_Gross Picture._
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. XXXIX
and XL).
_Histological Picture._
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]
[Illustration:
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.
]
[Illustration:
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.
]
[Illustration:
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 common and 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. XII and
L), 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. XLVIII
and XLIX).
_Summary._
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.