Management of Stable COPD
Management of Stable COPD
Author: Vincenza Snow, MD, Senior Medical Associate, Scientific Policy, American College of Physicians—American Society of Internal Medicine, Philadelphia, Pa.
Editor’s Note—In the past 3 years, several important new guidelines on the management of chronic obstructive pulmonary disease (COPD) have appeared in the literature. The Veterans Health Administration/ Department of Defense (VHA/DOD) published updated comprehensive guidelines on the management of COPD in 1999.1 In 2001, the World Health Organization/National Heart Lung and Blood Institute (WHO/NHLBI) issued comprehensive guidelines for the management of COPD, also known as the GOLD guidelines.2 Additionally in 2001, the American College of Physicians-American Society of Internal Medicine and the American College of Chest Physicians (ACP-ASIM/ACCP) issued guidelines specifically addressing the management of acute exacerbations of COPD.3,4 This article is the second of 2 covering these latest developments in the management of COPD. The previous one covered the management of acute exacerbations of COPD; this one will cover the management of stable COPD.
Chronic obstructive pulmonary disease affects 16 million adults, accounting annually for 110,000 deaths, more than 16 million office visits, 500,000 hospitalizations, and 18 billion dollars in direct health care costs.4 COPD is the fourth leading cause of death in the United States, and it is estimated that it will be the third leading cause of death worldwide by 2020.5 COPD is a progressive disease and is associated with an abnormal inflammatory response of the lungs. It is characterized by chronic airflow obstruction that is not fully reversible and episodic increases in dyspnea, cough, and sputum production that are commonly called "exacerbations."
General practice for the management of stable COPD encompasses many aspects of care, from counseling for smoking cessation, to multiple inhaled medications, to pulmonary rehabilitation, to surgery. In other words, it is a very complex and multi-tiered strategy. Previous practice in the management of stable COPD was guided by consensus guidelines from the American Thoracic Society and the European Respiratory Society.6,7 However, more evidence has become available since their publication in 1995, and medical groups are moving away from consensus-based guidelines to evidence-based guidelines. The VHA/DOD, ACP-ASIM/ACCP, and GOLD guidelines are examples of such evidence-based efforts.
Introduction/Epidemiology
COPD is characterized by chronic airflow obstruction that is not fully reversible, episodic increases in dyspnea, and cough and sputum production that are commonly called "exacerbations." COPD is a progressive disease and is associated with an abnormal inflammatory response of the lungs.1 The prevalence and mortality from COPD is increasing in most populations8 and it is estimated that by 2020 COPD will become the third leading cause of death all over the world.6 Prevalence and morbidity data probably underestimate the total numbers of affected patients because COPD is usually not diagnosed until it is clinically apparent and more advanced. The same applies to mortality data, in that COPD is less likely to be listed as a cause of death than it is to be listed as a contributing factor.9
Risk factors for COPD include both host factors and environmental exposures, and most likely from an interaction of the two. Known and suspected risk factors for lung function decline and COPD include smoking, occupational exposures, air pollution, airway hyper-responsiveness, and certain genetic variations. The most well-documented genetic variation is a rare hereditary deficiency in a1-antitrypsin. This deficiency leads to premature and accelerated development of panlobular emphysema and decline in lung function, which is further worsened by smoking. Table 1 lists the indications for screening for a-1-antitrypsin deficiency. While most patients who develop COPD are smokers, most smokers do not develop COPD. This supports the theory that the risk for COPD is a combination of interactions between environmental and genetic factors.
| Table 1. | |
| Indications for Screening for a-1-antitrypsin Deficiency (Adapted from ATS, GOLD, VHA) | |
|
|
|
| • | Chronic bronchitis with airflow obstruction in a never smoker |
| • | Bronchiectasis, especially in the absence of clear risk factors for the disease |
| • | Premature onset of COPD with moderate or severe impairment by or before age 50 |
| • | A predominance of basilar emphysema |
| • | Development of unremitting asthma, especially in a person under the age of 50 (screening is indicated even in the presence of atopy) |
| • | A family history of a-1-antitrypsin deficiency or of COPD onset before age 50 |
| • | Cirrhosis without apparent risk factors |
|
|
|
Pathophysiology
COPD is characterized by chronic inflammation throughout the airways, lung parenchyma, and pulmonary vasculature. In addition to inflammation, 2 other processes are thought to be important in the pathogenesis of COPD. It is postulated that these are an imbalance between the normal equilibrium of proteinases and antiproteinases in the lung and oxidative stress. This imbalance of proteinases and antiproteinases can result from genetic factors or the action of inflammatory cells and mediators, and it is thought to be the major contributing mechanism behind emphysematous lung destruction. The inflammation of the lungs is secondary to exposure to inhaled noxious particles and gases. Studies have shown that cigarette smoke can induce inflammation and cause direct damage to the lungs.10,11 While there are no comparable studies demonstrating any link between other kinds of inhaled particles and lung inflammation, it is generally thought that other risk factors initiate a similar inflammatory response.12,13 It is believed that this chronic inflammation leads to COPD.
Pathologic changes characteristic of COPD are found throughout the lung parenchyma and airways, and even in the pulmonary vasculature. In the central airways, inflammatory cells infiltrate the epithelium, mucus-secreting glands are enlarged, and there is an increase in the number of goblet cells. In the peripheral airways, chronic inflammation leads to a vicious circle of injury and repair of the airway wall. As a result of this repair process, there is structural remodeling of the airway wall, with increased collagen content and scar tissue formation leading to narrowing of the lumen and, consequently, fixed airways obstruction.
The characteristic pattern of lung parenchyma destruction in patients with COPD manifests as centrilobular emphysema. These lesions are seen more frequently in the upper lung regions, particularly in milder cases, but in advanced disease they may appear diffusely throughout the entire lung and also involve destruction of the pulmonary capillary bed. The changes in pulmonary vasculature seen in COPD are characterized by thickening of the vessel wall that begins early in the course of the disease. Thickening of the intima is the first structural change followed by an increase in smooth muscle and the infiltration of the vessel wall by inflammatory cells. As is the case in other lung territories, the vicious circle of inflammation causes greater amounts of smooth muscle and collagen to further thicken the wall.
These pathologic changes in the lung lead to the corresponding physiologic changes characteristic of COPD. These include hypersecretion of mucus, ciliary dysfunction, airflow limitation, pulmonary hypertension, and cor pulmonale. Generally, mucus hypersecretion and ciliary dysfunction lead to chronic cough and sputum production. These symptoms are one of the hallmarks of the presentation of COPD and can be present very early on, before other symptoms or respiratory abnormalities develop. Expiratory airflow limitation is primarily caused by fixed airway obstruction, which leads to an increase in airway resistance. Destruction of alveolar attachments, which inhibits the ability of the small airways to maintain patency, plays a smaller role.
As COPD advances, peripheral airways obstruction, parenchymal destruction, and pulmonary vascular abnormalities reduce the lung’s capacity for gas exchange, producing hypoxemia and, ultimately, hypercapnea. Pulmonary hypertension is the major cardiovascular complication of COPD and is associated with the development of cor pulmonale and a poor prognosis.14 It also tends to develop later on in the course of COPD.
Diagnosis and Severity Assessment
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. Currently there is no evidence for screening asymptomatic smokers with office spirometry or peak flow measurements. Table 2 provides some key indicators for considering a diagnosis of COPD (as adapted from GOLD). Table 3 provides a partial differential diagnosis for COPD.
| Table 2. |
| Key Indicators for Considering a Diagnosis of COPD (adapted from GOLD) |
| Chronic cough |
| Present intermittently or every day |
| Often present throughout the day, seldom only nocturnal |
| Chronic sputum production |
| Any pattern of chronic sputum production may indicate COPD |
| Dyspnea |
| That worsens over time (progressive) |
| Is present every day (persistent) |
| Described by the patient as "increased effort to breathe" "heaviness," "air hunger," or "gasping" |
| Worsened on exertion |
| Worse during upper respiratory infections |
| Presence of risk factors |
| Tobacco smoke |
| Occupational dusts and chemicals |
| Smoke from home cooking and heating fuels |
|
|
| Table 3. | |
| Differential Diagnosis of COPD | |
|
|
|
| • | Asthma |
| • | Congestive Heart Failure |
| • | Bronchiectasis |
| • | Tuberculosis |
| • | Obliterative bronchiolitis |
| • | Diffuse panbronchiolitis |
|
|
|
The diagnosis of COPD is confirmed by spirometry, which is the gold standard for measuring airflow obstruction. The presence of a postbronchodilator FEV1 < 80% of predicted value in combination with an FEV1/FVC < 70% confirms the presence of airflow limitation that is not fully reversible. Disease severity has been classified in many ways by different groups (see Tables 4 and 5). The one common measure for all of the severity scales is FEV1. This is because FEV1 is the one measure that has clear prognostic value, while the other measures, particularly symptoms, do not correlate well with prognosis. Most importantly, these systems serve to direct management strategies.
| Table 4. |
| Table 4. GOLD Classification of Severity |
| Stage O: At Risk |
| Normal spirometry |
| Chronic symptoms (cough, sputum production) |
| Stage I: Mild COPD |
| FEV1/FVC < 70% |
| FEV1 > 80% predicted |
| With or without chronic symptoms |
| Stage II: Moderate COPD |
| FEV1/FVC < 70% |
| FEV1< 80% and > 30% predicted |
| IIA is FEV1 < 80% and > 50% predicted |
| IIB is FEV1 < 50% and > 30% predicted |
| With or without chronic symptoms |
| Stage III: Severe COPD |
| FEV1/FVC < 70% |
| FEV1 < 30% predicted or the presence of respiratory failure |
| (PO2< 60 mm Hg and PCO2 > 50 mm Hg on RA) or clinical signs of right heart failure |
|
|
| Table 5. | |||
| Other Available Severity Scales for COPD | |||
| Staging System | Mild | Moderate | Severe |
|
|
|||
| American Thoracic Society | Type 1 | Type 2 | Type 3 |
| FEV1 | > 50% | 35-49% | < 35% |
| British Thoracic Society | |||
| FEV1 | 60-79% | 40-59% | < 40% |
| Cough | "smoker’s cough" | cough w/ or w/o sputum on exertion w/ w/o wheeze | prominent cough on exertion or rest hyperinflation, wheeze, cyanosis, edema |
| Dyspnea | minimal | ||
| Findings on lung exam | normal | ||
| Findings on other examination | normal | normal | |
| European Respiratory Society | > 70% | 50-69% | < 50% |
| FEV1 | |||
|
|
|||
For moderate COPD or beyond, the GOLD and VHA recommend several other diagnostic measures in addition to spirometry. These are: bronchodilator reversibility testing, glucocorticosteroid reversibility testing, chest radiography, and arterial blood gases. Bronchodilator reversibility testing is generally performed once, at the time of diagnosis. It is useful to help rule out a diagnosis of asthma, to estimate a patient’s prognosis, and to direct treatment decisions. However, even patients who do not show a significant FEV1 (ie, spirometric) response to a short-acting bronchodilator test can benefit symptomatically from long-term bronchodilator treatment.
The glucocorticosteroid reversibility test is a simple and relatively safe way to identify patients most likely to respond to long-term glucocorticosteroid treatment. According to GOLD the treatment trial of inhaled glocucorticosteroids should last for 6-12 weeks using as criteria for reversibility an increase in FEV1 of 200 cc or 15% above baseline.15 This effect on FEV1 should be measured as improvement in addition to that of regular treatment with a broncholdilator. According to the VHA, a trial of high-dose inhaled glocucorticosteroids (equivalent of 880 µg or more of fluticasone, or 800 µg or more of budesonide, or 1500 µg of beclomethasone a day) for 14-21 days should be used, or prednisone (40-60 mg/d) for 10-14 days, with pre- and post-treatment spirometry to document an objective improvement in FEV1 of > 20% from baseline.16
Chest radiography is rarely diagnostic for COPD unless there is obvious bullous disease, but its value lies in excluding alternative diagnoses. Other imaging studies such as computed tomography (CT) of the chest, or high-definition CT, are not recommended for diagnostic purposes. If the COPD is moderate or advanced upon diagnosis, then measurement of arterial blood gases (ABG) is important. An ABG should be obtained in patients with an FEV1 < 40% predicted or with clinical signs suggestive of respiratory failure or right heart failure, such as central cyanosis, peripheral edema, and increased central venous pressure. Respiratory failure is defined as PaO2 < 60 mm Hg with or without PaCO2 > 50 mm Hg while breathing room air. Pulse oximetry is not recommended for diagnostic purposes since it is much less reliable.
Management of Stable COPD
General Principles. The overall approach to managing stable COPD should be characterized by a stepwise increase in treatment, depending on the severity of the disease, on an individual patient’s response to various therapies, and on patient’s preferences. Disease severity is determined by the degree of airflow limitation and magnitude of symptoms, as well as other factors, such as the frequency and severity of exacerbations, complications, respiratory failure, comorbidities (cardiovascular disease, sleep-related disorders, etc), and the general health status of the patient.
Although patient education in itself does not improve exercise tolerance or spirometry results, it can play an important role in improving patients’ skills and ability to cope with illness, and their health status. The topics that are recommended by GOLD and VHA for an education program to cover include: smoking cessation, basic information about COPD and pathophysiology of the disease, general approach to the therapy and specific aspects of medical treatment such as use of delivery systems; self-assessment and self-management skills; strategies to help minimize dyspnea such as rehabilitation and environment control; advice about when to seek help; and advance directives and end-of-life issues.
Management of Risk Factors. Smoking cessation results in small improvements in lung function and a slowing of the rate of decline to a rate similar to that seen in patients of the same age who have never smoked. It is the single most important and cost-effective way to reduce the risk of developing COPD and stop its progression. At the very least, every smoker at every visit should be advised to quit. Numerous effective pharmacotherapies for smoking cessation exist now. Except for certain special circumstances, pharmacotherapy is recommended when counseling is not sufficient to help patients quit smoking. The US Public Health Service put out guidelines on smoking cessation strategies in 2000.17
Although it is not known how many individuals are at risk of developing respiratory disease from occupational exposures, 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.18 Persons with severe COPD should monitor public announcements of air quality and should stay indoors when air quality is poor. Air cleaners, be it for use for indoor or outdoor pollutants, have not been shown to have health benefits.
Pharmacologic Treatment
Pharmacologic therapy is used to prevent and control symptoms, reduce the frequency and severity of exacerbations, improve health status, and improve exercise tolerance. None of the existing medications (with the exception of O2) for COPD has been shown to modify the long-term decline in lung function that is the hallmark of this disease. However, this should not preclude efforts to use medications to control symptoms. All medications should be used at the lowest level that satisfactorily relieves symptoms and maximizes activity level. Before escalating therapy, be sure that the patient has been compliant in the use of the medication and has used it properly.
Bronchodilators. Bronchodilator medications are central to the symptomatic management of COPD. They are given either on an as-needed basis for relief of persistent or worsening symptoms, or on a regular basis to prevent or reduce symptoms. When treatment is given by the inhaled route attention to effective drug delivery and training in inhaler technique is essential. The classes of bronchodilators drugs commonly used in treating COPD are: inhaled short-acting and long-acting ß2-agonists, inhaled anticholinergics, and methylxanthines.
Short-acting ß2-agonists can be delivered in several ways: by metered dose inhaler, dry powder inhaler, or by wet nebulization. Studies of inhaled short-acting ß2-agonists in COPD have shown significant improvements in FEV119 and significant decreases in breathlessness.20 For these reasons inhaled short-acting ß2-agonists are the preferred first-line therapy for COPD both in the GOLD and the VHA guidelines. Additionally, a recent Cochrane Review came to the same conclusion.21 It is recommended that the inhaled short-acting ß2-agonists be used for PRN use in most symptomatic patients with mild COPD, with a maximum dose of 12 puffs per day. In moderate to severe COPD, inhaled short-acting ß2-agonists may be used on a regular basis to control symptoms.
Inhaled anticholinergic bronchodilators, such as ipratropium, are available as metered dose inhalers or as wet nebulizations. Ipratropium, like the inhaled short-acting ß2-agonists, increases FEV122 and improves exercise tolerance.23 While it has a slower onset of action, it also has a longer duration of action, thus it is preferred as a maintenance medication. The starting dose of ipratropium should be at least 2 puffs t.i.d., and improvement in pulmonary function is maximal at 6 to 14 puffs as a single dose.24
Combinations of inhaled short-acting ß2-agonists and inhaled anticholinergic bronchodilators are now available. It is recommended that patients with COPD whose symptoms are inadequately controlled with the recommended doses of either an inhaled short-acting ß2-agonist or anticholinergic alone can now be treated with the combination of the 2 agents. Both medications may be also administered in conjunction, but independently, rather than in a prepackaged combination. Regardless of the maintenance therapy, patients should continue to use short-acting ß2-agonists PRN for breakthrough symptoms.
The long-acting ß2-agonist salmeterol has been shown to be effective in COPD, particularly in reducing symptoms of breathlessness and improving quality of life.25 The bronchodilator effect of salmeterol is prolonged and therefore is recommended for control of nocturnal symptoms. Additionally, it may increase compliance due to its less frequent dosing schedule. The GOLD guidelines support its use based on ease of use and the VHA recommends its use only in patients who experience a clear symptomatic benefit from it.
The methylxanthine bronchodilators, such as theophylline, have proven efficacy in COPD, but the risk for potentially serious side effects and their narrow therapeutic window make their use more problematic. As a result, the GOLD and VHA only recommend its use when therapy with the inhaled agents is suboptimal. Both entities also recommend the use of only the sustained release formulations of theophylline, with careful monitoring of serum levels.
Glucocorticosteroids. Prolonged treatment with inhaled or oral corticosteroids does not modify the long-term decline in FEV1 in patients with COPD.26,27 The GOLD guidelines recommend regular treatment with inhaled glucocorticosteroids only for symptomatic COPD patients with a documented spirometric response to inhaled glucocorticosteroids or in those with FEV1 < 50% predicted and repeated exacerbations requiring treatment with antibiotics or oral glucocorticosteroids. The "trial" recommended by GOLD consists of 6 weeks to 3 months of treatment with inhaled glucocorticosteroids, but recommended test doses are not described. The VHA’s recommended "corticosteroid test" uses both inhaled or oral corticosteroids (equivalent of 880 µg or more of fluticasone, or 800 µg or more of budesonide, or 1500 µg of beclomethasone a day for 14-21 days, or prednisone 40-60 mg/d for 10-14 days). GOLD recommends against using oral corticosteroids in testing for response because of mounting evidence that a short course of oral corticosteroids is a poor predictor of the long-term response to inhaled corticosteroids.28,29
Long-term treatment of COPD with oral glucocorticosteroids is not recommended by GOLD based on their determination that the side effects outweighed the benefits.30-32 The VHA guidelines recommend that inhaled steroids be preferred, but they also recommend the use of oral steroids in those patients who show a definite improvement.16,33,34 Adverse effects of oral glocucorticosteroids include: hypertension, hyperglycemia, weight gain, immunosupression, skin thinning, personality changes, purpura, mental status changes, depression, glaucoma, cataracts, and adrenal suppression. COPD patients who may already be on oral steroids should be evaluated for osteoporosis risk and preventive measures should be instituted (ie calcium and vitamin D supplementation, etc).
Tables 6 and 7 detail the step-wise approaches for pharmacotherapy recommended by both GOLD and VHA.
| Table 6. | |||
| Step Care in COPD as Recommended by the VHA Guidelines | |||
| Step | Symptoms and FEV1 | Therapy | |
|
|
|||
| 1 | Asymptomatic and FEV1 > 50% of predicted | Smoking cessation, vaccination, education | |
| 2a | Symptoms less than daily and FEV1 > 50% of predicted | Smoking cessation, vaccination, education. Inhaled short-acting ß2-agonist (2 puffs PRN up to 12 puffs a day) | |
| 2b | Asymptomatic and FEV1 < 50% of predicted | Smoking cessation, vaccination, education. Inhaled anticholinergic (2 puffs q.i.d.). Consider use of inhaler containing both a short-acting ß2-agonist and an anticholinergic. | |
| 2c | Symptoms less than daily and FEV1 < 50% of predicted OR daily symptoms | Smoking cessation, vaccination, education. Inhaled anticholinergic (2 puffs q.i.d.). Inhaled short-acting beta2-agonist (2 puffs PRN up to 12 puffs a day). Consider use of inhaler containing both a short-acting ß2-agonist and an anticholinergic. | |
| 3 | Symptoms not controlled | Increase dose of both: Inhaled anticholinergic (2-6 puffs q.i.d.) and inhaled short-acting ß2-agonist (2-4 puffs PRN up to 12 puffs per day) | |
| 4 | Symptoms still not controlled | Consider adding long-acting inhaled ß2-agonist * | |
| 5 | Symptoms still not controlled | Consider a theophylline trial (slow release theophylline adjusted to serum levels of 5-12 µg/mL).** | |
| 6 | Symptoms still not controlled | Consider a corticosteroid trial.*** Consider consultation by specialist | |
| 7 | Symptoms not controlled | Refer to specialist | |
|
|
|||
| * Inhaled long-acting ß2-agonists are not to be used for rescue therapy. Nighttime symptoms are frequently better controlled with long-acting ß2-agonists. | |||
| **Theophylline should be used with caution because of potential severe side effects and its narrow therapeutic window. Theophylline should be discontinued if no benefits in symptoms or other objective measures are not evident within several weeks. | |||
| ***Recommended corticosteroids trials vary from one organization to another. | |||
|
|
|||
| Table 7. | |
| Step Care Recommendations Adapted from GOLD | |
| Stage | Recommended Therapies |
|
|
|
| I | Short-acting bronchodilators when needed |
| IIA | Regular treatment with one or more bronchodilators |
| Rehabilitation | |
| Inhaled glucocorticosteroids if significant response on trial | |
| IIB | Regular treatment with one or more bronchodilators |
| Rehabilitation | |
| Inhaled glucocorticosteroids if significant response on trial or if repeated exacerbations | |
| III | Regular treatment with one or more bronchodilators |
| Inhaled glucocorticosteroids if significant response on trial or if repeated exacerbations | |
| Treatment of complications | |
| Rehabilitation | |
| Long-term oxygen therapy if indicated (respiratory failure) | |
| Consider surgical treatments | |
| ALL | Avoidance of risk factors, influenza vaccination |
|
|
|
Other Pharmacological Agents
Antibiotics
• There is no evidence for the use of antibiotics in stable COPD.
Mucolytics
• While not recommended by GOLD nor VHA, a recent Cochrane review concluded that treatment with mucolytics produced a small reduction in exacerbations and a somewhat greater reduction in the total number of days of disability in a population of patients with chronic bronchitis and/or COPD.35 But, it is not clear whether that benefit is large enough to justify the regular use of mucolytics in all patients with COPD.
Antitussives
• Antitussives should not be used in stable COPD, since cough serves a protective role.
Respiratory Stimulants
• The use of agents such as doxapram and almitrine bismesylate is not recommended in stable COPD.
Narcotics
• Narcotics are contraindicated in COPD due to their respiratory depressant effects and potential to worsen hypercapnea.
Others
• Nedocromil, leucotriene inhibitors, and alternative medicines, such as herbals or acupuncture, have not been adequately studied and tested in COPD patients and are currently not recommended by GOLD or VHA.
Nonpharmacological Treatment
Vaccines. Influenza vaccines can reduce serious illness and exacerbations in patients with COPD and is recommended by both the GOLD and VHA. Vaccines containing killed or live, inactivated viruses are recommended once yearly in the Fall. A pneumococcal vaccine containing the 23 virulent serotypes does not have enough evidence to support its general use in COPD patients and is not included in the recommendations by the GOLD or VHA.
Rehabilitation. The principle goals of pulmonary rehabilitation are to reduce symptoms, improve quality of life, and increase physical activity and exercise tolerance in order to preserve functionality in everyday activities. To accomplish these goals, pulmonary rehabilitation covers a range of non-pulmonary problems, including physical deconditioning, social isolation, and mood alterations, particularly depression. 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.36,37
Oxygen Therapy. The long-term administration of oxygen (>15 h/d) to patients with chronic respiratory failure has been shown to increase survival.38 Long-term oxygen therapy is indicated for patients with COPD who on room-air ABG show: 1) PaO2 at or below 55 mm Hg or SaO2 at or below 88% with or without hypercapnea; or 2) PaO2 between 55 mm Hg and 60 mm Hg or SaO2 at or below 89%, if there is evidence of pulmonary hypertension, peripheral edema suggestive of congestive heart failure, or polycythemia (Hct > 55%). The goal of long-term oxygen therapy is to increase the baseline PaO2 to at least 60 mm Hg or to reach SaO2 of at least 90%. The prescription should always include the source of the supplemental oxygen (gas or liquid), the method of delivery, duration of use, and the flow rate at rest, during exercise, and during sleep. A decision about the use of long-term oxygen should be based on the waking PaO2 values.
Ventilatory Support. To date there is no convincing evidence that mechanical ventilatory support has a role in the routine management of stable COPD and is not recommended for general use by the GOLD or VHA.
Surgical Treatments
Bullectomy
• In carefully selected patients, this procedure is effective in reducing dyspnea and improving lung function, but more studies are needed before it can be recommended on a widespread basis.
Lung Volume Reduction Surgery
• Although there are some encouraging reports, LVRS is still an unproven palliative surgical procedure, and is not recommended by the GOLD or VHA for widespread use.
Disclaimer
The recommendations in this paper reflect the author’s summary of the guidelines and works of others and in no way reflect the policy or views of the American College of Physicians—American Society of Internal Medicine
References
1. The Chronic Obstructive Pulmonary Disease Workgroup: Veterans Health Administration/Department of Defense. Clinical practice guidelines for the management of chronic obstructive pulmonary disease. August 1999. Version 1.1a. www.humanitas.com/vha. Accessed December 1, 2001.
2. Pauwels RA, et al. Global strategy for the diagnosis, management, and prevention of COPD. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop Report. Am J Respir Crit Care Med. 2001;163:1256-1276. www.goldcopd.com. Accessed December 1, 2001.
3. Snow V, Lascher S, Mottur-Pilson C. Evidence base for the management of acute exacerbations of chronic obstructive pulmonary disease. Clinical practice guideline, part 1. Ann Intern Med. 2001;134:595-599.
4. Bach PB, et al. Management of acute exacerbations of chronic obstructive pulmonary disease: A summary and appraisal of published evidence. Ann Intern Med. 2001;143:600-620.
5. Viegi G, et al. Epidemiology of chronic obstructive pulmonary disease (COPD). Respiration. 2001;68(1):4-19.
6. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;152:S77-S121.
7. Siafakas NM, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The European Respiratory Society Task Force. Eur Respir J. 1995;8(8): 1398-1420.
8. Chen JC, Mannino DM. Worldwide epidemiology of chronic obstructive pulmonary disease. Curr Opin Pulm Med. 1999; 5(2):93-99.
9. Mannino DM, et al. Obstructive lung disease deaths in the United States from 1979 through 1993: An analysis using multiple-cause mortality data. Am J Respir Crit Care Med. 1997;156: 814-818.
10. Niewoehner DE, et al. Pathologic changes in the peripheral airways of young cigarette smokers. N Engl J Med. 1974;291: 755-758.
11. Hunninghake GW, Crystal RG. Cigarette smoking and lung destruction: accumulation of neutrophils in the lungs of cigarette smokers. Am Rev Respir Dis. 1983;128:833-838.
12. Salvi S, et al. Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers. Am J Respir Crit Care Med. 1999; 159:702-709.
13. VonEssen SG, et al. Neutrophilic respiratory tract inflammation and peripheral blood neutrophilia after grain sorghum dust extract challenge. Chest. 1995;108:1425-1433.
14. McNee W. Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease. Part two. Am J Respir Crit Care Med. 1994;150:1158-1168.
15. American Thoracic Society. Lung function testing: selection of reference values and interpretive strategies. Am Rev Respir Dis. 1991;144:1202-1218.
16. Callahan CM, Dittus RS, Katz BP. Oral corticosteroids for patients with stable chronic obstructive pulmonary disease. Ann Intern Med. 1991;114:216-223.
17. The tobacco use and dependence clinical practice guideline panel, staff, and consortium representatives. A clinical practice guideline for treating tobacco use and dependence. JAMA. 2000; 28:3244-3254.
18. The COPD Guidelines Group of the Standards of Care Committee of the BTS. BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax. 1997;52(suppl 5):S1-S28.
19. Vathnen AS, et al. High-dose inhaled albuterol in severe chronic airflow limitation. Am Rev Respir Dis. 1988;138(4):850-855.
20. Belman MJ, et al. Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1996;153(3): 967-975.
21. Sestini P, et al. Short-acting beta 2 agonists for stable chronic obstructive pulmonary disease (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford: Update Software.
22. Rennard SI, et al. Extended therapy with ipratropium is associated with improved lung function in patients with COPD. A retrospective analysis of data from seven clinical trials. Chest. 1996; 110(1):62-70.
23. Blosser SA, et al. Is an anticholinergic agent superior to a beta-2 agonist in improving dyspnea and exercise limitation in COPD? Chest. 1995;108:730-735.
24. Ikeda A, et al. Comparative dose-response study of three anticholinergic agents and fenoterol using a metered dose inhaler in patients with chronic obstructive pulmonary disease. Thorax. 1995;50(1):62-66.
25. Appleton S, et al. Long-acting beta-2 agonists for chronic obstructive pulmonary disease (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford: Update Software.
26. Pauwels RA, et al. Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. European Respiratory Society Study on Chronic Obstructive Pulmonary Disease. N Engl J Med. 1999; 340:1948-1953.
27. The Lung Health Study Research Group. Effects of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med. 2000;343: 1902-1909.
28. Burge PS, et al. Randomized, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ. 2000;320:1297-1303.
29. Senderovitz T, et al. Steroid reversibility test followed by inhaled budesonide or placebo in outpatients with stable chronic obstructive pulmonary disease. The Danish Society of Respiratory Medicine. Respir Med. 1999;93:715-718.
30. Rice KL, et al. Withdrawal of chronic systemic corticosteroids in patients with COPD: a randomized trial. Am J Respir Crit Care Med. 2000;162:174-178.
31. Decramer M, et al. Corticosteroids contribute to muscle weakness in chronic airflow obstruction. Am J Respir Crit Care Med. 1994; 150:11-16.
32. Decramer M, Sias KJ. Corticosteroid induced myopathy involving respiratory muscles in patients with chronic obstructive pulmonary disease or asthma. Am Rev Respir Dis. 1992;146: 800-802.
33. Weir DC. Response to corticosteroids in chronic airflow obstruction: relationship to emphysema and airways collapse. Eur Respir J. 1991;4(10):1185-1190.
34. Weir DC. Corticosteroid trials in nonasthmatic chronic airflow obstruction: a comparison of oral prednisolone and inhaled beclomethasone diproprionate. Thorax. 1990;45(2):112-117.
35. Poole PJ, Balck PN. Mucolytic agents for chronic bronchitis (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford: Update Software.
36. Berry MJ, et al. Exercise rehabilitation and chronic obstructive pulmonary disease stage. Am J Respir Crit Care Med. 1999;160: 1248-1253.
37. Lacasse Y, et al. Meta-analysis of respiratory rehabilitation in chronic obstructive pulmonary disease. Lancet. 1996;348: 1115-1119.
38. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: A clinical trial. Ann Intern Med. 1980;93:391-398.
Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.