Amir Qaseem, MD, PhD, MHA; Vincenza Snow, MD; Paul Shekelle, MD, PhD; Katherine Sherif, MD; Timothy J. Wilt, MD, MPH; Steven Weinberger, MD; Douglas K. Owens, MD, MS; Clinical Efficacy Assessment Subcommittee of the American College of Physicians*
Note: Clinical practice guidelines are guides only and may not apply to all patients and all clinical situations. Thus, they are not intended to override clinicians' judgment. All ACP clinical practice guidelines are considered automatically withdrawn or invalid 5 years after publication or once an update has been issued.
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Grant Support: Financial support for the development of this guideline comes exclusively from the ACP operating budget.
Potential Financial Conflicts of Interest: Stock ownership or options (other than mutual funds): S. Weinberger (GlaxoSmithKline). Grants received: V. Snow (Centers for Disease Control and Prevention, Agency for Healthcare Research and Quality, Novo Nordisk, Pfizer Inc., Merck & Co. Inc., Bristol-Myers Squibb, Atlantic Philanthropies, Sanofi Pasteur).
Requests for Single Reprints: Amir Qaseem, MD, PhD, MHA, American College of Physicians, 190. N. Independence Mall West, Philadelphia, PA 19106; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. Qaseem, Snow, and Weinberger: 190 N. Independence Mall West, Philadelphia, PA 19106.
Dr. Shekelle: 1776 Main Street, Santa Monica, CA 90401.
Dr. Sherif: 219 North Broad Street, 6th Floor, Philadelphia, PA 19107.
Dr. Wilt: 1 Veterans Drive (111-0), Minneapolis, MN 55417.
Dr. Owens: 117 Encina Commons, Stanford, CA 94305.
Qaseem A., Snow V., Shekelle P., Sherif K., Wilt T., Weinberger S., Owens D., ; Diagnosis and Management of Stable Chronic Obstructive Pulmonary Disease: A Clinical Practice Guideline from the American College of Physicians. Ann Intern Med. 2007;147:633-638. doi: 10.7326/0003-4819-147-9-200711060-00008
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Published: Ann Intern Med. 2007;147(9):633-638.
In patients with respiratory symptoms, particularly dyspnea, spirometry should be performed to diagnose airflow obstruction. Spirometry should not be used to screen for airflow obstruction in asymptomatic individuals. (Grade: strong recommendation, moderate-quality evidence.)
Treatment for stable chronic obstructive pulmonary disease (COPD) should be reserved for patients who have respiratory symptoms and FEV1 less than 60% predicted, as documented by spirometry. (Grade: strong recommendation, moderate-quality evidence.)
Clinicians should prescribe 1 of the following maintenance monotherapies for symptomatic patients with COPD and FEV1 less than 60% predicted: long-acting inhaled Î²-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids. (Grade: strong recommendation, high-quality evidence.)
Clinicians may consider combination inhaled therapies for symptomatic patients with COPD and FEV1 less than 60% predicted. (Grade: weak recommendation, moderate-quality evidence.)
Clinicians should prescribe oxygen therapy in patients with COPD and resting hypoxemia (Pao2 â‰¤55 mm Hg). (Grade: strong recommendation, moderate-quality evidence.)
Clinicians should consider prescribing pulmonary rehabilitation in symptomatic individuals with COPD who have an FEV1 less than 50% predicted. (Grade: weak recommendation, moderate-quality evidence.)
*This paper, written by Amir Qaseem, MD, PhD, MHA; Vincenza Snow, MD; Paul Shekelle, MD, PhD; Katherine Sherif, MD; Timothy J. Wilt, MD, MPH; Steven Weinberger, MD; and Douglas K. Owens, MD, MS, was developed for the Clinical Efficacy Assessment Subcommittee of the American College of Physicians (ACP): Douglas K. Owens, MD, MS (Chair); Donald E. Casey Jr., MD, MPH, MBA; J. Thomas Cross Jr., MD, MPH; Paul Dallas, MD; Nancy C. Dolan, MD; Mary Ann Forciea, MD; Lakshmi Halasyamani, MD; Robert H. Hopkins Jr., MD; and Paul Shekelle, MD, PhD. Approved by the ACP Board of Regents on 14 July 2007.
Chronic obstructive pulmonary disease (COPD) is a slowly progressive lung disease involving the airways and/or pulmonary parenchyma, resulting in a gradual loss of lung function. The symptoms of COPD range from chronic cough, sputum production, and wheezing to more severe symptoms, such as dyspnea, poor exercise tolerance, and signs or symptoms of right-sided heart failure. In the United States, COPD affects more than 5% of the adult population and is the 4th leading cause of death and the 12th leading cause of morbidity (1, 2).
The purpose of this guideline is to present the available evidence on the diagnosis and management of COPD. The target audience for this guideline is all physicians, and the target patient population is all adults with COPD. These recommendations are based on the systematic evidence review in this issue by Wilt and colleagues (3) and the Agency for Healthcare Research and Quality–sponsored Minnesota Evidence-based Practice Center evidence report (4).
The literature search included studies from MEDLINE and the Cochrane database from 1966 to May 2005 (4). In addition, searches for oxygen, inhaled therapies, and disease management were updated through March 2007. The exclusion criteria were children or individuals with asthma, restrictive lung disease, or α1-antitrypsin deficiency. The methods of Schulz and colleagues (5) were used to assess the quality of randomized, controlled trials. Results from the individual studies were aggregated to produce pooled estimates. Heterogeneity was assessed by using the chi-square and I2 tests (6), and the DerSimonian–Laird random-effects model was used (7). Details about the methods used for the systematic evidence review may be found in detail in the background paper by Wilt and colleagues in this issue (3).
This guideline grades the evidence and recommendations by using the American College of Physicians' clinical practice guidelines grading system adopted from the classification developed by the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) workgroup (Table 1).
The objective of this guideline is to analyze the evidence for the following questions:
1. What is the value of clinical examination for prediction of airflow obstruction (AO)?
2. What is the incremental value of spirometry for case finding and diagnosis of adults who are COPD treatment candidates?
3. What management strategies are effective for the treatment for COPD (inhaled therapies, pulmonary rehabilitation programs, and supplemental long-term oxygen therapy)?
The National Health and Nutrition Examination Survey III and a systematic review of 19 studies examining the accuracy of clinical examination to predict AO were used to estimate the prevalence of COPD and AO and clinical diagnostic accuracy (8, 9). Cigarette smoking is the most common cause of COPD. A 70–pack-year history of smoking was the best predictor of AO, with a positive likelihood ratio of 8.0 but a sensitivity of only 40%. The literature showed that findings from physical examination also had high specificity (>90%) but poor sensitivity. In addition, sputum production or wheezing was also associated with an increased likelihood of AO. Evidence to assess the utility of combining items that were included in a clinical examination to predict AO showed that combinations of findings were more helpful for diagnosing the presence of AO (10–15). The best combination to exclude COPD included never having smoked, no reported wheezing, and no wheezing on examination. A patient with any combination of 2 findings (≥70–pack-year history of smoking, history of COPD, or decreased breath sounds) can be considered likely to have AO (defined as FEV1 less than 60% predicted or FEV1–FVC ratio less than 0.60) (positive likelihood ratio, 34) (9–15).
Spirometry may be useful to identify patients who may benefit from initiating therapy (Table 2). The evidence supports inhaled treatment in patients who have symptoms and FEV1 less than 60% predicted. The literature also showed that respiratory symptom status is not a reliable indicator of the presence of AO. However, as spirometric values worsened, individuals reported more respiratory symptoms, such as cough, sputum, wheezing, or dyspnea. But 33% of individuals with normal spirometric values reported respiratory symptoms. In addition, 21% of individuals who had severe to very severe AO by spirometry reported no symptoms. Nearly 80% of persons reporting any respiratory symptom had normal airflow, and only 3% to 4% had severe to very severe AO (8).
Evidence is insufficient to support widespread use of spirometry for testing adults with no respiratory symptoms, including those with current and past exposure to COPD risk factors. Spirometry may be beneficial in symptomatic adults who have an FEV1 greater than 60% predicted for determining when to initiate therapy. The evidence does not support periodic spirometry after initiation of therapy to monitor ongoing disease status or to modify therapy. Furthermore, no high-quality evidence supports the use of obtaining and providing spirometry results to improve smoking cessation, identify and treat asymptomatic individuals to prevent future respiratory symptoms, or reduce spirometric decline in lung function.
The literature showed that monotherapy with long-acting inhaled β-agonists, a long-acting inhaled anticholinergic, or inhaled corticosteroids was superior to placebo or short-acting anticholinergics in reducing exacerbations. Tiotropium (relative risk, 0.84 [95% CI, 0.78 to 0.90]), long-acting β-agonists (relative risk, 0.87 [CI, 0.82 to 0.93]), and corticosteroids (relative risk, 0.85 [CI, 0.75 to 0.96]) reduce the relative risk for at least 1 exacerbation compared with placebo. However, ipratropium, a short-acting anticholinergic, was not superior to placebo (relative risk, 0.95 [CI, 0.78 to 1.15]). In comparison studies, long-acting β-agonists were as effective as ipratropium (relative risk, 0.89 [CI, 0.72 to 1.10]), corticosteroids (relative risk, 1.06 [CI, 0.84 to 1.34]), or a long-acting anticholinergic (tiotropium) (relative risk, 1.11 [CI, 0.93 to 1.33]). Also, long-acting β-agonists were slightly superior to dual D2 dopamine receptor–β2-agonist (sibenadet) (relative risk, 0.80 [CI, 0.63 to 1.02]), and tiotropium was more effective than ipratropium (relative risk, 0.77 [CI, 0.62 to 0.95]). Compared with tiotropium alone, the combination of tiotropium with a long-acting β-agonist and inhaled corticosteroid has been shown to improve respiratory symptoms related to quality of life and lung function (16). Patients treated with tiotropium plus a long-acting β-agonist and inhaled corticosteroid had an increase of greater than 4 points on the St. George Respiratory Questionnaire, which is considered to be clinically significant (16).
Evidence comparing the combination of inhaled corticosteroids and long-acting β-agonists with either monotherapy or placebo was evaluated in 5 multigroup studies that lasted from 6 to 23 months in patients with a mean baseline FEV1 less than 50% predicted (17–21). Combination therapy with long-acting β-agonists and inhaled corticosteroids showed an absolute risk decrease in the percentage of individuals with at least 1 exacerbation compared with placebo. The combination of long-acting β-agonists and corticosteroid therapy did not reduce the percentage of individuals with at least 1 exacerbation compared with inhaled corticosteroid monotherapy (17, 18, 20, 21). However, adding an inhaled corticosteroid to a long-acting β-agonist may reduce exacerbations compared with long-acting β-agonist monotherapy (3). The combination of a short-acting β-agonist (albuterol) and ipratropium reduced exacerbations compared with albuterol alone (22–24).
Use of tiotropium (absolute risk difference, −2% [CI, −4% to −1%) (25–28) and ipratropium (absolute risk difference, −4% [CI, −10% to 1%]) reduced hospitalizations for patients with COPD (29). However, the Lung Health Study I and II trials showed no significant difference in hospitalizations per 100 person-years of exposure between ipratropium and placebo or between inhaled corticosteroids and placebo (30, 31). The TORCH (Towards a Revolution in COPD Health) study (32) showed that use of a combination of a long-acting β-agonist and an inhaled corticosteroid reduces deaths compared with use of an inhaled corticosteroid alone (relative risk, 0.79 [CI, 0.67 to 0.94]). Results from a meta-analysis by Salpeter and colleagues (33) showed an increase in respiratory deaths with long-acting β-agonists and a decrease with anticholinergics. However, a recently released TORCH study found no difference in deaths due to pulmonary causes between placebo and salmeterol (34). In addition, serious adverse effects occurred in 10% of the persons receiving inhaled corticosteroids as monotherapy or combination therapy compared with 6% of persons receiving placebo or long-acting β-agonists (34).
Evidence for withdrawals from treatment and nonadherence showed that individuals using long-acting β-agonists, tiotropium, or inhaled corticosteroids were less likely to withdraw from treatment for any reason compared with those receiving placebo (17, 18, 21, 26, 27, 29, 35, 36). In trials of combination therapy with corticosteroids and long-acting β-agonists, withdrawals were lower for combination therapy than for placebo but were similar to either type of monotherapy (17, 18, 21, 26, 27, 29, 35, 36). Adverse events during follow-up also were minor and were similar to those with placebo. The main adverse reactions included oropharyngeal candidiasis and a moderate to severe degree of easy bruising with inhaled corticosteroids (18, 37, 38), dry mouth with tiotropium (39), and minor cardiovascular events with β-agonists (40). Results from 2 randomized, controlled trials (37, 38) showed that the incidence of fracture during 3 years was similar with inhaled corticosteroids and with placebo (1.4% vs. 2.0%, respectively). However, after 3 years, lumbar spine and femur bone density was lower in the triamcinolone group of the Lung Health Study II (31).
The evidence is not sufficient to evaluate the effectiveness of long-acting β-agonists in symptomatic individuals with FEV1 greater than 50% predicted or in asymptomatic individuals regardless of spirometric values. Evidence on other inhaled therapies used for at least 1 year found little or no improvement in respiratory outcomes or deaths among individuals with mild or moderate AO or in those with normal airflow but chronic sputum production (18, 30, 31, 41, 42). Modifying existing therapy for COPD or monitoring disease status according to spirometric values was not evaluated in trials.
The main components of most pulmonary rehabilitation programs included endurance or exercise training, education, behavioral modification, and outcome assessment. Three studies found clinically significant improvement in dyspnea and fatigue (43–45). Pulmonary rehabilitation did not result in reduction in deaths, but the studies had small sample sizes and short durations (46). A review of 6 small RCTs in patients with baseline FEV1 less than 40% predicted showed a reduction in hospitalizations and clinically significant improvement in health status and exercise capacity (47).
The evidence did not show any effect of disease management programs or patient education on deaths, COPD exacerbations, reduction in all-cause readmissions, hospital length of stay, visits to primary care physicians, clinically meaningful improvement in the St. George Respiratory Questionnaire health status score, patient satisfaction, self-management skills, or adherence to treatment (46, 48).
Two trials showed that supplemental oxygen used 15 or more hours daily to maintain a Pao2 greater than 60 mm Hg reduced deaths in individuals who have very severe AO (FEV1 <30% predicted) and resting hypoxemia (mean resting Pao2 ≤55 mm Hg) (49, 50). Two other studies showed no effect on relative risk for death with use of supplemental oxygen (9 to 13 hours daily) during the day or at night in patients with similar severity of AO but with daytime Pao2 greater than 60 mm Hg (51, 52). In addition, studies showed no effect of ambulatory oxygen on respiratory health status measures (53, 54).
History and clinical examination are poor predictors of AO and its severity. Evidence does not support using spirometry as a diagnostic strategy for individuals not reporting respiratory symptoms. However, adding spirometry to clinical examination for individuals with respiratory symptoms, especially dyspnea, has demonstrated benefits. Treatment benefits for COPD are primarily related to reduced exacerbations among patients who are more likely to have exacerbations, dyspnea that limits activity, or severe to very severe AO. Inhaled corticosteroids and long-acting bronchodilators are more effective in reducing exacerbations than are short-acting inhalers. The reduction in deaths is associated with the use of long-term supplemental oxygen therapy for patients with very severe AO and resting hypoxemia.
Recommendation 1: In patients with respiratory symptoms, particularly dyspnea, spirometry should be performed to diagnose airflow obstruction. Spirometry should not be used to screen for airflow obstruction in asymptomatic individuals. (Grade: strong recommendation, moderate-quality evidence.)
Targeted use of spirometry for diagnosis of AO is beneficial for individuals with respiratory symptoms, particularly dyspnea. Evidence does not support the use of spirometry to screen for AO in asymptomatic individuals, including those who have risk factors for COPD. No high-quality evidence supports obtaining and providing spirometry results to improve smoking cessation, or to identify and treat asymptomatic individuals to prevent future respiratory symptoms or reduce spirometric decline in lung function.
Recommendation 2: Treatment for stable COPD should be reserved for patients who have respiratory symptoms and FEV1 less than 60% predicted as documented by spirometry. (Grade: strong recommendation, moderate-quality evidence.)
Evidence shows that individuals who will benefit the most from therapy are those who have respiratory symptoms and clinically significant AO (FEV1 <60% predicted). No evidence supports treating asymptomatic patients, because treatment does not improve outcomes. The evidence does not support periodic spirometry after initiation of therapy to monitor ongoing disease status or to modify therapy. This recommendation does not address the occasional use of bronchodilators for acute symptomatic relief.
Recommendation 3: Clinicians should prescribe 1 of the following maintenance monotherapies for symptomatic patients with COPD and FEV1 less than 60% predicted: long-acting inhaled β-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids. (Grade: strong recommendation, high-quality evidence.)
Monotherapy with a long-acting inhaled β-agonist, a long-acting inhaled anticholinergic, or an inhaled corticosteroid is beneficial in reducing exacerbations. Inhaled corticosteroids and long-acting inhaled bronchodilators have similar effectiveness but differ in adverse effects, reductions in deaths, and hospitalizations. The review did not systematically evaluate all other outcomes. Evidence is insufficient to recommend 1 monotherapy over another.
Recommendation 4: Clinicians may consider combination inhaled therapies for symptomatic patients with COPD and FEV1 less than 60% predicted. (Grade: weak recommendation, moderate-quality evidence.)
When to use combination therapy instead of monotherapy has not been clearly established. In the TORCH trial (32), combination therapy with long-acting β-agonists and corticosteroids reduced exacerbations more than did monotherapy. Although deaths with combination therapy decreased in the trial compared with monotherapy, the reduction did not reach the predetermined level of statistical significance. In a recent randomized trial (16), addition of salmeterol–fluticasone to tiotropium therapy did not statistically influence rates of COPD exacerbation but did improve lung function, quality of life, and hospitalization rates in patients with moderate to severe COPD. However, studies of combination therapies do not consistently demonstrate benefits of combination therapy over monotherapy.
Recommendation 5: Clinicians should prescribe oxygen therapy in patients with COPD and resting hypoxemia (Pao2 ≤55 mm Hg). (Grade: strong recommendation, moderate-quality evidence.)
Use of supplemental oxygen for 15 or more hours daily can help improve survival in patients with severe AO (FEV1 <30% predicted) and resting hypoxemia.
Recommendation 6: Clinicians should consider prescribing pulmonary rehabilitation in symptomatic individuals with COPD who have an FEV1 less than 50% predicted. (Grade: weak recommendation, moderate-quality evidence.)
Evidence supports the use of pulmonary rehabilitation programs for patients with severe AO, because they reduce hospitalizations and improve health status and exercise capacity. However, the evidence is not clear for individuals with FEV1 greater than 50% predicted.
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Video News Release - New Guidelines for Diagnosis and Treatment of Stable Chronic Obstructive Pulmonary Disease
Emmanuel M Bhaskar
Sri Ramachandra Medical College and Research Institute,Porur,Chennai-600116,India
November 5, 2007
Effectiveness of Immunization for patients with Chronic Obstructive Pulmonary Disease
To the Editor,
The guideline on diagnosis and management of stable chronic obstructive pulmonary disease [COPD] by Qaseem and colleagues is commendable (1).However a recommendation on immunization for patients suffering from COPD is strikingly absent.It is possible that the guideline was not meant to address this issue. But the third objective of this guideline ," What management strategies are effective for the treatment for COPD ", should include immunization for influenza and pneumococcal infection , the former being an important cause for morbidity and mortality among patients suffering from COPD (2,3). Adult immunization strategies are an important need of the hour(4).
Here, I wish to summarize two Cochrane systematic reviews on effectiveness of immunization among COPD patients.
Poole et al (5) in their review on influenza vaccine for COPD patients analysed six randomized controlled trials [RCTs] and observed a significant reduction in total number of exacerbations per vaccinated subject compared to patients who received placebo ( Weighted mean difference[WMD] -0.37 , 95% confidence interval -0.64 to -0.11 , p=0.006 ). This favourable effect was observed three to four weeks after the administration of vaccine. There was a mild and transient increase in the occurrence of local adverse reactions due to vaccine , but they are outweighed by the long term benefits of vaccination. Addition of intranasal live attenuated virus to the inactivated vaccine was of no added benefit. Further the sample size of the studies were too small to detect any effect on mortality.
Granger et al (6) in their review on injectable vaccines for preventing pneumococcal infection in patients with COPD analyzed four RCTs for outcomes like acute exacerbation, development of pneumonia,rates of hospital admissions and emergency department visits. However, a major disadvantage of this review was that only three studies had some data on outcome variables and based on that,pneumococcal vaccination had no favourable effect on patients with COPD. The authors conclude saying that there is no evidence from RCTs that pneumococcal vaccines have a significant impact on morbidity or mortality among patients with COPD. However the conclusion should be interpreted with caution , since there is absence of evidence with respect to favourable effect of pneumococcal vaccination in patients with COPD and not evidence of absence for the same.
To conclude, evidence at this point of time suggests that inactivated influenza vaccination for patients with COPD is probably beneficial and efficacy of pneumococcal vaccination for COPD patients in reducing morbidity and mortality needs further studies.
1.Amir Qaseem, Vincenza Snow, Paul Shekelle, Katherine Sherif, Timothy J. Wilt,Steven Weinberger, Douglas K. Owens, et al. Diagnosis and Management of Stable Chronic Obstructive Pulmonary Disease: A Clinical Practice Guideline from the American College of Physicians . Ann Intern Med. 2007;147:633-638.
2.Nichol KL, Baken L, Nelson A. Relation between influenza vaccination and outpatient visits, hospitalization, and mortality in elderly persons with chronic lung disease.
Ann Intern Med 1999; 130:397"“403
3.Rothbart PH, Kempen BM, Sprenger MJW. Sense and nonsense of influenza vaccination in asthma and chronic obstructive pulmonary disease. American Journal of Respiratory & Critical Care Medicine 1995;151:1682"“6.
4. Gregory A.Poland, John W.Gnann, Myron J.Levin. An Update on Adult Immunizations for vaccine preventable diseases. Available at http://www.medscape.com/viewprogram/7621 (accessed on 12/9/07)
5.Poole PJ, Chacko E,Wood-Baker RWB, Cates CJ. Influenza vaccine for patients with chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2006, Issue 1. Art. No.: CD002733. DOI: 10.1002/14651858.CD002733.pub2.
6.Granger R, Walters J, Poole PJ, Lasserson TJ, Mangtani P, Cates CJ, Wood-Baker R. Injectable vaccines for preventing pneumococcal infection in patients with chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD001390. DOI: 10.1002/14651858.CD001390.pub2.
Christian Medical College and Hospital Ludhiana,India
November 7, 2007
Role of nutrition and education in the management of stable COPD
The guideline on diagnosis and management of stable chronic obstructive pulmonary disease [COPD] by Qaseem and colleagues is highly appreciable (1).However, recommendation on nutrition , education and immunization are lacking. Emmanuel M Bhaska has very well taken the role of Immunization for patients with Chronic Obstructive Pulmonary Disease .We would like to share the literature on the role of education and nutrition in the management of stable COPD Although patient education is an essential component of care for any chronic disease, assessment of the value of education in COPD may be difficult because of the relatively long time required to achieve improvements in objective measurements of lung function. Patient education alone does not improve exercise performance or lung function (2-5), but it can play a role in improving skills, ability to cope with illness, and health status (6). Patient education regarding smoking cessation has the greatest capacity to influence the natural history of COPD . Education also improves patient response to exacerbations (7, 8) . Prospective end-of-life discussions can lead to understanding of advance directives and effective therapeutic decisions at the end of life (9) . Ideally, educational messages should be incorporated into all aspects of care for COPD and may take place in many settings: consultations with physicians or other health care workers, home-care or outreach programs, and comprehensive pulmonary rehabilitation programs. Education should be tailored to the needs and environment of the individual patient, interactive, directed at improving quality of life, simple to follow, practical, and appropriate to the intellectual and social skills of the patient and the caregivers. The topics that seem most appropriate for an education program include the following: smoking cessation; basic information about COPD and pathophysiology of the disease, general approach to therapy and specific aspects of medical treatment, self- management skills, strategies to help minimize dyspnea, advice about when to seek help, self management and decision making during exacerbations, and advance directives and end-of-life issues.
Weight loss, as well as a depletion of fat-free mass (FFM), may be observed in stable COPD patients, irrespective of the degree of airflow limitation, and being underweight is associated with an increased mortality risk (10). Nutritional screening is recommended in the assessment of COPD. Simple screening can be based on measurements of BMI and weight change. Patients are considered underweight (BMI< 21 kg.m-2; age>50 yrs), normal weight (BMI 21"“25 kg.m-2), overweight (BMI 25"“30 kg.m-2) or obese (BMI â‰¥ 30 kg.m-2). Criteria to define weight loss are weight loss >10% in the past 6 months or >5% in the past month. Weight loss and particularly muscle wasting contribute significantly to morbidity, disability and handicap in COPD patients. Weight loss and loss in fat mass is primarily the result of a negative balance between dietary intake and energy expenditure, while muscle wasting is a consequence of an impaired balance between protein synthesis and protein breakdown. In advanced stages of COPD, both energy balance and protein balance are disturbed. Therefore, nutritional therapy may only be effective if combined with exercise or other anabolic stimuli (11, 12).
2 Reis AL. Response to bronchodilators. In: Clausen J, editor. Pulmonary function testing: guidelines and controversies. New York: Academic Press; 1982.
3 . Janelli LM, Scherer YK, Schmieder LE. Can a pulmonary health teaching program alter patients' ability to cope with COPD? Rehabil Nurs 1991;16:199"“202.
4 . Ashikaga T, Vacek PM, Lewis SO. Evaluation of a community-based education program for individuals with chronic obstructive pulmonary disease. J Rehabil 1980;46:23"“27.
5. Toshima MT, Kaplan RM, Ries AL. Experimental evaluation of rehabilitation in chronic obstructive pulmonary disease: short-term effects on exercise endurance and health status. Health Psychol 1990;9:237"“252.
6. Celli BR. Pulmonary rehabilitation in patients with COPD. Am J Respir Crit Care Med 1995;152:861"“864.
7. Stewart MA. Effective physician-patient communication and health outcomes: a review. CMAJ 1995;152:1423"“1433.
8. Clark NM, Nothwehr F, Gong M, Evans D, Maiman LA, Hurwitz ME, Roloff D, Mellins RD. Physician-patient partnership in managing chronic illness. Acad Med 1995;70:957"“959.
9. Heffner JE, Fahy B, Hilling L, Barbieri C. Outcomes of advance directive education of pulmonary rehabilitation patients. Am J Respir Crit Care Med 1997;155:1055"“1059.
10. Schols AMWJ, Soeters PB, Dingemans AMC, Mostert R, Frantzen PJ, Wouters EF. Prevalence and characteristics of nutritional depletion in patients with stable COPD eligible for pulmonary rehabilitation. Am Rev Respir Dis 1993; 147: 1151"“1156.
11. Schols AM, Soeters PB, Mostert R, et al. Physiologic effects of nutritional support and anabolic steroids in patients with chronic obstructive pulmonary disease: A randomized controlled trial. Am J Respir Crit Care Med 1995; 152: 1248"“1274.
12. Creutzberg EL, Wouters EFM, Mostert R, et al. Efficacy of nutritional supplementation therapy in depleted patients with chronic obstructive pulmonary disease. Nutrition 2003; 19: 120"“127.
Paul A. Selecky
July 8, 2008
Clinical Practice Guideline for COPD
To the Editor:
On behalf of the joint taskforce of American College of Chest Physicians (ACCP) and American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR), we wish to comment on the recommendation concerning pulmonary rehabilitation for patients with chronic obstructive pulmonary disease (COPD) that was included in the recently published Clinical Practice Guideline from the American College of Physicians (ACP).1,2 In general, we laud the ACP for publishing this important guideline highlighting the increasing prominence of COPD in the general medical community, the growing evidence base in this field, and the need for all physicians to be versed in appropriate management strategies for this often under-recognized and sub-optimally managed disease. In our view, the systematic review and recently published clinical practice guideline on pulmonary rehabilitation published by ACCP and AACVPR3,4 cast a wider net in its systematic review of the pulmonary rehabilitation literature and, as a result, graded key recommendations regarding pulmonary rehabilitation as stronger than the more narrowly focused review conducted by ACP.
In general, we agree with the statement in the ACP Guideline that "Evidence supports the use of pulmonary rehabilitation programs for patients with severe airflow obstruction, because they reduce hospitalizations and improve health status and exercise capacity." Based on the ACCP/AACVPR Guideline3,4, as well as the statement recently published by the American Thoracic Society (ATS) and European Respiratory Society (ERS)5 and the most recent Cochrane Review6, we believe that the strength of evidence supporting the use of pulmonary rehabilitation is much stronger than implied by the recommendation in the ACP Guideline. This difference in opinion about the strength of the recommendations regarding whether the "benefits do clearly outweigh risks" (strong recommendation) or the "benefits, risks and burdens are finely balanced" (weak recommendation) is due, at least in part, to the fact that the ACP review was limited primarily to clinical trials, meta-analyses and reviews that evaluated only outcomes of comprehensive pulmonary rehabilitation program interventions incorporating multiple components such as "exercise training, education, behavioral modification and outcome assessment". Although this certainly represents current state of the art treatment in pulmonary rehabilitation, it misses a wealth of evidence and clinical research justifying the treatment components in COPD that form a key basis of inclusion of such treatment modalities in pulmonary rehabilitation. For instance, in evaluating the effect of pulmonary rehabilitation on exercise tolerance, the ACP Guideline comments only on improvements in the 6-minute walk distance in the few trials of pulmonary rehabilitation that examined this particular outcome measure. This misses the large body of evidence about exercise for patients with chronic lung disease that strongly supports endurance exercise training for the lower extremities (1A Recommendation in ACCP/AACVPR Guidelines), upper extremity exercise training (important for activities of daily living, 1A Recommendation), and strength-training (1A Recommendation) and does not support routine use of inspiratory muscle training in pulmonary rehabilitation (1B Recommendation).3,4 In addition, the well established and accepted effect of pulmonary rehabilitation on health-related quality of life (HRQOL) has led to its use as a gold standard against which new measures of HRQOL are evaluated.7
In addition, we wish to emphasize a cautionary note in the ACP statement regarding the severity of patients for whom pulmonary rehabilitation may be considered. The ACP guideline states "However, the evidence is not clear for individuals with FEV1 greater than 50% predicted" and the wording of the ACP Recommendation indicates that "Clinicians should consider pulmonary rehabilitation in symptomatic individuals with COPD who have an FEV1 less than 50% predicted." While we agree that most of the patients with COPD included in the trials of pulmonary rehabilitation examined in the ACP review had moderate to severe disease with severe impairment of lung function, a key principle of rehabilitation medicine is that such treatment should be based on symptoms and disability and not on any arbitrary lung function measure. There are many symptomatic patients with FEV1 above 50% predicted who could, and do, benefit from pulmonary rehabilitation and its treatment components. We are concerned that a recommendation worded like the one in the ACP Guidelines might encourage health providers and payors to deny access to pulmonary rehabilitation for such patients. The inference from this recommendation might suggest that patients with FEV1 above 50% predicted do not benefit from pulmonary rehabilitation. There is no such evidence. In commenting on the effect of pulmonary rehabilitation on mortality, the ACP document appropriately acknowledges that "sample size and study duration were insufficient to adequately evaluate this end-point." We believe that the same principle should be applied to the use of pulmonary rehabilitation for patients with less severe disease than the arbitrary cutoff of 50% predicted FEV1. Given the modest costs and high benefits/risks ratio of pulmonary rehabilitation for such patients, we believe that rehabilitation is reasonable to recommend for appropriate patients. In the absence of evidence, much of medical treatment is based on clinical judgment and common sense. This is another example of the adage that "absence of proof is not proof of absence."
Overall, we are encouraged by the growing body of evidence supporting the use of pulmonary rehabilitation as a standard of care for patients with chronic lung disease and believe that the ACP Guideline, interpreted appropriately, will add weight to this evidence.
Alvin V. Thomas, MD, FCCP President American College of Chest Physicians
Larry Hamm, PhD, FAACVPR, FACSM President American Association of Cardiovascular and Pulmonary Rehabilitation
1. Qaseem A, Snow V, Shekelle P et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2007; 147:633-638.
2. Wilt TJ, Niewoehner D, MacDonald R et al. Management of stable chronic obstructive pulmonary disease: a systematic review for a clinical practice guideline. Ann Intern Med 2007; 147:639-653.
3. Ries AL, Bauldoff GS, Carlin BW et al. Pulmonary rehabilitation executive summary: joint American College of Chest Physicians/American Association of Cardiovascular and Pulmonary Rehabilitation evidence-based clinical practice guidelines. Chest 2007; 131(suppl)(5_suppl):1S-3S.
4. Ries AL, Bauldoff GS, Carlin BW et al. Pulmonary rehabilitation: joint ACCP/AACVPR evidence-based clinical practice guidelines. Chest 2007; 131(suppl)(5):4S-42S.
5. American Thoracic Society, European Respiratory Society. ATS/ERS statement on pulmonary rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1413.
6. Lacasse Y. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2006; Issue 4. Art. No.: CD003793. DOI: 10.1002/14651858.CD003793.pub2.
7. Schunemann HJ, Griffith L, Jaeschke R et al. Evaluation of the minimal important difference for the feeling thermometer and the St. George's Respiratory Questionnaire in patients with chronic airflow obstruction. J Clin Epidemiol 2003; 56:1170-1176.
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