Andrew L. Ries
Chronic obstructive pulmonary disease (COPD) refers to a group of disorders that have in common the presence of persistent and progressive airflow obstruction that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lung to noxious particles or gases, primarily caused by cigarette smoking.
From the viewpoint of the pathologist, chronic bronchitis and emphysema are distinct processes, the former limited to the airways and the latter to the pulmonary parenchyma. From the viewpoint of the clinician, such a distinction is difficult for several reasons: (1) some degree of each may coexist in the same patient; pure forms of chronic bronchitis and emphysema are exceptions rather than the rule; (2) both are characterized by expiratory flow obstruction on simple spirometric testing; (3) patients with both processes often present with the same symptom—dyspnea on exertion; and (4) the presence of airway hyperreactivity (asthma, acutely reversible airways disease) in many patients with chronic bronchitis or emphysema further complicates the distinction. Faced with such complexities, it is understandable that the clinician often lumps together patients with chronic expiratory obstruction under the label COPD.
Nevertheless, distinct advantages are found in attempting to distinguish chronic bronchitis from emphysema, or at least to define the relative extent of each in a given patient. Such advantages relate particularly to the selection of therapy and to the natural history of these disorders, which is reflected in the individual patient’s prognosis. For example, recent studies have indicated that mucous gland hypertrophy and mucus hypersecretion—both hallmarks of chronic bronchitis—are not major factors in causing airflow obstruction. Attempts at distinction also are essential to determine the pathogenetic differences between chronic bronchitis and emphysema, although the dominant role of cigarette smoking in both is clear.
The confusion between chronic bronchitis and emphysema has been compounded by the manner in which they have been defined by various scientific societies, in different studies, and in different nations. In defining chronic bronchitis and emphysema, three options are available: pathologic, clinical, and physiologic. In fact, all three options have been used. This is not surprising because pathologic evidence is rarely sought (or advisable) while the patient is alive; the physiologic techniques that allow distinction are still not generally applied; and attempts to provide clinical definitions were useful when neither pathologic nor physiologic criteria were available.
Chronic bronchitis has long been defined in clinical terms. The most widely used definition is that of the American Thoracic Society, which defines chronic bronchitis as “a clinical disorder characterized by excessive mucous secretion … manifested by chronic or recurrent productive cough … on most days for a minimum of three months in the year and for not less than two successive years.” This clinical definition is now known to have serious deficits. First, other disorders with similar manifestations must be excluded, such as bronchiectasis, tuberculosis, and lung abscess. Furthermore, patients with predominant asthma or emphysema may fit this definition. Finally, many patients with pathologic or physiologic hallmarks of chronic bronchitis may not qualify under this definition (i.e., they do not cough).
If pathologic findings were used to define chronic bronchitis, the task would be relatively easy. Pathologically, the hallmark of chronic bronchitis is the hyperplastic and hypertrophied mucous glands found in the submucosa of large cartilaginous bronchi. The ratio of bronchial gland thickness to bronchial wall thickness (Reid index) is increased. The small airways (noncartilaginous bronchioles <2 mm in diameter) may also be involved, demonstrating mucous plugging, mural fibrosis and narrowing, goblet-cell hyperplasia, and inflammatory cell infiltrates. Thus, in the absence of parenchymal change, these findings in the airways would characterize pure chronic bronchitis.
Because such pathologic evidence is not conveniently available, much effort has been devoted to correlating pathologic data with physiologic tests. By physiologic testing, the pure chronic bronchitis patient should demonstrate
1. Relatively normal total lung capacity (TLC) with modest elevation of the residual volume (RV) and functional residual capacity (FRC)
2. Some degree of expiratory and inspiratory flow obstruction (both flows are abnormal because the airway lumen is narrowed)
3. Flow obstruction not acutely improved by bronchodilator administration
4. Significant disturbances of gas exchange producing hypoxemia because of ventilation–perfusion imbalance. Hypercapnia can develop with more severe disease
5. Normal diffusing capacity for carbon monoxide.
In contrast with the clinical description of chronic bronchitis, emphysema has long been defined in anatomic–pathologic terms. The widely used American Thoracic Society definition states that emphysema is present when there is “an anatomical alteration of the lung characterized by an abnormal enlargement of the airspaces distal to the nonrespiratory bronchioles, accompanied by destructive changes of the alveolar walls.” Thus, pure emphysema is a parenchymal (airspace) disease in which the bronchi are not involved. In recent years, high-resolution computed tomography has been used to detect emphysema based on anatomic changes in the lung parenchyma.
Pathologically, emphysema is characterized by disruption of the alveolar walls at some location within the acinus, which is the lung division distal to the terminal bronchiole that includes the respiratory bronchioles, alveolar ducts, and terminal alveoli. Depending on the dominant site of involvement, emphysema is defined pathologically as centrilobular (proximal acinar), in which the proximal part of the acinus is involved, or as panacinar, in which the whole acinar structure is involved.
A clinical definition of emphysema is lacking; if one did exist, it would be dominated by the historic finding of effort dyspnea.
Physiologically, patients with pure emphysema demonstrate distinct features:
1. The lung volumes show evidence of hyperinflation, namely, an elevated FRC, RV, and RV:TLC ratio. Often, TLC is increased. Early in the course of disease, vital capacity (VC) may be preserved (i.e., concomitant elevation in RV and TLC). With more severe disease, VC may be reduced in proportion to the elevation in RV when further elevation in TLC is limited by the chest wall. Such measurements are best made in a body plethysmograph, because the lung volume measured by gas dilution techniques (e.g., helium dilution, nitrogen washout) may underestimate the lung volume in emphysema due to airspaces that communicate poorly with the airways.
2. Significant expiratory flow obstruction is present with preservation of inspiratory flows. This observation is most dramatically demonstrated by flow–volume curves that show normal flow rates during inspiration but severely reduced flow rates on expiration.
3. Expiratory obstruction is not immediately improved by bronchodilator administration.
4. Elastic recoil is low (i.e., low pleural pressures exist at TLC and other specified lung volumes) and compliance is increased (i.e., small pleural pressure changes are associated with large increases in lung volume). These findings are the physiologic correlates of alveolar disruption and are the hallmarks of emphysema.
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