Here, as in the discussion of the involvement of the lymphadenoid
tissue, the most outspoken changes are in the thorax. Frequently thrombi
are encountered in the vessels of the lung (34, 138). This does not
include the capillary thrombi associated with damage to the alveolar
walls already discussed. It has not been possible to demonstrate an
association between the hemorrhagic, infarct-like foci in the lung and
these vascular complications (47). The thrombi, histologically, are most
frequently propagated, but occasionally an indication of their etiology
is found in a destructive lesion of the vessel wall (19, 47, 50, 108,
156). This arteritis or phlebitis may be embedded either in a pneumonic
zone or in relatively normal lung. The vessel wall may be obscured by a
cellular infiltrate throughout its circumference or only at one point.
The cells, on account of karyorrhexis often difficult to identify, are,
partly at least, polymorphonuclear leucocytes, and the thrombus which
forms upon the inflammatory nucleus, as a rule, is fairly rich in these
cells (Fig. LII).
This vascular lesion may involve either artery or vein and may be found
either within the lung or at distant points. Not infrequently, pulmonary
embolus terminates influenza. One instance of this is incorporated in
the group of chronic influenzal cases detailed above (Fig. LIII). In
this instance, the thrombus originated in the right iliac veins; and,
although no attempt was made to demonstrate the primary vascular lesion,
so many similar cases are recorded (7, 82), and vascular damage is so
frequent in this disease, that the hypothesis attributing pulmonary
embolus to a thrombus initiated by a phlebitis is strongly supported.
Parenchymatous and skeletal lesions of hemorrhagic type, although
variable quantitatively, are frequent and involve the muscles, the
parenchymatous organs,—the adrenal especially,—and the mucosa of the
alimentary canal. They have been described already with regard to the
pleural surface and they may occur in other serous membranes.
[Illustration:
FIG. XXXII. AUTOPSY NO. 100. A HIGHER MAGNIFICATION OF THE LESION
ILLUSTRATED IN FIGURE XXXI. THE ALVEOLAR WALL IS ENTIRELY NECROTIC:
BACTERIA AND POLYMORPHONUCLEAR LEUCOCYTES ARE ABUNDANT.
]
[Illustration:
FIG. XXXIV. AUTOPSY NO. 87. CROSS SECTION THROUGH THE AREA OF GANGRENE
SHOWN IN FIGURE XXXIII.
]
[Illustration:
FIG. XXXV. AUTOPSY NO. 160. MICROSCOPIC DRAWING OF THE GANGRENOUS
CAVITY ILLUSTRATED IN FIGURES XXXIII AND XXXIV.
]
Only two examples of hemorrhage in the recti muscles[11] were
encountered in the ninety-five autopsies. In other localities this
lesion has not only been more frequent but also more extensive (2, 47,
50, 128, 140, etc.). However, it has been fortunate that the two
instances in this series represent a fresh hemorrhage and the healing
lesion, respectively. The fresh hemorrhage is quite characteristic of
Zenker’s necrosis involving muscles. Grossly, it is a small lesion and
does not involve the entire width of the rectus muscle, as may happen,
with a resulting rupture of this structure (12, 162). Microscopically,
many of the muscle cells have lost their striation, are irregularly
swollen, and, as fractures in them indicate, are apparently brittle.
Between the muscle fibers and where these are lacking, the predominating
element of exudate is the red blood cell, but there is a considerable
amount of fibrin and also some serum between these cells (Fig. LVI). The
absence of polymorphonuclear leucocytes is noteworthy. The second
example of a muscular lesion occurred in a patient who died on the
twenty-fifth day of the disease. Grossly, this also was a small lesion,
although the muscle fibers at its site were obviously ruptured.
Histologically, the lesion is a healing one. Regeneration of the muscle
fibers (47, 156), as illustrated by the formation of typical spindles,
is handicapped by the rapid development of the fibrous scar (Fig. LVII).
Suppuration had not occurred and this also has been true for the focal,
hemorrhagic, inflammatory processes which were encountered in many
different localities throughout the body.[12]
Perhaps the focal hemorrhagic lesions were most frequent in the adrenal
gland. Generally, they were located in the cortex, although medullary
hemorrhages were encountered. The extent of the process varied from
minute hemorrhages, associated with necrosis of only a few cells, to
extensive ones involving half of the adrenal. The microscopic
examination of the exudate revealed the same elements and in
approximately the same proportions as described for the similar process
in the muscles. Not infrequently, mitotic figures in the adrenal cells
indicated an attempt at repair of a minute damage.
Hemorrhages in the mucosa of the alimentary canal, including the stomach
and intestines, similar to those so common at the post-mortem table in
many different types of acute infectious disease, are, of course, common
in influenza; but, in one case especially, a lesion was encountered
which adds significance to these hemorrhages (47). Here areas of mucosa,
usually round or oval and varying from one-half to two centimeters in
diameter, often with ulceration in their centers, show, microscopically,
bacterial emboli in the vessels of the mucosa with a hemorrhagic
effusion which obliterates the architecture of this coat and extends at
some points into the submucosal and muscular layers (Fig. LVI). Here,
the occurrence of bacterial emboli in association with the lesion
suggests that they may be etiologically related to similar processes in
other parts of the body.
The above example of hemorrhage in the mucosa of the alimentary canal
has seemed of especial interest, not only for its possible value in
explaining the etiology of the lesion here and elsewhere, but as an
interpretation of the findings in Autopsy No. 185, an abstract of which
is appended below. There a hemorrhagic lesion in the wall of the urinary
bladder led to rupture and brought the patient to the surgical clinic of
the hospital.
_Autopsy No. 185._
A white female, aged 46 years, was admitted to the New Haven Hospital on
January 4, 1919, complaining of “cough and headache.” Five days
previously she had a “cold” that she was able to “break up” with quinine
and aspirin. The “cold” recurred two days ago, and since then she has
had “frequent chills, aches all over, and feels weak.” Her family and
past histories were unimportant.
Physical examination on admission showed congestion of the pharynx.
Below the inferior angle of the scapula on the right, there was
dullness, bronchovesicular breath sounds, and a few fine râles. The
examination was otherwise negative. Three days later the signs in the
lungs disappeared. The next day, after an attack of coughing, she
complained of something having “burst” within her abdomen and of
generalized abdominal pain. A diagnosis of ruptured bladder was made and
1,400 cubic centimeters of bloody urine were withdrawn by catheter.
Immediate operation was decided upon and the bladder was found a hand’s
breadth above the symphysis pubis; the posterior wall was very thin and
presented a tear extending from the trigone upward in the mid line for 7
centimeters. Fully 500 cubic centimeters of clotted blood and urine were
removed from the pelvis, but there was no marked evidence of
peritonitis. A permanent mushroom catheter was placed in the urethra,
and the tear was sutured. The abdomen was closed with provision for
drainage. The patient was returned to the ward in doubtful condition.
Her temperature at entrance was 104°F., and it fell by lysis to 99°F.
just before operation. After the operation it fell to 97°F., and in a
few hours rose to 99°F. Thirty-six hours after operation she had a chill
lasting ten minutes, and her temperature rose to 105°F. in eight hours,
when death occurred. The respirations were thirty per minute until the
rupture of the bladder when they rose to forty per minute and
corresponding to the final rise in temperature rose to 60 per minute.
The pulse ran a parallel curve to the temperature, ranging from 100 to
160 per minute.
The autopsy was held two hours after death, and the essential findings
were as follows:—
The body was that of a moderately obese woman. Rigor mortis had not
developed, but there was a distinct heliotropic hue of the face and
neck. The recent surgical wound between the symphysis pubis and
umbilicus was in good condition. The peritoneum was slightly dulled in
the lower half of the abdomen, and there was about 100 cubic centimeters
of faintly cloudy, blood-tinged, thin fluid in the pelvis. The left
pleural cavity contained about 200 cubic centimeters of slightly turbid,
amber fluid, but the right side was free from fluid. While the pneumonia
had not been prominent clinically, both lungs were found extensively
involved by a necrotizing and organizing bronchopneumonia with purulent
bronchitis similar to what has already been described. As the lesion of
the bladder is the distinctive one in this case, and as the other organs
show nothing that has not been described elsewhere, further description
will be confined to it.
The wall of the bladder was thin and soft, and grossly the sutured wound
appeared in good condition. Posteriorly there was a hemorrhagic zone
about 3 centimeters in width most marked beneath the mucosa, but
involving all of the coats. The mucosa was superficially ulcerated along
this area, and was covered by a thin, patchy, fibrinous exudate. In
addition, there were scattered beneath the mucosa several smaller
hemorrhagic foci, quite distinct from the larger one.
Microscopically, one striking feature was the erosion of the mucosa,
with hemorrhages most marked along the line of rupture but occurring
elsewhere in the subjacent tissues. This condition was found in all the
sections studied. Another feature was the lack of inflammatory exudate
and the very slight attempt to repair the injury, only a very rare
polymorphonuclear cell and fibroblast being seen. Sections of the
peritoneum showed only a patchy deposit of fibrin with a rare
polymorphonuclear cell.