B. LESIONS OF THE BLOOD VESSELS AND ELSEWHERE IN THE BODY
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.
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.
FIG. XXXIV. AUTOPSY NO. 87. CROSS SECTION THROUGH THE AREA OF GANGRENE SHOWN IN FIGURE [XXXIII].
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.