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Chronic Obstructive Pulmonary Disease: Diagnostic Considerations MARVIN DEWAR, M.D., J.D., and R

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Chronic Obstructive Pulmonary Disease: Diagnostic Considerations MARVIN DEWAR, M.D., J.D., and R Chronic Obstructive Pulmonary Disease: Diagnostic Considerations MARVIN DEWAR, M.D., J.D., and R. WHIT CURRY, JR., M.D. University of Florida College of Medicine, Gainesville, Florida Chronic obstructive pulmonary disease is characterized by the gradual progression of irrevers- ible airflow obstruction and increased inflammation in the airways and lung parenchyma that is generally distinguishable from the inflammation caused by asthma. Most chronic obstructive pulmonary disease is associated with smoking, but occupational exposure to irritants and air pollution also are important risk factors. Patients with chronic obstructive pulmonary disease typically present with coughing, sputum production, and dyspnea on exertion. However, none of these findings alone is diagnostic. The Global Initiative for Chronic Obstructive Lung Disease diagnostic criterion for chronic obstructive pulmonary disease is a forced expiratory volume in one second/forced vital capacity ratio of less than 70 percent of the predicted value. Severity is further stratified based on forced expiratory volume in one second and symptoms. Chest radiog- raphy may rule out alternative diagnoses and comorbid conditions. Selected patients should be tested for G1-antitrypsin deficiency. Arterial blood gas testing is recommended for patients pre- senting with signs of severe disease, right-sided heart failure, or significant hypoxemia. Chronic obstructive pulmonary disease also is a systemic disorder with weight loss and dysfunction of respiratory and skeletal muscles. (Am Fam Physician 2006;73:669-76, 677-8. Copyright © 2006 American Academy of Family Physicians.) S Patient Information: he global burden of chronic limitation that is not fully reversible and A handout on chronic obstructive pulmonary disease that is associated with an abnormal inflam- obstructive pulmonary disease, written by the (COPD) is increasing; the disease matory response of the lungs to noxious authors of this article, is is projected to be the third leading particles or gases. provided on page 677. causeT of death and fifth leading cause of over- Patients with COPD present with a S 1 See related editorial all disability worldwide by 2020. Men and variety of clinical findings, including ele- on page 590. women seem to be at an equal risk, and the ments of chronic bronchitis and emphy- death rate attributable to COPD is increasing sema.6-8 Although COPD and asthma are significantly in both sexes.1,2 The economic both associated with airflow obstruction consequences of COPD are substantial. In and inflammation of the lung and airways, 2002, the estimated total societal cost of asthma-related airflow obstruction is more COPD in the United States was $32 billion.2 reversible and the disease course is more variable than with COPD.6,8,9 Definition COPD is a heterogeneous disorder that Risk Factors encompasses traditional clinical entities such Exposure to tobacco smoke is the most as emphysema and chronic bronchitis.3,4 significant risk factor for COPD, with 80 to The Global Initiative for Chronic Obstruc- 90 percent of all cases attributable to smok- tive Lung Disease (GOLD),5 a ing.6 Evidence linking tobacco smoke expo- collaborative effort from the sure and COPD predominantly comes from Smokingcessationcangive National Heart, Lung, and population-based studies that have consis- a former smoker the Blood Institute; the National tently shown that smoking is associated with same average ongoing Institutes of Health; and the diminished lung function, more frequent loss of lung function as World Health Organization, respiratory symptoms, and increased COPD- a never-smoker. defines COPD as a usually pro- related deaths.5,10-13 Pipe and cigar smoking gressive disease with airflow are associated with increased COPD risk, $OWNLOADEDFROMTHE!MERICAN&AMILY0HYSICIAN7EBSITEATWWWAAFPORGAFP#OPYRIGHT¥2006!MERICAN!CADEMYOF&AMILY0HYSICIANS&ORTHEPRIVATE NONCOMMERCIAL USEOFONEINDIVIDUALUSEROFTHE7EBSITE!LLOTHERRIGHTSRESERVED#ONTACTCOPYRIGHTS AAFPORGFORCOPYRIGHTQUESTIONSANDORPERMISSIONREQUESTS COPD SORT: KEY RECOMMENDATIONS FOR PRACTICE Evidence Clinical recommendation rating References Spirometry should be used as the first-line diagnostic tool when C 5, 6 evaluating patients for COPD. A FEV1/FVC ratio of less than 70 percent of the predicted value suggests COPD. Patients with suspected COPD should receive chest radiography C6, 31 to exclude other diagnoses and comorbidities. G1-Antitrypsin deficiency testing should be performed in select C15 patients (e.g., COPD in never-smokers, idiopathic cirrhosis, family history of G1-antitrypsin deficiency, predominantly lower lung emphysema, “premature” COPD, and refractory asthma at a young age). ABG testing should be performed if the patient presents with C 5 right-sided heart failure or has more severe COPD. COPD = chronic obstructive pulmonary disease; FEV1 = forced expiratory volume in one second; FVC = forced vital capacity; ABG = arterial blood gas. A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evi- dence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 573 or http://www.AAFP.org/afpsort.xml. but at a lesser rate than with cigarette smok- fuels, commonly used for indoor cooking ing.5,6 Although cigarette smoking is a sig- and heating, is a risk factor for COPD, par- nificant risk factor for COPD, only about ticularly in the developing world.5,6,9,19,20 20 percent of cigarette smokers develop clinically significant COPD.6,8,13 Natural History The second most significant documented Patients with COPD may present with loss risk factor for COPD is G1-antitrypsin defi- of lung function beyond normal age-related ciency. Although G1-antitrypsin deficiency decreases. Clinical disease develops fairly increases the risks associated with smok- late in the disease course, after lung function ing, COPD can develop in never-smokers drops below threshold values. with G1-antitrypsin deficiency. One percent After 25 years of age, a nonsmoking adult’s of COPD cases are attributable to severe forced expiratory volume in one second 5,6,14,15 G1-antitrypsin deficiency. (FEV1) decreases by an average of 20 to 40 mL Certain occupational exposures are per year. In some smokers, FEV1 decreases by associated with increased risk of COPD two to five times this amount, making them (Table 116-18). Exposure to solid biomass particularly susceptible to COPD.6,8,12,13,21,22 Smoking cessation may cause slight initial improvement in FEV1 (approximately 50 mL TABLE 1 in the first year).21 More importantly, smok- Occupational Irritants That ing cessation can give a former smoker the IncreasetheRiskofCOPD same average ongoing loss of lung function as a never-smoker.13,21 Figure 113,21 illustrates Occupation Irritant the progressive loss of lung function in a Agricultural worker Endotoxin variety of settings. Coal miner Coal dust Patients with COPD usually have a smok- Concrete worker Mineral dust ing history of at least 20 pack-years. Wheez- Construction worker Dust ing and dyspnea on exertion generally occur Gold miner Silica when the FEV1 is less than 50 percent of the Hard rock miner Mineral dust predicted value, and significant physical Rubber worker Industrial chemicals disability usually occurs when the FEV1 is less than 35 to 40 percent of the predicted COPD = chronic obstructive pulmonary disease. value.4,22,23 Patients who started smoking in Information from references 16 through 18. their 20s and have already sustained appre- ciable FEV1 loss by their 40s are likely to 670 American Family Physician www.aafp.org/afp Volume 73, Number 4 U February 15, 2006 COPD develop significant COPD if they continue matous changes are most prominent in the to smoke. Those in their mid-40s who have upper lung fields. Loss of the structural sup- normal FEV1 values, however, probably will ports that keep the airways open allows the not develop symptomatic disease.13 bronchioles to collapse during expiration; the resulting nonfunctioning alveolar units Pathophysiology reduce the amount of lung area available for COPD involves a chronic inflammatory pro- gas exchange.4-6,24 cess, primarily in the peripheral airways and Patients with COPD have high neutro- the lung parenchyma. Airway irritation causes phil, macrophage, and CD8+ T-lymphocyte mucous gland enlargement, hypersecretion, counts in the airways and lung parenchyma. ciliary dysfunction, and squamous metaplasia These cells release inflammatory cytokines early in the disease course. An ongoing cycle and proteases that cause an imbalance of the of inflammation and repair ultimately nar- pro-inflammatory and protective mediators rows the airway lumen and obstructs air- found in healthy lungs.5,8,20,25 flow. Patients with emphysema experience destruction of the structural constituents Diagnosis of the alveolar walls, causing permanent Common differential diagnosis of COPD enlargement of the air spaces distal to the ter- includes asthma, heart failure, bronchiecta- minal bronchioles. In early COPD, emphyse- sis, bronchiolitis obliterans, cystic fibrosis, Lung Function Decline in Smokers and Nonsmokers Average nonsmoker 4 Severely susceptible smoker who stops smoking at 40 years 3 of age (L) 1 Clinical symptoms develop FEV 2 Susceptible smoker Severely susceptible smoker Severe disability 1 0 25 45 65 85 Age (years) Figure 1. The natural history of lung function decline. Smokers who are susceptible
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