THE RADIOLOGIST AND OBSTRUCTIVE AIRWAY DISEASE

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Abstract
1. There has been a marked increase in reported deaths from chronic bronchitis and emphysema in recent years, to a point where they now account for as many deaths as carcinoma of the lung. Perhaps of greater importance is their serious economic impact, respiratory disease comprising the most important cause of work incapacity and restricted activity in both the U.S.A. and the U.K. Control thus becomes a vital aim of the medical profession. In this selective review of the subject of obstructive airway disease, an attempt is made to place in proper perspective the role of the radiologist in this control. 2. In recent years, intensive research has revealed the prominent place occupied by the peripheral airways in the pathogenesis and pathophysiology of obstructive pulmonary disease. Since early peripheral airway disease is potentially reversible, and since it is known that once a patient with chronic obstructive pulmonary disease develops symptoms he will usually manifest progressive deterioration, control must be directed towards early recognition of obstruction in small airways. 3. Chest roentgenograms are virtually always normal at a stage when disease is potentially reversible. Thus, it is evident that in the present state of our knowledge, the radiologist can play no useful role in early recognition and therefore in the control of the disease. This being the case, the responsibility of the radiologist lies in the recognition of already established disease so that institution of appropriate therapeutic measures might prevent complications or control reversible elements. 4. The recent literature pertaining to the site of airway obstruction has been reviewed. It has been shown that the peripheral airways—2 mm. in diameter or less—contribute only a small fraction to total pulmonary resistance from the alveoli to the mouth, and that extensive obstruction of these airways may have little effect on specific measurements of airway resistance or indeed on indirect assessment of resistance by measurement of FEV. In view of these limitations, it has been necessary to devise new techniques for the identification of early disease of small airways, Three such techniques have been developed which offer much promise: frequency dependence of compliance; Xe133 studies of ventilation and perfusion; and most recently, closing volume. Although only preliminary investigations have been carried out, it appears probable that the estimation of closing volume—a simple, inexpensive laboratory procedure—will become a valuable aid in the diagnosis of early small-airway disease at a stage when standard tests of pulmonary function are still normal. 5. Although the radiologist, employing plain roentgenographic studies, can play no useful role in diagnosis at this early stage, research currently in progress offers some hope that in vivo roentgenographic visualization of bronchioles may permit assessment of the dynamic behavior of the small airways. Structures as small as alveoli have already been visualized through a combination of tantalum bronchography and either primary roentgenographic or electronic magnification, and their dynamic changes measured during inflation and deflation of the lungs. It is entirely feasible that such techniques will permit correlation of the dynamic activity of small airways roentgenographically with physiologic studies of airway closure and the closing volume phenomenon. 6. The roentgenographic appearances of uncomplicated chronic bronchitis are inadequately documented, but it is probable that the major function of radiology in this condition is to exclude other diseases (such bronchiectasis) which may mimic it clinically. 7. In 3 large reported series of patients with chronic bronchitis, the chest roentgenogram was considered normal in less than 50 per cent. However, it is highly probable that this figure is much too low; if one were to obtain roentgenograms of the chest of a number of cigarette smokers, picked at random from passers-by on the street, each of whom satisfied the clinical criteria for the diagnosis of chronic bronchitis, it is very likely that the great majority would show no changes suggesting that diagnosis. Abnormalities, when present, are relatively non-specific and highly subjective: prominence of lung markings (the "dirty chest"); and overinflation. Work in progress suggests that bronchial wall thickening as assessed from bronchi visualized end-on in the parahilar zones may aid roentgenologic discrimination of the chronic bronchitic from the normal. 8. In chronic bronchitis without emphysema, the presence of overinflation of the lungs as assessed from roentgenograms exposed in full inspiration is difficult to equate with physiologic observations, since function-test values for total lung capacity are characteristically within the predicted range and the elastic properties of the lungs are normal. It is suggested that reports of roentgenographic overinflation could be due to over-reading of the roentgenograms, function-test underestimation of TLC, the presence of unrecognized emphysema, or a combination of these. 9. It is emphasized that chronic bronchitis is not a roentgenologic diagnosis; changes may be observed on the plain chest roentgenogram which suggest that bronchitis may be present, but it is inappropriate for the radiologist to do other than indicate that the findings are compatible with or suggestive of that diagnosis. 10. In a review of the morphologic and roentgenologic characteristics of pulmonary emphysema, it has been shown that the roentgenologic diagnosis is highly accurate in cases of severe disease and reasonably precise in those of less severity. The roentgenographic signs of morphologically proved disease consist in 2 distinctly different patterns, "arterial-deficiency" (AD) and "increased-markings" (IM). If only the traditional criteria of emphysema are recognized—general pulmonary overinflation and oligemia—many patients with severe emphysema who manifest the IM pattern roentgenographically will not be recognized, including those with clear-cut evidence of pulmonary hypertension and cor pulmonale. 11. Although the relationships are by no means complete, there is some indication that patients who manifest the arterial-deficiency pattern roentgenographically have panlobular emphysema morphologically and present clinically as "pink puffers;" and that those who show the increased-markings pattern have centrilobular emphysema and present as "blue bloaters." It is probable that the latter represent the severe chronic bronchitic with cardiac decompensation described in the U.K. Which label one wishes to place on this roentgenographic pattern of disease is probably more of semantic than of practical importance; its pathologic characteristics are unclear at present and are the subject of some debate among morphologists. Whether or not the pathophysiology of the disease is related to the presence of emphysema requires to be clarified by the pathologist and need not engender dispute among radiologists. In view of the uncertainties surrounding its fundamental nature, it is recommended that this pattern of obstructive airway disease be designated by the radiologist as "the IM pattern of COPD" or alternatively "the chronic bronchitic pattern of COPD with arterial hypertension." 12. In patients with chronic obstructive pulmonary disease, studies of the dynamic behavior of the larger airways by cinebronchography, combined with simultaneous recording of pressures and flows, have revealed 2 levels of obstruction: one in the small airways is relatively fixed, present during both inspiration and expiration and but little affected by changes in lung volume; and the other in the large airways is highly variable, present only during expiration and markedly increased at low lung volume. Expiratory flow in patients with COPD may be limited by large airways, small airways or both. Segments that limit flow can be identified by assessment of the dynamic activity of the tracheobronchial tree cinebronchographically; the caliber of segmental bronchi changes only slightly when flow is limited by the lobar bronchus, but reduces significantly when the small airways limit flow. 13. Finally, it has been speculated that the following chain of events may constitute the pathogenesis of chronic obstructive airway disease (excluding the influence of proteolysis): (a) ciliary paralysis associated with increased mucus production leads to chronic cough; (b) disproportionate collapse of large airways limits the effectiveness of cough, leading to the retention of secretions; and (c) retention of secretions results in mucus plugging, recurrent episodes of bronchiolitis, and eventual fibrous obliteration—"small-airway disease." An additional factor, replacement of the normal surfactant lining of small airways by mucus, may result in instability, premature closure, and air-trapping.

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