As the definition of COPD indicates, there are clinically significant manifestations of the disease that are not accurately measured by indices of airflow obstruction. A number of classification systems have been developed in an attempt to better capture the total impact of the disease. The most widely used of these is the BODE Index, developed by Celli and colleagues, that incorporates Body Mass Index, Airflow Obstruction, Symptoms of Dyspnea, and Exercise Tolerance in a scoring system that has been demonstrated to better predict mortality than using airflow obstruction alone. The BODE Index is presented in table 33.2.

Table 33.2 BODY INDEX (RANGE 0-10 POINTS)

SOURCE: Adapted from Celli R, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med. 2004;350:1005–1012.

The BODE Index more accurately correlates with prognosis than systems that use spirometry alone to classify patients. Recently, GOLD has proposed a multidimensional system that incorporates airflow obstruction, symptoms, and exacerbation frequency. Currently there are not enough published prospective data to establish whether it has improved performance over the GOLD classification based on spirometry alone.

CLINICAL PRESENTATION

The majority of persons diagnosed with COPD initially present for medical evaluation in one of two ways: with gradually progressive symptoms that include dyspnea on exertion or with an acute illness characterized by an abrupt increase in cough, sputum, and dyspnea (COPD exacerbation). In the latter scenario, questioning usually reveals antecedent gradual increase in exertional dyspnea and/or chronic cough.

DEMOGRAPHICS AND SYMPTOMS

The typical patient presents between the ages of 50 and 70 and frequently has a history of significant cigarette use. As mentioned above, the most frequently cited symptom is dyspnea on exertion, which has usually been gradually increasing for months to years. Given the age and demographic characteristics of patients with COPD, the increase in dyspnea is often attributed to aging, deconditioning, weight gain, or concomitant comorbid medical conditions. Cough, particularly morning cough with sputum production, is common and frequently accepted by patients as “a normal smoker’s cough.”

    In addition to chronic symptoms, patients may also report episodic exacerbations in symptoms with a syndrome of increased cough, increase and/or change in characteristics of sputum production and increased dyspnea. This may be accompanied by fever, myalgias, and other symptoms suggesting viral infection. Not infrequently, patients will report a repeated seasonal occurrence of such events, stating “every winter I get a cold and it settles in my chest” or similar descriptions.

PHYSICAL EXAMINATION

In patients with mild or moderate disease, the history of symptoms in the appropriate exposure setting is the key to pursuing evaluation, as the physical examination is frequently normal. As airflow obstruction becomes more severe, the physical examination may reveal a prolonged expiratory phase of the respiratory cycle, inspiratory basilar rhonchi or crackles, and expiratory polyphonic wheezing. Supportive signs on the physical examination may include stigmata of cigarette smoking, including dental changes, skin thinning and wrinkling, and nicotine staining of fingers. Clubbing is not seen in COPD and its presence should prompt evaluation for other causes, most frequently lung cancer.

    In patients with severe or very severe COPD, there may be skeletal muscle wasting, the use of accessory muscles of respiration at rest with patients seeking positions that allow them to brace the shoulder girdle to provide mechanical advantage for these muscles. These positions include the classic “tripod” position while seated, and using the handles on a shopping cart or wheelchair while ambulating. Examination of the chest reveals markedly prolonged expiratory phase, symmetrically diminished breath sounds, and medial and inferior displacement of the cardiac PMI to the subxiphoid position. It is unusual for patients to present with signs of overt right heart failure (“cor pulmonale”) or physical findings of severe pulmonary hypertension.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of a middle-aged person presenting with dyspnea on exertion is broad. It includes COPD, asthma, interstitial lung disease, anemia, congestive heart failure, coronary artery disease, and deconditioning. Given the nonspecificity of the presenting symptoms and physical examination, the ability to diagnose COPD depends on obtaining spirometry as part of the initial evaluation of the patient. The presence of airflow obstruction as manifest by a reduction in the FEV₁/FVC that does not normalize after the administration of an inhaled bronchodilator strongly supports the diagnosis (Figure 33.1). The importance of ordering spirometry is underlined by the fact that NHANES 3 survey data suggest that at least 50% of patients with airflow obstruction have not been diagnosed with COPD and are not receiving any therapy.

PULMONARY FUNCTION TESTING

All patients with COPD have, by definition, incompletely reversible airflow obstruction on pulmonary function testing. Measurements of lung volumes will reveal increases in functional residual capacity (FRC), the ratio of residual volume to total lung capacity (RV/TLC), and TLC, all indicative of hyperinflation that is in proportion to the degree of airflow obstruction.

    Measurement of the diffusing capacity for carbon monoxide (Dlco) may show a reduction. The magnitude of this reduction is in proportion to the amount of emphysematous destruction of the lungs in an individual patient.

ARTERIAL BLOOD GASES AND ASSESSMENT OF OXYGENATION

As discussed below, the data demonstrate that patients with COPD and chronic resting hypoxemia, defined as Po₂ <55 mm Hg or Sao₂ <88%, benefit from supplemental oxygen therapy. It is appropriate to assess oxygenation with either an arterial blood gas measurement or oximetry in patients with moderate or greater disease or those presenting with an increase in symptomatology. Measurement of arterial blood gases provides information not only about oxygenation but also acid–base status and pco₂. Knowledge of the latter two parameters is important in the assessment of acute respiratory failure.

THORACIC IMAGING

Imaging of the chest can be performed with conventional chest radiography, computed tomography (CT), and/or magnetic resonance imaging (MRI).

    Chest x-rays (CXRs) are frequently normal in patients with mild or moderate disease. Signs of hyperinflation with increase in anterior-posterior dimension and/or flattening of the diaphragms are nonspecific but are consistent with the presence of COPD (Figure 33.2). Some smokers may manifest a nonspecific increase in interstitial markings (“dirty lungs”). In patients with more advanced disease, the images may demonstrate increased lucency of the lung fields consistent with the tissue destruction of emphysema, a diminishment in visualized vascularity, and medial and inferior displacement of the cardiac silhouette (Figure 33.3). Focal areas of hyperlucency are suggestive of bullous disease. In patients presenting with acute respiratory decompensation, the x-ray should be carefully reviewed for evidence of congestive heart failure, pneumonia, or pneumothorax. The latter can be difficult to distinguish from severe bullous changes in some individuals with marked underlying emphysema.

    Chest CT scanning may be normal in mild disease. It is the current test of choice for assessing the presence of emphysema. It is much more sensitive than plain chest radiography for demonstrating emphysematous changes. Qualitatively, these changes can be described as consistent with centriacinar, panlobular, or paraseptal emphysema. In addition, the distribution of the changes can be described: upper-lobe predominant, diffuse, lower-lobe predominant. The latter is suggestive of underlying alpha-1-antiprotease deficiency. More recently, tools are being developed to provide a more precise quantitation of emphysema on CT scanning. Although still largely a research tool, these approaches have been used to evaluate patients considering surgical therapy for COPD. The CT scan is also the test of choice to evaluate for the presence of bronchiectasis. The presence of enlarged airways (greater in diameter than the associated blood vessel), nontapering airways, or airways visible within 1–2 cm of the pleural surface are findings of bronchiectasis; airway thickening may also be seen involving these structures.

    Chest CT scanning with intravenous contrast is frequently used to evaluate patients with suspected pulmonary embolism and may be ordered in a patient with COPD presenting with chest pain or acute respiratory decompensation.

    In addition to demonstrating emphysema, chest CTs performed in patients with significant smoking history and COPD frequently demonstrate pulmonary nodules (10– 30% depending on the definition used), a minority of which represent malignancy (Figure 33.4). If such a nodule is detected, further evaluation is required. Published guidelines utilize the size of the nodule and the underlying risk factors of the patient to recommend evaluation and monitoring strategies.

    The issue of whether to use chest CT scans to screen asymptomatic middle-aged smokers for the presence of lung cancer was the subject of a large government-funded multicenter trial in the United States (National Lung Screening Trial [NLST]). This study demonstrated a 20% reduction in lung cancer mortality in individuals between the ages of 55 and 74 with 30 or more pack-years of cigarette smoking. It is likely that this study and others will result in a more widespread institution of lung cancer screening programs using low-dose CT scans.

    The current role of CT scanning in the assessment of a patient with known or suspected COPD is in evolution. Agreed-upon indications include the evaluation of patients considering surgical therapy for COPD such as bullectomy, lung volume reduction surgery, or lung transplantation; evaluation of large airways in patients in whom a focal anatomic abnormality is in the differential diagnosis; establishing the presence and extent of emphysema in individuals with alpha-1antiprotease deficiency; and (with contrast) to evaluate possible pulmonary embolism in a patient with underlying COPD and acute decompensation.

    MRI scanning of the chest has its greatest utility in visualizing the mediastinum, trachea, and proximal large airways. The nature of the lung parenchyma, with its large air content, limits the applicability of MRI in imaging the lung parenchyma. Although current research in the field includes the development of functional imaging techniques in COPD, there is currently little role for chest MRI scanning in the evaluation and management of patients with COPD.

BLOOD TESTS

There are no specific blood tests that establish the presence or absence of COPD. Traditionally, it has been recommended to obtain an alpha-1-antitrypsin (also known as alpha-1-antiprotease) level in patients with a strong family history of COPD, patients presenting at a young age (<45–50), patients with basilar predominant emphysema, and patients with unexplained bronchiectasis and/or liver disease. More recent guidelines have recommended checking a level in every patient diagnosed with COPD. Those with a low A1AT level should be evaluated for replacement therapy and counseled concerning the genetics of Al AT deficiency. In patients with unexplained bronchiectasis, evaluation of IgG subclass deficiency (IgG2, IgG4), IgA deficiency, cystic fibrosis, and immotile cilia syndrome should be considered.

SUMMARY OF DIAGNOSIS OF COPD

Middle-aged or older patients complaining of unexplained or worsening dyspnea should be evaluated for COPD; this is particularly true of those individuals with a significant cigarette smoking history. For patients with mild to moderate disease, the physical examination may be relatively normal. Establishing the diagnosis requires consideration of COPD in the differential diagnosis and obtaining spirometry before and after bronchodilator. Spirometry alone is usually enough to establish the diagnosis; lung volumes and diffusing capacity provide additional information concerning degree of hyperinflation and emphysema and may be useful in situations where there is concern about the presence of an additional disease process (interstitial lung disease, weakness, neurologic disease), as part of preoperative evaluation for chest surgery, or in patients being considered for therapy specific for emphysema.

CONTROVERSIES CONCERNING SCREENING FOR COPD

Given that COPD has a strong association with cigarette smoking and that 20+% of lifelong smokers will develop clinically significant COPD, there is a school of thought that advocates performing spirometry on all middle-aged smokers regardless of the presence of symptoms. The logic is that identification of early airflow obstruction, prior to the onset of symptoms, will provide an opportunity for early intervention. The only intervention determined to influence the natural history of early COPD is smoking cessation. The available data are relatively limited, but those available do not establish that the knowledge of early signs of COPD results in a higher smoking cessation rate than smoking cessation interventions irrespective of spirometry results. The opposing school of thought reasons that (a) all smokers should be counseled to quit and provided appropriate cessation therapy regardless of the results of spirometry; and (b) the majority of smokers with normal lung function may be inappropriately reassured that they are not at risk for smoking-related disease(s). As a result, screening for COPD is not in widespread practice.

THERAPY FOR COPD

GOALS OF THERAPY

Treatment of any chronic disease has the goals of improving current symptoms, eliminating the disease or reducing the rate of progression, and reducing mortality. These combine to produce an improvement in health-related quality of life. In addition, the most desirable goal of therapy is to prevent the development of disease in the first place. COPD is somewhat unique in medicine, as the strategy to prevent development of disease in the majority of patients is very clear: prevent people from starting to smoke cigarettes.

Disease Prevention

As noted above, there is compelling evidence implicating cigarette smoking as the major risk factor for the development of COPD. There are data suggesting that there is (are) genetic predisposition(s) to develop COPD, and COPD is frequently cited as an example of gene–environment interactions. While the majority of patients with COPD are cigarette smokers (80–90+% in most series), the majority of smokers do not develop COPD.

    Given that cigarette smoking is a risk factor for disease development, it is logical to assume that smoking cessation will have a favorable impact on disease course. This hypothesis is supported by data from the Lung Health Study, which demonstrate that individuals with early airflow obstruction that are able to cease smoking experience an improvement in the rate of decline of lung function back to normal rates for age and reduced mortality in 15 year follow-up.

    Clearly, the most desirable approach is to prevent individuals from starting smoking. Public health campaigns have succeeded in reducing the proportion of US adults who smoke, but the prevalence of smoking in the US adult population is still approximately 20%. For such individuals who express a desire to quit, the current recommendations are to consider pharmacotherapy to aid in smoking cessation, based on reports that the chances of success are significantly improved with such therapy. Options for therapy are presented in table 33.3.

Table 33.3 PHARMACOTHERAPY FOR SMOKING CESSATION

THERAPY OF CHRONIC STABLE DISEASE

A variety of pharmacologic and nonpharmacologic therapies are available for COPD. Pharmacologic therapy includes medications intended to produce bronchodilation, antiinflammatory medications, mucolytics, antioxidants, and protease inhibitors. Although there is some controversy about their efficacy (discussed below), the majority of available data suggest that pharmacotherapy does not alter the rate of decline in lung function or mortality. Thus, they are best viewed as intended to improve current symptoms.

    Other available therapies include supplemental oxygen, surgical therapy, and pulmonary rehabilitation. Of these, supplemental oxygen and lung volume reduction surgery have been demonstrated to reduce mortality in appropriately selected patients.

    The algorithm published by the Global Initiative on Chronic Obstructive Lung Disease recommends a step-wise escalation of therapy with worsening airflow obstruction. These recommendations are summarized in Figure 33.5.

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