Secondary Lobule Research Articles

Pulmonary tuberculosis and centrilobular emphysema. The "upright theory" of apical localization.

<h3>Introduction</h3> Emphysema may be defined as dilatation of respiratory air spaces with destruction of the intervening septa. Understanding of the pathologic anatomy of emphysema has been greatly enhanced by studies of inflation-fixed lung specimens carried out over the past two decades. We have recently reviewed the literature on this topic¹and will not do so here. Briefly, two major anatomic patterns have emerged from these studies. They have been named centrilobular and panlobular emphysema on the basis of their localization in the secondary lung lobule of Miller.²Centrilobular emphysema presents as a focal area of air space dilation located at or near the center of the secondary lobule; the air spaces at the periphery of the lobule tend to be preserved till the disease is far advanced. The process has been shown to start with dilation of the respiratory bronchiole with subsequent involvement of adjacent air spaces. Panlobular

The Circulation of the Secondary Lobule of the Human Lung

Microscopic dissection of corrosion models of normal human lungs permitted us to make the following observations: 1. The capillary networks of the alveoli of the secondary lobule derive their blood supply in one of three ways. (a) From branches of the arterial vessel entering the secondary lobule together with the bronchiole. These vessels supply primarily the central core of the lobule. (b) From branches of vessels on the surface of the secondary lobule. These branches may penetrate to the level of the respiratory bronchioles. They supply primarily the alveoli of the peripheral zone of the secondary lobule as well as alveoli on the surface of the lobule. A variable number of alveoli on the surface of the secondary lobule are supplied directly from the vessels located in the tissues betwen secondary lobules. 2. Extensive anastomoses exist between the capillary networks derived from the same parent vessel as well as between capillary networks derived from different types of parent vessels. 3. Several patterns used in the formation of capillary networks have been described. 4. The physiologic importance of the multiple blood supply to the secondary lobule and the richness of the anastomoses between vessels feeding the capillary networks and between the capillary networks themselves, has been discussed.

Panlobular Emphysema: Anatomy and Pathodynamics

Based upon the structural concept of the secondary lobule of Miller, it is apparent that a common anatomic pattern of emphysema involving principally the terminal air ducts and sacs may be recognized on a localized or generalized basis. This form of emphysema we have labelled the panlobular type, as the entire secondary lobule of Miller shows overdistension and air sac rupture, and in advanced cases uniform bullous fields. An accompaniment of advancing degrees of emphysema is the presence of numerous alveolar fenestrations of major importance in the progression of this form of irreversible lung distension. Panlobular emphysema is a morphologic denominator common to such heterogeneous conditions as primary kyphotic chest deformities, localized hilar scleroses or neoplastic states producing laryngeal or large bronchial airway deformities and congenital lobar emphysema. Less well-defined is the airway obstruction in chronic bronchitis and bronchiectasis observed in many cases of established panlobular emphysema. An additional emphysematous group without structural bronchial deformity was also found. These were usually associated with lesser degrees of emphysema. Bronchial disturbances may produce not only an obstructive airway mechanism leading to air trapping, but indirectly influence surface tension phenomena within the lung or impair clearance of entrapped pollutants and in this way initiate erosion of the air sac membranes. Hypertrophy of the right ventricle was a frequent companion of established cases of generalized panlobular emphysema. The air-to-blood exchanging surface—the pulmonary contribution to homeostasis—is progressively destroyed through alveolar sac dissolution with the concurrent loss of the perfusing lung bed being responsible for the common clinical manifestations of cor pulmonale. Other determinants involved in the development of cor pulmonale are pathologic by-passes from artery to vein, bronchopulmonary shunting particularly in emphysema with fibrosis and a decompensating portal azygos-pulmonary vein system. These morphologic findings reflect the primary importance of the pulmonary-cardiac disease in the natural history of this form of emphysema.

The secondary lobule in the adult human lung, with special reference to its appearance in bronchograms.

The secondary lobule in the adult human lung, with special reference to its appearance in bronchograms.

The histology of generalized pulmonary emphysema. II. Diffuse emphysema.

SUMMARYThe evolution of morphological changes in the air passages from the early focal lesions of emphysema to those associated with the clinical disease is presented.Progress of the focal lesions leads to involvement of the whole of the secondary lobule, at which stage the emphysema is no longer focal but “diffuse”. This diffuse change occurs at different stages of development of the focal lesions in different lungs ; the morphological evolution of both early and late change is described along with some of the more common intermediate forms.Observations supporting the hypothesis of pathogenesis of emphysema presented in Part I of this paper have been made, and the hypothesis is extended to account for diffuse change. These diffuse lesions are aggravated by bronchospasm and, relatively late in the morphological evolution of the disease, by expiratory collapse of bronchioles. The emphysematous changes themselves, in turn, aggravate this last factor.The hypothesis of pathogenesis is reviewed, and morphological evidence is correlated with several aspects of physiological observations on alterations of lung function in the disease.The relation of chronic bronchitis to emphysema is analysed in view of these observations, and it is concluded that chronic bronchitis cannot be said to “cause” emphysema, but, rather, both are related by way of the common factor of inflammatory disease of the bronchioles.

The histology of generalized pulmonary emphysema. I. The genesis of the early centrolobular lesion: focal emphysema.

SUMMARYThe histological appearances of structural changes in air passages in the early lesions of generalized pulmonary emphysema are presented. The earliest lesions were found in respiratory bronchioles and alveolar ducts near the middle of secondary lobules ; one form was an acute lesion associated with bronchiolar obstruction proximally, whereas the other was “ chronic “, with no evidence of recent change or obstruction.The chronic form evolved either towards diffuse emphysema or towards macroscopically visible focal emphysema in which sharply localized dilated air spaces occupy the middle of the lobule.An hypothesis of origin of these early subclinical lesions is presented. It rests on two propositions : first, that distending forces exist in patent air passages beyond an obstruction (particularly in those just distal to such an obstruction) and that these forces have a disruptive effect ; second, that obliteration of bronchioles, due to past inflammation, occurs diffusely and extensively in emphysema, even in these early examples. Both phenomena have been shown to be closely related to acute bronchiolitis (McLean, 1956b, 1957) so that the disease is regarded as a sequel of repeated incidents of acute bronchiolitis, progressing more rapidly when such incidents are severe or prolonged.This hypothesis is consistent not only with pathological observations on the emphysematous lung but also with morphological, clinical and physiological observations concerning the broader subject of the evolution of inflammatory disease of the bronchioles.Concurrently, the nature of the black pigment of the lung and its relation to focal emphysema were examined. It was concluded that, in most cases, part of this pigment is endogenous hæmosiderin derived largely from the hemoglobin of cells found in the exudate in acutely inflamed respiratory bronchioles and branches. Evidence that part is carbon rests on less conclusive evidence, although it is not denied that inhaled carbon can contribute to this pigmentation. Excessive retention of carbon or hæemosiderin in the peripheral passages was considered to result in accentuation of the focal form of emphysema.

Intrapulmonary septal lymphatic lines (B lines of Kerley): Their significance and their prognostic evaluation before mitral valvotomy

One hundred and thirty-four patients with mitral disease and subjected to cardiotomy have been reviewed with reference to their pulmonary artery and capillary pressures, effort disability, presence of B lines and post-operative progress. Anatomical, pathological, and theoretical evidence is presented to determine the causation of the B lines seen on chest radiographs. They are caused by an increase in the radio-opacity of the septa between the peripheral pulmonary secondary lobules, usually due to œdema and lymphatic dilatation. Their visibility on the chest radiographs of patients clinically selected for mitral valvotomy is a very favourable prognostic sign.

The morbid anatomy and histology of asbestosis

The result of dust inhalation in pulmonary asbestosis is different from that seen in other dust diseases owing to the peculiar long needle-like shape of the asbestos particles. The fibrosis is diffuse, and the nodules characteristic of silicosis are not seen. The variation of conditions in the asbestos industry reders it probable that as time goes on unusual forms of asbestosis will occur. In the pleura the disease is marked by the obliterative nature of the process. The lung of the uncomplicated case as seen in the post-mortem room is characterised by dense blue-black areas corresponding to the secondary lobules, surrounded by thick bands of interlobular connective tissue, generally with a reddened background of terminal bronchopneumonia in the less affected portions of the lung. The naked-eye signs of disease in other organs are few.

The X-ray Shadows of Secondary Infection in Lung Tuberculosis

ON account of the physical conditions in the lungs, their radiologic densities are susceptible of finer analysis than are those of any other part of the body. Further, nothing in this field is of more interest and value than the differentiation, whenever possible, of lesions caused by tuberculosis from those produced by other infections. It is well recognized that there are no pathognomonic physical signs of lung tuberculosis; however, radiologists believe that their particular contribution to the physical examination of the chest, when skillfully interpreted, will more accurately indicate the nature of a lesion, as well as its location and extent, than will any other part of that examination. Since the criteria which the clinician accepts in physical findings as suggesting tuberculosis and those which point the radiologist to this conclusion are based on the same fundamental anatomy and pathology, there should be no antagonism. The radiologist must always remember that his contribution to the physical examination is supplementary, even on those occasions when the supplement, like a woman's postscript, furnishes the real meat of the examination. The fundamental investigations of Miller and Dunham, many years ago, regarding the architectural structure of the lung, the method of invasion by tubercle bacilli and the pathology produced pointed the way to our subsequent observations that tuberculous infection and infection by other bacterial invaders produce different kinds of shadows in the lung field. If we will base our interpretations upon the fundamental investigations of Miller and Dunham, to which there have been no material additions, we will be in position to differentiate etiological factors with a reasonable degree of certainty. It is our belief that wherever we have departed from the fundamentals mentioned and interpreted shadows as tuberculosis, without proper regard for the underlying pathology which must produce such densities, we have been out on the thin ice of conjecture and have too often been wrong in our conclusions. We know that tuberculosis invades lung tissue through the lymph channels; therefore, that the infection first surrounds the lobules, because the lymphatic vessels enclose each anatomical lung unit very much as a fishnet holds its contents. The smallest visible tuberculous lesion, therefore, is the dim outline of a secondary lobule, with its congested lymphatics and beginning granulomatous consolidation. Such a lesion is essentially parenchymatous, and since the lung parenchyma fills all the space between the hilus and the pleura, the tuberculous density may occur anywhere in this lung field. The lesion has a definite relation to the bronchial tree, and this relation can be traced by the striation densities which mark the blood vessels accompanying the bronchi.