When the fatal illness has lasted more than two weeks, abundant new formation of fibrous tissue occurs in a zone surrounding the dilated bronchus. Adjacent alveolar walls are thickened by young fibrous tissue. Alveoli, much diminished in size, are filled by hyaline fibrin into which fibroblasts and newly formed blood vessels have penetrated. These changes are limited to a wide zone in immediate contact with the dilated bronchus, whereas at a greater distance alveolar walls have undergone no thickening and alveoli contain no fibrin.
Fig. 19.—Acute bronchiectasis; the bronchial wall indicated by engorged mucosa shows a varying degree of destruction, fissures extending into and through the bronchial wall. Autopsy 352.
Fig. 20.—Acute bronchiectasis; with destruction of bronchial wall exposing alveoli filled with fibrin; peribronchial fibrinous pneumonia is seen about several bronchi present in the section; Gram Weigert fibrin stain. Autopsy 425.
This stage is well represented by Autopsy 421 after an illness of nineteen days. Bronchiectatic cavities, from 3 to 6 mm. in diameter, are numerous in sections of the lung; their lumina are irregular in outline and often irregularly stellate. Microscopic examination shows the presence of clefts which interrupt the bronchial wall at intervals throughout its entire circumference. The original wall is well indicated by the very richly vascularized connective tissue containing scattered muscle bundles and is infiltrated with lymphoid and plasma cells in great number. Where fissures have occurred the adjacent edges of the interrupted wall have separated from one another, leaving a wide interval where underlying alveolar tissue is exposed. Two changes tend eventually to render the fissures inconspicuous, namely, regeneration of epithelium and new formation of fibrous tissue. Exposed alveoli filled with fibrin are in process of organization and epithelium which has assumed a squamous type has grown down over the exposed surfaces of the interrupted bronchial wall. It has begun to cover or in some instances has completely covered the surface of rents entering alveoli plugged with fibrin (Fig. 21). In the periphery of the bronchus alveolar walls are thickened and infiltrated with lymphoid and plasma cells. The same changes affect bronchi containing cartilage which is undergoing atrophy.
The reinforcement of the fissured bronchial wall by new formation of fibrous tissue, by thickening of the interalveolar walls and by organization of fibrin within the alveoli is well shown after four weeks (Autopsy 425; Fig. 28). There are spherical bronchiectatic cavities more than a centimeter in diameter surrounded by a dense fibrous wall in which are atrophied alveoli lined by epithelium of cubical form. Occasionally, the fibrous wall is interrupted and alveoli, plugged with organizing fibrin, are in immediate contact with the lumen. When these plugs of fibrin which are slowly absorbed disappear, evidence of preexisting rents in the bronchial wall are lost, and there are in this lung bronchiectatic cavities of which the wall is a continuous circle of dense fibrous tissue.
Fig. 21.—Bronchiectasis with fissures extending through the bronchial wall into alveolar tissue which is the site of fibrinous pneumonia; epithelium has grown down into these fissures and has covered the exposed surfaces. Autopsy 463.
