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Editorials |

“All That Wheezes Is Not Asthma” (or COPD)!Spirometry and COPD FREE TO VIEW

David A. Kaminsky, MD, FCCP
Author and Funding Information

From the Pulmonary Disease and Critical Care Medicine Division, College of Medicine, The University of Vermont.

CORRESPONDENCE TO: David A. Kaminsky, MD, FCCP, Pulmonary Disease and Critical Care Medicine, University of Vermont College of Medicine, Given D-213, 89 Beaumont Ave, Burlington, VT 05405; e-mail: david.kaminsky@uvm.edu


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(2):284-286. doi:10.1378/chest.14-1813
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Published online

This famous quote was made by Chevalier Jackson in the Boston Medical Quarterly in 1865.1 At the time, Jackson, an otolaryngologist, was concerned about foreign body aspiration causing wheezing and being misdiagnosed as asthma. Today, this adage reminds us that there are many causes of wheezing and shortness of breath besides the common and classic diagnosis of asthma. Among these causes is COPD. In fact, COPD is probably one of the most common diagnoses made in the older patient with a smoking history who complains of shortness of breath, wheezing, or chest tightness. However, COPD is frequently underdiagnosed and overdiagnosed. Patients are underdiagnosed when spirometry is not used to search for objective evidence of obstruction, and patients are overdiagnosed when spirometry is not used to confirm the “obstruction” in COPD. Overdiagnosis mislabels the patient with a disease they do not have, which can result in inappropriate prescription and use of costly medications that may have side effects. In addition, the focus on COPD shifts attention away from the possibility of other causes of the patient’s symptoms, such as obesity, deconditioning, heart disease, or depression, which may lead to a worsening of their true underlying condition.

This topic is highlighted by the current study by Collins and colleagues2 in this issue of CHEST (see page 369), in which the authors demonstrate that a significant percentage of patients diagnosed with COPD never received confirmation by spirometry. The study was cleverly designed by first identifying a cohort of patients from three Pacific Northwest Department of Veterans Affairs Medical Centers between 2003 and 2007 who had spirometry and then focusing only on those patients with an empirical, clinical diagnosis of COPD in the 2 years prior to spirometry who were also on inhaled medication in the 1 year prior to spirometry. This strategy thus defined patients who were diagnosed and treated empirically for COPD and had all undergone subsequent spirometry. Among those with a clinical diagnosis of and treated for COPD, only 62% had airflow limitation. The authors then used modified Poisson regression to identify risk factors independently associated with having airflow limitation, and found that such factors, not surprisingly, included older age, prior smoking status, and being underweight. What was fascinating were the factors associated with normal spirometry. These included congestive heart failure, depression, diabetes, sleep apnea, systemic hypertension, and obesity. Given that many of these factors are so commonly associated with shortness of breath, the authors concluded that many patients are incorrectly diagnosed with and inappropriately treated for COPD.

Unlike many studies investigating the accuracy of diagnosis of COPD, in which spirometry is often not performed, the current study had spirometric data on all patients. Even so, only a little more than one-half of them had documented airflow limitation despite diagnosis of and treatment of COPD! The results were robust to various sensitivity analyses including the use of GOLD (Global Initiative for Chronic Obstructive Lung Disease) vs lower limit of normal criteria, the use of more intensive inhaled therapy, and the use of prebronchodilator vs postbronchodilator spirometry. In addition, what makes this study unique is the finding that the lack of airflow limitation related to specific alternative diagnoses that may be associated with shortness of breath. Thus, it is reasonable to conclude that many of the patients in this study in fact had some of these other diagnoses, and not COPD. Interestingly, these conditions are well recognized as comorbidities in COPD,3 thus highlighting that many of our patients who do have COPD may be suffering from more than one reason for their shortness of breath. It is critical to recognize these comorbidities because they may also be risk factors for increased mortality in COPD.3

The current study is not without limitations. As noted by the authors, their study was performed in a select population of Department of Veterans Affairs patients, who are predominantly older men. There was no documentation of symptoms or longitudinal follow-up to ascertain the accuracy of the diagnoses or correlation with spirometry. A limitation of the study design was that all patients had spirometry within the year after medications were prescribed, so some of the patients who might have had reversible airflow limitation may have normalized their lung function by the time spirometry was performed. In addition, we do not know whether any of the patients who were found not to have airflow limitation subsequently were further investigated to identify other causes of dyspnea, and whether their medications were altered. As acknowledged by the authors, there is the possibility that some patients in fact had clinical COPD as suggested by symptoms of chronic bronchitis, but had normal spirometry,4 even though the benefit of treating such patients is unclear. Finally, spirometry itself is limited by the patient effort involved, the insensitivity to early peripheral airway changes, and the effects of thoracic gas compression5 and deep inhalation on FEV1.6 Other studies demonstrate that further lung function testing with lung volumes or diffusing capacity, in addition to characterization of airway and parenchymal abnormalities by CT scan, may improve the diagnostic accuracy of a clinical impression of COPD.7,8

The definition of COPD is becoming more complex as we learn more about the many phenotypic presentations of the disease.9 Indeed, the new GOLD guidelines try to capture this aspect of COPD by now incorporating symptoms and exacerbations in addition to spirometry into the classification of the disease.10 Use of other noninvasive methods to detect small airway disease, such as multiple breath nitrogen washout11 or forced oscillation,12 may help us define the disease earlier or in cases where spirometry is normal. Nevertheless, we need to remember that spirometry remains one of the best available, objective measures we have of defining the “O” in COPD so that we may render the most accurate and appropriate diagnosis in our patients who are short of breath or wheeze.

References

Jackson C. All that wheezes is not asthma. BMQ. 1865;16:86.
 
Collins BF, Feemster LC, Rinne ST, Au DH. Factors predictive of airflow obstruction among veterans with presumed empirical diagnosis and treatment of COPD. Chest. 2015;147(2):369-376.
 
Divo M, Cote C, de Torres JP, et al; BODE Collaborative Group. Comorbidities and risk of mortality in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2012;186(2):155-161. [CrossRef] [PubMed]
 
Martinez CH, Kim V, Chen Y, et al; COPDGene Investigators. The clinical impact of non-obstructive chronic bronchitis in current and former smokers. Respir Med. 2014;108(3):491-499. [CrossRef] [PubMed]
 
Sharafkhaneh A, Babb TG, Officer TM, Hanania NA, Sharafkhaneh H, Boriek AM. The confounding effects of thoracic gas compression on measurement of acute bronchodilator response. Am J Respir Crit Care Med. 2007;175(4):330-335. [CrossRef] [PubMed]
 
Scichilone N, La Sala A, Bellia M, et al. The airway response to deep inspirations decreases with COPD severity and is associated with airway distensibility assessed by computed tomography. J Appl Physiol (1985). 2008;105(3):832-838. [CrossRef] [PubMed]
 
Coxson HO, Leipsic J, Parraga G, Sin DD. Using pulmonary imaging to move chronic obstructive pulmonary disease beyond FEV1. Am J Respir Crit Care Med. 2014;190(2):135-144. [CrossRef] [PubMed]
 
Hesselbacher SE, Ross R, Schabath MB, et al. Cross-sectional analysis of the utility of pulmonary function tests in predicting emphysema in ever-smokers. Int J Environ Res Public Health. 2011;8(5):1324-1340. [CrossRef] [PubMed]
 
Agusti A, Sobradillo P, Celli B. Addressing the complexity of chronic obstructive pulmonary disease: from phenotypes and biomarkers to scale-free networks, systems biology, and P4 medicine. Am J Respir Crit Care Med. 2011;183(9):1129-1137. [CrossRef] [PubMed]
 
Global strategy for the diagnosis, managment and prevention of COPD. GOLD website. http://www.goldcopd.org. January 2014. Accessed July 22, 2014.
 
Verbanck S, Schuermans D, Meysman M, Paiva M, Vincken W. Noninvasive assessment of airway alterations in smokers: the small airways revisited. Am J Respir Crit Care Med. 2004;170(4):414-419. [CrossRef] [PubMed]
 
Faria AC, Costa AA, Lopes AJ, Jansen JM, Melo PL. Forced oscillation technique in the detection of smoking-induced respiratory alterations: diagnostic accuracy and comparison with spirometry. Clinics (Sao Paulo). 2010;65(12):1295-1304. [CrossRef] [PubMed]
 

Figures

Tables

References

Jackson C. All that wheezes is not asthma. BMQ. 1865;16:86.
 
Collins BF, Feemster LC, Rinne ST, Au DH. Factors predictive of airflow obstruction among veterans with presumed empirical diagnosis and treatment of COPD. Chest. 2015;147(2):369-376.
 
Divo M, Cote C, de Torres JP, et al; BODE Collaborative Group. Comorbidities and risk of mortality in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2012;186(2):155-161. [CrossRef] [PubMed]
 
Martinez CH, Kim V, Chen Y, et al; COPDGene Investigators. The clinical impact of non-obstructive chronic bronchitis in current and former smokers. Respir Med. 2014;108(3):491-499. [CrossRef] [PubMed]
 
Sharafkhaneh A, Babb TG, Officer TM, Hanania NA, Sharafkhaneh H, Boriek AM. The confounding effects of thoracic gas compression on measurement of acute bronchodilator response. Am J Respir Crit Care Med. 2007;175(4):330-335. [CrossRef] [PubMed]
 
Scichilone N, La Sala A, Bellia M, et al. The airway response to deep inspirations decreases with COPD severity and is associated with airway distensibility assessed by computed tomography. J Appl Physiol (1985). 2008;105(3):832-838. [CrossRef] [PubMed]
 
Coxson HO, Leipsic J, Parraga G, Sin DD. Using pulmonary imaging to move chronic obstructive pulmonary disease beyond FEV1. Am J Respir Crit Care Med. 2014;190(2):135-144. [CrossRef] [PubMed]
 
Hesselbacher SE, Ross R, Schabath MB, et al. Cross-sectional analysis of the utility of pulmonary function tests in predicting emphysema in ever-smokers. Int J Environ Res Public Health. 2011;8(5):1324-1340. [CrossRef] [PubMed]
 
Agusti A, Sobradillo P, Celli B. Addressing the complexity of chronic obstructive pulmonary disease: from phenotypes and biomarkers to scale-free networks, systems biology, and P4 medicine. Am J Respir Crit Care Med. 2011;183(9):1129-1137. [CrossRef] [PubMed]
 
Global strategy for the diagnosis, managment and prevention of COPD. GOLD website. http://www.goldcopd.org. January 2014. Accessed July 22, 2014.
 
Verbanck S, Schuermans D, Meysman M, Paiva M, Vincken W. Noninvasive assessment of airway alterations in smokers: the small airways revisited. Am J Respir Crit Care Med. 2004;170(4):414-419. [CrossRef] [PubMed]
 
Faria AC, Costa AA, Lopes AJ, Jansen JM, Melo PL. Forced oscillation technique in the detection of smoking-induced respiratory alterations: diagnostic accuracy and comparison with spirometry. Clinics (Sao Paulo). 2010;65(12):1295-1304. [CrossRef] [PubMed]
 
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