In the preceding description, the gross and microscopic anatomical changes in the lung have been discussed minutely. The picture presented persists, even though it becomes less intense, and forms a background upon which later variations may be superimposed. There is no justification for the opinion that the changes described are necessarily the most acute, but it is presumably correct to suppose that an aplastic, inflammatory reaction will terminate fatally more quickly than a cellular reaction (160), and upon this basis the sequential description in this narrative is arranged.
In the group of fatal cases of influenza, now to be discussed, the lesions of the pulmonary parenchyma are characterized by more definite lung consolidation. Thirty-nine examples presenting an average illness of ten days are included in the following description.
The external examination of the body includes nothing not described in the previous group.
FIG. XIX. AUTOPSY NO. 123. A SMALL AIR BUBBLE IN THE INTERSTITIAL TISSUE. COMPARE FIGUREXVIII.HELIOTYPE CO. BOSTON
FIG. XIX. AUTOPSY NO. 123. A SMALL AIR BUBBLE IN THE INTERSTITIAL TISSUE. COMPARE FIGUREXVIII.HELIOTYPE CO. BOSTON
FIG. XIX. AUTOPSY NO. 123. A SMALL AIR BUBBLE IN THE INTERSTITIAL TISSUE. COMPARE FIGUREXVIII.HELIOTYPE CO. BOSTON
FIG. XX. AUTOPSY NO. 90. THE ACUTE SEROFIBRINOUS EXUDATE INVOLVES NOT ONLY ALVEOLI, BUT ALSO SUBPLEURAL AND INTERLOBULAR BANDS OF CONNECTIVE TISSUE. COMPARE FIGURESXXI,XXII, ANDXXIII.HELIOTYPE CO. BOSTON
FIG. XX. AUTOPSY NO. 90. THE ACUTE SEROFIBRINOUS EXUDATE INVOLVES NOT ONLY ALVEOLI, BUT ALSO SUBPLEURAL AND INTERLOBULAR BANDS OF CONNECTIVE TISSUE. COMPARE FIGURESXXI,XXII, ANDXXIII.HELIOTYPE CO. BOSTON
FIG. XX. AUTOPSY NO. 90. THE ACUTE SEROFIBRINOUS EXUDATE INVOLVES NOT ONLY ALVEOLI, BUT ALSO SUBPLEURAL AND INTERLOBULAR BANDS OF CONNECTIVE TISSUE. COMPARE FIGURESXXI,XXII, ANDXXIII.HELIOTYPE CO. BOSTON
The fluid of the pleural cavities varies volumetrically as described in the preceding section. It is, however, usually not a clear fluid, but varies from a slightly turbid, blood-stained material to a typical purulent exudate. The cloudiness may be associated with minute flecks of suspended material, but in no instance has this fluid been of the thick inspissated type which formerly would have been designated as empyema.[8](This is mentioned with the knowledge that the term empyema is being applied now to less viscid, purulent, pleural exudates). The turgidity of the mediastinal tissue also persists, but it is very rare indeed to find anything more than a small amount of clear fluid in the pericardial sac. Only once was there a typical, fibrinous pericarditis with effusion, and this occurred where a most extensive pleural exudate was also present.[9]Where such complications have been described in serous membranes, the bronchial lymph glands, particularly at the hilum of the lung, are more involved and show, not only an increase in size and a red color on cross section, but frequently also focal areas of necrosis at the periphery, which appear as yellow patches and subsequently undergo suppurative disintegration (2, 47).
The lung remains increased in volume and its surface is mottled with vivid colors. Often these are an indication of deeper parenchymatous change. The pale pink zones, through the pleural surface of which distended alveoli are discernible, are still prominent in the upper lobe, around the margins, and on the anterior surface of the lung. The darker purple, slightly elevated, often circumscribed, infarct-like areas (25, 34, 108) may occur anywhere, but are more frequent in the lower lobes. Small, maroon, slightly depressed areas of atelectasis may also involve the borders of the lung, usually the posterior borders; or they may occur between larger and more elevated areas on either lobe. Besides the purple, firm, projecting foci, paler pink or grey nodules of similar consistence may be present and show no structure when viewed through the pleura. The distribution of the different types of change is variable, and, aside from the fact that they involve the middle and lower lobes more frequently than the upper, no general statement is possible. In a few instances, one lobe, almost always the lower, may be more voluminous than the others, and although its pleura often suggests lobular involvement, the masses tend to be confluent and suggest a pseudolobar change. Sometimes, though rarely, this approaches a true lobar type of consolidation. (Compare Figs.XIIIandXXVII.) Occasionally, the changes in the lung, except its increase in size, are obscured by pleural exudate which may form a thick, buttery, rather sticky mass on the surface (12, 19, 157) (Fig.XXXVII). Such pleural exudates are rare, and likewise it is uncommon to find so little pleural granulation as in the previous group. The roughening, as a rule, is not uniform, but is more prominent over the lower lobes and in the interlobar spaces than elsewhere. It may occur when there is no definite increase in the fluid content of the pleural sac.
The lung, now sectioned, presents a surface in accord with the changes suggested from the description of its external appearance. As compared with the first stage the amount of syrupy, blood-stained exudate may be definitely decreased, especially in the upper lobe or in those portions of the lung where the solidification is less marked. Its character, too, may be more cloudy, and more ropy, or viscid; it bathes the surface and is scraped off in abundance with the blade of a knife from the underlying consolidated foci (108, 156). The bronchi and bronchioles, however, may be prominent, irrespective of the change in the parenchyma itself. From their lumina, thick, yellow pus wells forth and their mucous membrane is intensely congested. Where such involvement occurs in unconsolidated portions of thelung, the bronchioles are even more striking than in the hepatized areas in which the more widespread changes obscure the process. The dilatation of the bronchioles, especially in their smaller ramifications, is still conspicuous.
The consolidated areas vary greatly in size and number;[10]often they are small and involve only single lobules, which now stand out as granular, generally elevated patches on the surrounding congested plane. Their color, as on the pleura, varies. They may be dark, almost hemorrhagic, fading through the reds, pinks, and greys. They may be firm, or, at the other extreme, honeycombed by small, often narrow, cavities, from which a material similar to that described on the surface wells forth. The latter change is more frequent if the consolidated area is large. It has occurred most often in the pseudolobar and in the lobar types of the process. The pseudolobar change is differentiated, not only by the confluence of more or less definite lobular patches and by its involvement of portions of contiguous lobes rather than a single lobe, but also by variations in the color and consistence of the different lobular foci. This is in contrast with lobar involvement where the entire lobe is affected by a uniform process usually at the same stage of development. Although the consistence may vary in different portions, usually the same color is present throughout. (Compare Figs.XIVandXXVIII.) In one instance where a solid, yellow lobe was found, its center contained an irregular, fresh blood clot (Fig.XVIII), which would be sufficient to differentiate this type of consolidation from that of respiratory disease in which the initial lesion is less destructive. Sometimes the softening in a hepatized lobule or group of lobules is much more evident, and the zone becomes divided by irregular channels filled with viscid, grey or brown material (108, 149, 162). When such a condition lies just beneath the pleural surface, it may be distinctly seen from without (Fig.XXXIII). The pleura bulges, the normal topography of the local zone is lost, and it appears as a dull, somewhat projecting, circumscribed patch, two or three or more centimeters in diameter, the surface of which has a more or less characteristic brown or brownish black opacity. As soon as this is sectioned there pours from the cavity the liquefied exudate in which the destroyed pulmonary parenchyma is mixed (Fig.XXXIV). Occasionally, strands of tissue still traverse the cavity, but, as a rule, it empties itself completely, and leaves a brownish black wall. The delicate, sweet but persistent and penetrating odor is not so marked as with typical gangrene.
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 FIGURESXX,XXII, ANDXXIII.HELIOTYPE CO. BOSTON
FIG. XXI. AUTOPSY NO. 95. A TYPICAL APLASTIC ALVEOLAR EXUDATE COMPOSED Of RED BLOOD CELLS, FIBRIN, AND BACTERIA. COMPARE FIGURESXX,XXII, ANDXXIII.HELIOTYPE CO. BOSTON
FIG. XXI. AUTOPSY NO. 95. A TYPICAL APLASTIC ALVEOLAR EXUDATE COMPOSED Of RED BLOOD CELLS, FIBRIN, AND BACTERIA. COMPARE FIGURESXX,XXII, ANDXXIII.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. XXIII. AUTOPSY NO. 175. NOTE THE ABSENCE OF ALVEOLAR EPITHELIUM, THE ENGORGEMENT OF THE VESSELS OF THE ALVEOLAR WALLS, AND THE SEROUS EXUDATE.
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 FIGURESXXIVANDXXVI.
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 FIGURESXXIVANDXXVI.
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 FIGURESXXIVANDXXVI.
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).
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.