Part 7

Sections from the least involved areas of the lung show a subsidence of the alveolar exudate and the walls are no longer intensely engorged. Perhaps the most prominent feature within the alveoli is the desquamated cells, presumably alveolar cells with broken or pyknotic nuclei. Despite the fact that so many cells of this type occupy the lumen of the alveolus, its wall has a prominent lining of cubical epithelium. Often mitotic figures abound in this new alveolar epithelial lining (Fig. XLVII), an evidence of rapid regeneration in that portion of the lung where the initial irritative process has subsided and where the destruction has not been as deep as elsewhere (79). This picture may be taken as positive evidence of an initial, diffuse, and general pulmonary involvement, which, with the subsidence of the primary reaction, is followed by localization resulting in the different types of consolidation now encountered.

FIG. XXI. AUTOPSY NO. 95. A TYPICAL APLASTIC ALVEOLAR EXUDATE COMPOSED Of RED BLOOD CELLS, FIBRIN, AND BACTERIA. COMPARE FIGURES XX, XXII, AND XXIII.

HELIOTYPE CO. BOSTON ]

FIG. XXIII. AUTOPSY NO. 175. NOTE THE ABSENCE OF ALVEOLAR EPITHELIUM, THE ENGORGEMENT OF THE VESSELS OF THE ALVEOLAR WALLS, AND THE SEROUS EXUDATE. ]

FIG. XXV. AUTOPSY NO. 92. THE EXUDATE CONSISTS ALMOST ENTIRELY OF A MASS OF RED BLOOD CELLS. THE DESQUAMATED ALVEOLAR EPITHELIUM IS SCATTERED THROUGH THE HEMORRHAGIC EXUDATE. COMPARE FIGURES XXIV AND XXVI. ]

However, in such areas of slight change, the bronchi and bronchioles may be distended and filled with polymorphonuclear leucocytes, exfoliated epithelium, and bacteria (Fig. X). It is, of course, possible that infection of the parenchyma may recur from these sources. Here the extent of involvement of the bronchiolar wall is variable and analogous to those described previously. Occasionally, too, where the alveolar change has subsided, the interstitial tissue, particularly that which divides groups of neighboring lobules, may retain its increased size with fibrous tissue framework spread apart by exudate and punctuated with an occasional circumscribed purulent mass (92, 95, 110, 156) (Fig. XXXVI). Such a miliary abscess within the lymphatics of the interstitial tissue may compress the neighboring air sacs, themselves entirely free of inflammatory involvement. That these strands of interstitial tissue, the conduits for the lymphatics, are important barriers against the spread of an inflammatory process from lobule to lobule by direct extension, is evidenced by the extreme variation in the amount and type of involvement in neighboring lobules (Fig. XXX). This variation is repeatedly encountered and the band of interstitial tissue, often prominent on account of its edema, separates these lobules the more clearly. In all probability, the sharp demarcation of the lobular consolidation as described in the gross picture depends upon the change in the interstitial tissue which tends to localize the infection (93). This fact suggests that the process within the pulmonary parenchyma spreads along the bronchial tree rather than from lobule to lobule.

Sections from those areas of the lung where the involvement is more marked may show a histological picture not unlike that described for the aplastic stage, but, in addition, there are groups of lobules where the exudate is typically purulent and pus cells not only form the greater part of the exudate in the lumen, but are prominent in the distended vessels of the alveolar wall (Fig. XXIX). Often these leucocytes are multilobed and frequently their protoplasm is granulated with phagocytized bacteria. The bacteria are also encountered free in the alveolus along with other elements; namely, red blood cells, strands of fibrin, or precipitated albumin (Fig. XXI). The bacteria, however, are not particularly conspicuous, for generally they are either single, in pairs, or in chains; and it is only when they become clumped to form large masses, often larger than any normal tissue cell, that they attract attention. When this appearance is encountered, the alveolar wall is no longer distinct and well preserved. Although the wall may still be made out, it often stains rather homogeneously and much of the finer architecture is lost in the thrombo-necrotizing process that has been instituted (Fig. XVII).

From this intermediary stage the picture of actual abscess with mortification of bronchiolar and alveolar tissue, as well as of the exudate itself, is readily approached (25, 48, 110, 140) (Fig. XXXI). In the necrotic mass that forms the center of such a focus, the most prominent feature is the bacteria. With hematoxylin they stain intensely as black, irregular masses, and their prominence is accentuated by the homogeneous staining qualities (with eosin) of the dead tissue, whether lung or exudate (Fig. XXXII). These abscesses may have central cavities which represent a discharge of their contents and may indicate the position of a bronchiole (Fig. XXXI). The necrosis of the alveolar walls, focal in its distribution as previously described, suggests itself as a forerunner of the more extensive necrosis encountered at this stage.

The most extreme form of mortification is seen in the wall of a gangrenous cavity, and several layers can be distinguished there. Beginning with that portion of the lung the least involved, the lesion may be limited to congestion of the alveolar wall with a serofibrinous exudate in the lumen, but this stage passes rather rapidly into another where cellular exudate, chiefly of polymorphonuclear leucocytes, predominates. Moreover, the leucocytes form not only the bulk of the alveolar content, but also distend the vessels and accumulate in the interstitial tissue around blood vessels and lymphatics. Passing toward the center of the gangrenous cavity, the lung rapidly changes in appearance. The blue zone of leucocytic infiltration makes more conspicuous the inner area of necrosis—where nuclei no longer stain and the alveolar wall is a homogeneous pink.

Gradually this phantom architecture, spotted only here and there with disintegrating polymorphonuclear leucocytes, ends in a ragged compressed border of a shaggy pink material which has no identifying qualities (Fig. XXXV). In the inner zone of pink an occasional vessel or, at times, a bronchiole more resistant to the process remains; frequently it is accentuated by the presence of partially destroyed polymorphonuclear leucocytes at its periphery. Probably these cells invade the necrotic areas along the sheath of the bronchus or vessel and not across the dead area. The thrombotic process described in the previous stage (Fig. LII) associated with an acute arteriolitis, may be associated with these gangrenous areas as well as with infarcts (82), but more likely gangrene is preceded by the acute diffuse necrosis of the alveolar wall which occurs in the fulminating cases. Furthermore, this is suggested where a typical grey hepatization is associated with marked thinning, but not actual disappearance, of the alveolar wall. Before concluding the description of this stage of the disease, mention should be made of the granular nodules of fibrin superimposed upon the swollen pleural cells and also of the older pleural exudate, either typically fibrinopurulent or more homogeneous with broken nuclear fragments (Fig. XXXVIII).

Summary.

In this stage of the disease the respiratory change is characterized by a localization of the inflammatory process with cellular invasion of the exudate. Pneumonia results, varying in extent from peribronchial to lobar, a pneumonia in which one of the most frequent complications is necrosis of the lung. Consequently, abscesses, even gangrene, are found.

(3) ORGANIZATION OF BRONCHIOLAR AND PNEUMONIC PROCESSES.

The processes described for the preceding group which involve not only the alveoli, but also the bronchi and the bronchioles, were predicted from the extensive hyalinization of these structures—a characteristic change in the more fulminating and acute phases of the disease. Likewise, it can be predicted that where death does not terminate the process such lesions will be followed by organization, which, by converting the exudate into scar, will produce deformities and offer serious mechanical interference with the ingress and egress of alveolar air and similar interference with the flow of blood through the pulmonary circulation (82).

FIG. XXIV. AUTOPSY NO. 92. AN ALMOST PURE HEMORRHAGIC ALVEOLAR EXUDATE. COMPARE FIGURES VI, XXV, AND XXVI. ]

FIG. XXVI. AUTOPSY NO. 103. THE LARGER ILLUSTRATION OF AN HEMORRHAGIC ALVEOLAR EXUDATE IS ELABORATED BY TWO HIGHER POWER DRAWINGS. THESE SHOW (1) AN ANEURSYMAL DILATATION OF A CAPILLARY IN THE ALVEOLAR WALL AND (2a) A RUPTURE OF THE CAPILLARY WALL WITH THE ESCAPE OF RED BLOOD CELLS INTO THE ALVEOLUS; (2b) NECROSIS WITH EARLY THROMBOSIS OF THE CAPILLARY IN THE ALVEOLAR WALL. ]

It is probable that chronic processes, not sufficiently severe to terminate fatally in a few weeks or months, may occur, but few examples of that kind have been observed. A total of twelve cases of our series in which organization of the bronchiolar (47), or alveolar exudate (156) was found, include three of the lobar, three of the pseudolobar, two of the lobular, and four of the peribronchial types. Such a differentiation, it will be understood, is purely arbitrary. The majority of the cases show, not only a reparative process, but also a continuance of the acute change, and, indeed, both gross and microscopic pictures of the lung may be complicated. It will be impossible to give an inclusive description of these changes, and therefore a few of the most diverse and characteristic will be presented in the form of case abstracts.

Autopsy No. 140.

A white female, aged 19 years, entered the New Haven Hospital after five days of fever, prostration, and cough. She was moderately cyanotic and dyspnœic, but examination of the lungs was negative except for a few râles at the right base. She was delivered of a six-months’ fœtus two days later. On the eleventh day of her illness, definite signs of consolidation had developed in the midback on both sides and spread gradually to include the left base and all of the right back to the level of the 4th dorsal spine. The temperature varied irregularly between 100°F. and 105°F. The pulse followed the temperature, but averaged 102 per minute, while the respirations remained about 40 per minute.

The white blood count on admission was 5,800, but rose gradually to 28,320 cells per cubic millimeter, with 90% of polymorphonuclear leucocytes. The patient died on the twenty-second day of the disease.

Post-mortem examination showed little of interest aside from the thorax. The left pleural cavity contained 75 cubic centimeters of slightly cloudy fluid. The right was almost completely obliterated by an organizing fibrinopurulent exudate which bound together the visceral and parietal layers. The left lung was partially collapsed and covered by a thickened pleura, bluish purple in color, which at the base and in the interlobar area was finely granular. Crepitation was present at the apex, the anterior surface, and the borders of the lung; elsewhere the consistency was increased. On section there was a frothy exudate from the apex and extreme base. These were deep red in color, while the intervening surface of the lung was paler, but broken by many small, white, elevated nodules which at first glance resembled tubercles (Fig. XXXIX). On close examination each of these was seen to have a small, depressed center from which pus could be expressed, and on dissection this was seen to be the wall of a bronchiole. The right lung was more voluminous and covered by a thick, grey, fibrinopurulent exudate except on the upper anterior border where there were a few small areas of interstitial emphysema. On section the pleural exudate was seen to be sharply demarcated from the lung parenchyma by a fine red line. The pseudotubercles of the other lung were here even more marked and from each exuded a yellow pus which partially obscured the pinkish-grey translucence of the surface (Fig. XL). The lumina of the larger bronchi were distended. The hilic and bronchial glands were enlarged and grey.

Microscopic examination of sections from the lung showed an extensive bronchopneumonia. The alveoli of an occasional group of lobules were filled with serum or red blood cells, while still other areas showed foci of necrotizing pneumonia, actual miliary abscesses in which there were large clumps of bacteria (Fig. XLI). Throughout the sections, however, the striking change was an organization of the exudate, which varied from a few fibroblasts to a well defined connective tissue almost obliterating the normal architecture (Figs. XLI and XLIV). The alveolar walls in some areas showed edema only, in others they were almost replaced by a thin line of fibrous tissue, and in still others, by a hyperplasia of the epithelium which almost filled their lumina. The bronchi exhibited similar changes, their lumina were filled with an exudate of desquamated epithelium and leucocytes, which in some places was organizing (Fig. XI), and there was a regeneration of epithelium evidenced by a piling up of the cells and the presence of mitotic figures in them. The interstitial tissue showed some edema. The tracheal epithelium was intact, but a few leucocytes and lymphocytes were scattered through the submucosa.

Pneumococcus Type II was recovered from the blood, pleural fluid, and lung. B. influenzæ was also demonstrated in the lung by smears and cultures.

In contrast to this example of a very diffuse, organizing pneumonia, associated with a marked peribronchial organization where the illness lasted for three weeks with hardly a remission throughout its course, the following example of necrotizing and organizing lobar pneumonia may be considered.

Autopsy No. 183.

A white male, aged 46 years, was admitted to the New Haven Hospital on January 9, 1919, complaining of “pneumonia.” The family history was unimportant. He stated that he was in the hospital twelve years ago with typhoid fever and again five years ago with acute cholecystitis.

His present illness began two weeks previous to admission with chills, fever, anorexia, nausea, vomiting, and a slightly productive cough. He was prostrated and drowsy, but could not sleep. On admission his temperature was 101.5°F., the pulse 124, and the respirations 34 per minute. He was cyanotic and dyspnœic. The right chest showed signs of consolidation, and fluid below the 3rd interspace. The white blood count was 8,200 cells per cubic millimeter, 89% being polymorphonuclear leucocytes. The patient died eighteen hours after admission.

The autopsy was held four hours after death and the essential findings were as follows:—