The pathology of influenza

by M. C. Winternitz; Frank P. McNamara; Isabel M. Wason

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.