS). Although there are some encouraging reports (Evidence C), LVRS is still an unproven palliative surgical procedure (154, 155). Several large randomized studies are now underway to investigate the effectiveness and cost of LVRS in comparison to vigorous conventional therapy (156). Until the results of these studies are known, LVRS cannot be recommended for widespread use.
Lung transplantation. In appropriately selected patients with very advanced COPD, lung transplantation has been shown to improve quality of life and functional capacity (Evidence C) (157). Criteria for referral for lung transplantation include FEV1 < 35% predicted, PaO2 < 7.3 to 8.0 kPa (55 to 60 mm Hg), PaCO2 > 6.7 kPa (50 mm Hg), and secondary pulmonary hypertension (161).
Component 4: Manage Exacerbations
Key Points
- Exacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD.
- The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of approximately one-third of severe exacerbations cannot be identified (Evidence B).
- Inhaled bronchodilators (particularly inhaled 2-agonists or
anticholinergics), theophylline, and systemic, preferably
oral, glucocorticosteroids are effective for treatments for
acute exacerbations of COPD (Evidence A).
- Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased volume and change of color of sputum, or fever) may benefit from antibiotic treatment (Evidence B).
- Noninvasive positive pressure ventilation (NIPPV) in acute exacerbations improves blood gases and pH, reduces in-hospital mortality, decreases the need for invasive mechanical ventilation and intubation, and decreases the length of hospital stay (Evidence A).
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