Early in the disease the congestion and the hemorrhages that have been described in the mucous membrane of the nasopharynx (14 and 94) are also conspicuous features in the lining of the trachea and bronchi (Fig.I). This membrane is swollen, turgid, red, and covered by a copious, mucous exudate which may be clear, but much more frequently is blood-stained or opaque and yellowish in color. The blood, variable in amount, may be fresh and red; and after the mucous exudate on the surface is removed, more intense red foci stand out on the congested base (47, 90, 157). Frequently, as the bronchi are approached, the red color of the mucosa becomes more intense and may have a garnet tinge. Membranes such as are encountered in the more usual necrotizing inflammatory processes, like diphtheria, have not occurred in the trachea and larger bronchi in this series (108, 128, 157).[3]The exudate peels off readily, and as indicated above, leaves a velvety red surface,dotted here and there with darker or more intensely red foci. Small ulcerations of the mucosa occur, but are inconspicuous (82, 156). As the finer ramifications of the bronchi are approached, the accumulation of the exudate in their lumina becomes more and more marked, and on cross section of the lung, they often stand out conspicuously on account of their increased size and projecting, seromucous, blood-stained content (101, 149, 162).
It is remarkable how long this picture in the trachea and bronchi may persist without showing any marked variation. It is encountered, not only in the most acute and fulminating types of the disease (that have been examined), but a similar picture may be present in cases which end fatally only after a period of weeks of severe illness. In the latter cases, however, the exudate, particularly in the bronchioles, assumes a more purulent character and after this accumulation is wiped away from the surface of the tube, the intensity of the dark red color of its lining membrane presents an even more striking contrast on account of the opaque, yellowish-green exudate in the lumen. At this stage, too, the bronchioles are more distended with pus, which oozes from each one when the lung is sectioned (1, 108, 110). In the cases still more chronic, the terminal bronchioles may be sharply outlined with a thick grey wall which surrounds the dilated opening from which the accumulated yellowish exudate oozes as soon as the pressure is relieved (Figs.XXXIXandXL).
The changes are less marked, perhaps, in the trachea than in its finer ramifications. The mucosa is constantly more or less destroyed and large areas, usually focal, are entirely devoid of their epithelial covering. This is replaced by a sparse exudate, composed largely of red blood cells, mucus, a small amount of fibrin, and nuclear fragments (Fig.II). It may dip into the submucosa for a short distance, but usually these indentures are associated with the ducts of the mucous glands into which the inflammatory reaction extends. A more striking feature than the exudate, however, is the edema and the congestion of the submucosa. The loose areolar tissue of the submucosa is spread widely apart, and throughout it distended blood vessels are very conspicuous. Occasionally such a vessel is broken and actual hemorrhage appears in the submucosa. Occasionally, too, the inflammation extends down the duct to the mucous gland itself, and here, also, aplastic inflammatory reaction is evident, inasmuch as the acini now stain intensely red with the cells undifferentiated from each other and specked here and there by broken remains of the dead nuclei (Fig.III). After the disease has continued for a short period, even at the end of five or six days, some regeneration of the epithelial lining may be seen (3) (Fig.IV). But despite this, the acute picture persists, and there goes on, side by side, an attempted repair characterized by epithelial regeneration and the same evidence of acute change. Since the lesion is essentially a superficial one, scars or contractures of any extent are not encountered in the trachea, even in examples of the disease that have ended fatally only after many weeks.[4]
FIG. VIII. AUTOPSY NO. 97. ALTHOUGH THE EPITHELIUM IS STILL VISIBLE AS A HYALINE BAND LIFTED FROM THE UNDERLYING MUCOSA, BOTH MUCOSA AND SUBMUCOSA ARE INVOLVED IN A NECROTIZING PROCESS. BACTERIA ARE ABUNDANT IN THE DEAD TISSUE.
FIG. VIII. AUTOPSY NO. 97. ALTHOUGH THE EPITHELIUM IS STILL VISIBLE AS A HYALINE BAND LIFTED FROM THE UNDERLYING MUCOSA, BOTH MUCOSA AND SUBMUCOSA ARE INVOLVED IN A NECROTIZING PROCESS. BACTERIA ARE ABUNDANT IN THE DEAD TISSUE.
FIG. VIII. AUTOPSY NO. 97. ALTHOUGH THE EPITHELIUM IS STILL VISIBLE AS A HYALINE BAND LIFTED FROM THE UNDERLYING MUCOSA, BOTH MUCOSA AND SUBMUCOSA ARE INVOLVED IN A NECROTIZING PROCESS. BACTERIA ARE ABUNDANT IN THE DEAD TISSUE.
FIG. IX. AUTOPSY NO. 105. THE NECROTIC EPITHELIUM IS INVADED BY POLYMORPHONUCLEAR LEUCOCYTES AND THESE, AS WELL AS ROUND CELLS, CAUSE A THICKENING OF THE BRONCHIOLAR WALL.
FIG. IX. AUTOPSY NO. 105. THE NECROTIC EPITHELIUM IS INVADED BY POLYMORPHONUCLEAR LEUCOCYTES AND THESE, AS WELL AS ROUND CELLS, CAUSE A THICKENING OF THE BRONCHIOLAR WALL.
FIG. IX. AUTOPSY NO. 105. THE NECROTIC EPITHELIUM IS INVADED BY POLYMORPHONUCLEAR LEUCOCYTES AND THESE, AS WELL AS ROUND CELLS, CAUSE A THICKENING OF THE BRONCHIOLAR WALL.
FIG. X. AUTOPSY NO. 106. THE SMALL BRONCHIOLE IS FILLED WITH PUS CELLS, WHICH, IN SOME PLACES, EXTEND THROUGH ITS WALL.
FIG. X. AUTOPSY NO. 106. THE SMALL BRONCHIOLE IS FILLED WITH PUS CELLS, WHICH, IN SOME PLACES, EXTEND THROUGH ITS WALL.
FIG. X. AUTOPSY NO. 106. THE SMALL BRONCHIOLE IS FILLED WITH PUS CELLS, WHICH, IN SOME PLACES, EXTEND THROUGH ITS WALL.
There is considerable evidence to support the view that the disease spreads from bronchus to bronchus, and in keeping with this view, various stages in the inflammatory processes are more readily determined in these smaller structures than in the trachea. Furthermore, it must be emphasized that even the mildest and the most extreme of these stages are not infrequently encountered in the same lung. The earliest lesion is manifested by an increased homogeneity of the protoplasm of the epithelial lining of the bronchus. The cell protoplasm loses its normal granulation and the nucleus, somewhat darker than usual, becomes conspicuous on a red base (Fig.V). In the lumen of such a tube a serous exudate, perhaps mixed with mucus, is encountered, and there is some spreading apart of the surrounding muscular tissue with engorgement of the vessels. This picture merges gradually into one where the epithelium appears as a homogeneous, red-staining ribbon, devoid of nuclei, often exfoliated, in part at least, from the underlying submucosa (92). The change is traceable through the larger bronchi, even to the ducti alveolares, and not infrequently, bacteria, either as a diffuse, minute dotting or in the form of circumscribed, colony-like formations, are spread through the red, ribbon-like strand (Fig.XVI). With the exfoliation of the epithelial lining, the submucous vessels become more and more conspicuous and may bulge into the lumen of the tube (Fig.VI). That they actually weep into the lumen is proved by the presence of red blood cells in the exudate, now rich in mucus, broken-down nuclei, and desquamated cells. The necrotizing process may not extend deeper than the epithelial lining as is the status described above (140, 162), but it also frequently involves the underlying submucous and muscular layers, so that these lose their identity and stand out as homogeneous masses, in which fragmented nuclei and bacterial accumulations are prominent. Such deeper necrotizing areas may be focal (Fig.VII), or may involve the entire circumference of the tube (Fig.VIII). Occasionally, the epithelium, now dead and staining homogeneously, is lifted from the underlying submucosa in the form of a blister (66), and has very much the same appearance as the well known, early reaction which follows the application of croton oil to the rabbit’s ear. Where this occurs, the submucosa is less involved, as though the necrotizing agent had not penetrated to the same depth and the serous reaction beneath were actually a beneficent exudate. These blisters are in contrast with the deeper areas where the fibrinous mass, mixed with the dead tissue, forms an intensely staining ring or band, which extends through the bronchiolar wall even to the surrounding alveoli.
In the early stage of this process one of the most outstanding features is the absence of polynuclear leucocytes in the reactionary process, but gradually as the dead tissue sloughs away, these cells wander into the exudate and form a purulent ring, more intense in the lumen, but extending for a variable distance through the still viable wall of the structure (47) (Fig.IX). Later mononuclear cells accumulate in this wall and occur either as a diffuse mottling or as circumscribed foci in the muscle and submucous layer of the bronchiole, just as they do in the trachea. Occasionally, a striking change is found in a small bronchiole within a portion of the lung which is otherwise uninvolved by an inflammatory process. Perhaps the alveoli were the seat of a change which has subsided, but, whatever the history, the purulent mass in the bronchiole and involving its wall, stands out effectively (Fig.X).
Sooner or later, with the subsidence of the irritating agent, repair begins in the bronchus or bronchiole. If its walls have been destroyed and the lesion has extended into the surrounding alveoli to form an abscess of greater or lesser extent, or if the necrotizing process has been superficial and confined to the epithelium in large part, the reparative process is very much the same. Mitotic figures in the fibroblasts and in the endothelial cells of the capillaries abound in the young granulations (Fig.XI). However, the granulation tissue does not have an unrestricted path of growth, for if a remnant of epithelium remains, this is stimulated to grow probably in this disease as in no other. Mitotic figures are commonand the young epithelial cells stretch across the denuded submucosa or granulation (Fig.XLVIII) and extend downward into the surrounding alveoli, not only as strands, but also as solid nests of cells (47) (Fig.XLIX). The bronchioles, therefore, show changes dependent upon the extent of the damage suffered by their walls. The vast majority, in all probability, will be restored; but if the wall has actually been necrotized, the bronchioles may be converted into small, saccular, bronchiectatic cavities (48, 110, 162) (Figs.XIIandL), or obliterating bronchiolitis may result from the organization of the exudate within their lumina (82) (Fig.XI). The importance of the epithelial proliferation cannot be ignored; in many cases, it invades the surrounding lung tissue and a typical, histological picture results—an infiltrating, malignant, epithelial neoplasm (Figs.XLVIIIandXLIX).
The lesions of the trachea and of the larger bronchi, even though they persist in their acute form for a period of weeks, are superficial and do not lead to extensive or deep scarring. In contrast to the larger respiratory passages, that portion of the bronchial tree which is not supported by cartilaginous rings becomes more and more intensely involved, not only on its surface, but in its deeper structures, and the changes in the bronchioles and the neighboring air sacs are among the more characteristic anatomical manifestations in this disease. Therefore, while it will be unnecessary to refer again to the larger air passages, further consideration of the smaller ones, which are constantly associated with the lesions of the pulmonary parenchyma, will be included in the subsequent discussion of the pulmonic involvement.