The spleen is very large (14 × 11 × 5 cm.) and firm.
The spinal fluid is cloudy and blood vessels over the lumbar enlargement and lower thoracic region are congested; in the upper thoracic region the cord is covered by purulent exudate.
Bacteriologic examination demonstrates the presence of hemolytic streptococci in the blood of the heart; plates from the left lung contain a few colonies of S. aureus and Pneumococcus IV; plates from the right main bronchus contain S. aureus and a large bacillus which does not stain by Gram’s method. Three plates from the spinal meninges contain Pneumococcus IV.
Fig. 25.—Advanced bronchiectasis throughout lower left lobe. Autopsy 445.
Microscopic examination shows that the cavities which have been described are lined by very vascular connective tissue containing many cells; there is no epithelial lining and the surface is in places covered by fibrin. On the surface polynuclear leucocytes are numerous, but immediately below, large mononuclear cells occur and frequently contain one or several ingested polynuclear leucocytes. None of the structures peculiar to the bronchi can be identified in the wall of these cavities, and in many places it is evident that lung tissue has undergone destruction, for in places the lining of vascular connective tissue is interrupted and an extension of the cavity penetrating into the lung substance is surrounded by alveoli filled with fibrin; in contact with the cavity there is some necrosis.
The cavities communicate with the bronchi and are lined in part by vascular connective tissue which may in part represent preexisting bronchial walls, but no epithelium is present and the relation to the bronchi cannot be established with certainty. These cavities have extended by necrosis which has broken the vascular connective tissue of their wall and penetrated into adjacent lung tissue. Death has been the result of purulent meningitis caused by pneumococcus, and the histologic changes in the walls of the cavities suggest that the activity of the inflammatory reaction here is subsiding, for large mononuclear cells are numerous and are ingesting polynuclear leucocytes. The changes described would, if continued, result in the formation of cavities lined by fibrous tissue and resembling many of those formed as the result of dilatation of the bronchi.
A study of the progress of the changes which result in the formation of bronchiectatic cavities has shown how the inflammatory irritant within the bronchus destroys the epithelium of the bronchus, penetrates into the deeper tissues and produces fissures which extend through the entire thickness of the bronchial wall at one or usually several places. These longitudinal fissures, which at first often give a stellate outline in cross section to the cavity of the affected bronchus, permit the separation of the edges of the fissure, so that an increase in the circumference occurs. The base of the fissure is formed by surrounding alveolar tissue and its edges are the site of necrosis. Tears may extend into the surrounding alveolar tissue, thus permitting further stretching of the bronchial wall. The consequences of rupture of the small bronchi into the adjacent alveoli are to some extent overcome by the inflammatory reaction which plugs the adjacent alveoli with fibrin.
Compression of the lungs by forced expiration, even though the glottis were closed as in coughing, would not dilate the bronchi, because pressure outside and within the bronchi would be equally elevated (Thornton and Pratt[[89]]). The pressure within the bronchi does not differ greatly from atmospheric pressure, whereas the negative pressure within the pleural cavity may vary from approximately 6 mm. of mercury during quiet inspiration to 30 mm. with forced inspiration. Excess of pressure upon the inner surface of the bronchial walls will vary with coughing and other respiratory efforts, between these limits depending upon the readiness with which pressure is equalized within and without the bronchi by penetration of air into the alveoli. The presence of viscid mucopurulent fluid within bronchioles will obstruct these tubules and retard the entrance of air into alveoli.
Weakening of the bronchial wall by the changes which have been described will cause lasting dilatation of the bronchi. Whatever increases pressure within the bronchi will increase the tendency to dilatation; the bronchi being filled with mucopurulent exudate dilatation usually appears first at the bases of the lung, since gravity increases intrabronchial pressure here. New formation of fibrous tissue within the wall of the bronchus, thickening of adjacent alveolar walls, and organization of fibrin reinforce the weakened bronchial wall and limit the dilatation which follows injury to the wall. Regeneration of epithelium covering the dilated tube will further obscure the early changes which have made dilatation possible. The changes which weaken the bronchial wall permit dilatation at a time when there is no new formation of fibrous tissue. When the bronchial lesion has persisted several weeks, chronic pneumonia is associated with it. It has been suggested that the contraction of newly formed fibrous tissue within the substance of the lung might cause bronchi to be enlarged by traction upon their walls. Newly formed connective tissue is most abundant in the wall of the bronchiectatic cavity, and here contraction would tend to diminish the size of the cavity.