The changes which take place subsequent to the stage of gray hepatization, and the modifications due to age, remain to be considered.
Croupous pneumonia may terminate—1, in resolution [recovery]; 2, in suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5, and very rarely, in chronic (fibroid) pneumonia.
1. During resolution the lung is moist, lighter than in the stage of hepatization, has a yellow or yellowish-green color, and still shows a marked loss in elasticity. On section, the lung appears to be non-granular, and a tenacious, puruloid fluid escapes when the section is pressed upon. Some oedema may still remain. When examined under the microscope the alveolar capillary vessels are seen to have returned to their normal calibre; the alveolar epithelium is restored; the cells in the air-sacs are degenerated, broken down, and resolved into a detritus. The degeneration of these cells is both fatty and mucoid, and the coloring matter of the blood gives origin to the granular pigment which is scattered throughout the disintegrated and liquefied mass. Some of the pigment is supposed to come from the connective tissue between the alveoli. In this condition the alveolar contents are either expelled by expectoration or undergo absorption, the lung being finally restored to its normal condition.
2. When purulent infiltration or suppuration of the lung occurs, its surface becomes yellow—more so than in any of the preceding conditions; it is soft, moist, and friable, and gives somewhat the sensation of an abscess. It is well described as miry.7
7 Pneumonia, Sturges, 1876, pp. 110, 113.
On section, a diffluent, purulent fluid exudes from a surface whose yellow color is due both to the large number of cells which are undergoing fatty degeneration, and to the anæmia which results from over-distension of the alveoli with these cell-elements.
When examined under the microscope, the cells are found not only crowding the alveoli, but infiltrating the inter-alveolar tissue. This corpuscular infiltration of the alveolar walls may so interfere with their nutrition that they will undergo softening and degeneration. Whether these cells (in all respects resembling pus-cells) have emigrated from the blood-vessels or are the result of epithelial changes is still unsettled. Reason and analogy seem to point to a dual origin. Now and then these cells are pigmented. Occasionally the alveolar walls become thinned, indistinct, and finally rupture.
There has been much discussion over the term suppuration of the lung, but the appearances reported by those who uphold, as well as by those who protest against, the term are identically the same, all agreeing that the "lung is filled with pus."
3. Abscess of the lung, as a termination of croupous pneumonia, is exceedingly rare, and is always preceded by extensive cellular or interstitial oedema; small abscesses are formed by the rupture of several of the alveolar septa. It may follow purulent infiltration. These abscesses vary in size from that of a pea to one which may occupy the greater part of a lobe. They may have a thick, well-defined, irregular wall, their interior being crossed by shaggy shreds of broken-down lung-tissue, or they may form irregular excavations in softened lung-tissue. They may be single or multiple. Several abscesses are often found in the same lobe. They increase in size by peripheral growth or by fusion of several small abscesses.
Abscesses are more common in the upper than in the lower lobes; their frequency is variously estimated as 1 in 30 or 60 cases. These pus-cavities, if of small size, may ultimately close by cicatrization, in which case they may open into a bronchus of sufficient size to allow of the discharge of their contents. Under such circumstances the contents of the abscess are expectorated; interstitial inflammation is set up around their site, which after a time encloses them in a firm connective-tissue wall; contraction ensues, and finally only a line of cicatricial tissue marks their former situation. Or if no such bronchial opening occurs, the abscess becomes encapsulated in firm cicatricial tissue, and the contents undergo cheesy and calcareous transformation. Sometimes these abscesses perforate the pleura and discharge their contents into the pleural cavity, causing pyo-pneumothorax. External fistulous openings have occurred, but they are a rare termination of pulmonary abscess.