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

Abstract

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.