As a rule, occasional red blood-corpuscles are also permitted to escape through the vessel walls in the process of diapedesis to give to the surface mucus its characteristic tinge, and punctate submucous hemorrhage is very frequently seen.
The pressure of the swollen, softened mucosa upon the sensitive nerves, and the irritation of the acrid intestinal contents, are often invoked to account for the constant desire of defecation (tenesmus) which constitutes such an essential symptom of the disease; but both the tenesmus and the colicky pains (tormina) precede the anatomical changes, and are much more rationally explained by the direct action upon the nerves of the cause of the disease, or by the derangement of innervation effected through changes in the circulation.
An acute case of catarrhal dysentery may exhibit no further lesions, and in the lightest cases even these may have entirely disappeared post-mortem, so that no change at all may be observed at the autopsy.
In a more severe or protracted case the other alterations which constitute the more complete cycle of the inflammatory process follow the stage of hyperæmia. The arrest of circulation becomes more or less complete, and the white corpuscles emigrate from the vessels to form the pus-cells. Fibrin, or the elements which compose it, also escapes to infiltrate the mucous membrane and remain upon its surface. The pseudo-membranous or diphtheritic process is now developed, and may vary in intensity from a mere frosting of the surface to dense infiltration of the entire thickness. The false membrane, as well as the mucous membrane, next suffers necrosis to form more or less extensive sloughs. These sloughs are grayish-white when fresh, dark-brown when stained by the intestinal contents, or greenish or black when undergoing gangrene. They may cover patches of the mucosa or the whole mucosa from the ileo-cæcal valve to the rectum. They soon become soft and pultaceous, hang in flaps or festoons in the interior of the intestinal tube, or, detached, are voided in fragments or shreds. One such fragment nine inches long is recorded in Woodward's exhaustive description of the pathology of this disease. Examined under the microscope, they are seen to consist of coagulated fibrin, red and white blood-corpuscles, epithelial cells and débris, necrotic pieces of mucosa, and myriads of micrococci and other micro-organisms.
The fall of the sloughs leaves the dysenteric ulcer. Its edges are irregular and ragged, its base uneven like a crater, and its surface is more or less covered with pultaceous débris. The submucous connective tissue may form its base, or, this structure having been also destroyed, the muscularis may be exposed, or in more extensive necrobiosis the peritoneum itself may be laid bare. Occasionally this last barrier is broken down, and perforation occurs. Or an acute peritonitis may be developed, in dysentery as in typhoid fever, by simple extension of the inflammatory process without perforation. Perforation is very rare in cases of follicular ulceration, and is by no means frequent in the diphtheritic process, but it is the most frequent cause of peritonitis in chronic dysentery. It may occur in any part of the colon, but does occur most frequently in the cæcum. The resulting peritonitis is fatal as a rule, but the danger is obviated sometimes, as in typhoid fever, by agglutination of the gut to a contiguous structure or viscus. Perforation usually occurs late in the disease, but it may occur very early. Thus Nägele reports from the Franco-Prussian War a case in which perforation took place on the fourth day, the diagnosis having been confirmed by an autopsy. In rare cases a perityphlitis may ensue, with its natural consequences, or periproctitis may be developed with perineal abscess, or, finally, fistulæ may form to burrow about and discharge themselves anywhere in or upon the surface of the abdomen, the lumbar region, or the thigh. Bamberger describes cases of perityphlitis attending dysentery, in some of which resorption occurred, while in others pus was discharged upon the surface of the abdomen; and the writer of this article once saw, in consultation with T. A. Reamy, a case of fistula which extended from the descending colon to the vagina. Through the opening made to discharge the pus from a fluctuating abscess pointing in the vaginal vault an india-rubber tube could be passed for six to eight inches. The patient finally died from marasmus.
Chronic dysentery is distinguished by the alterations which occur in inflammation developing more gradually and extending over a longer period of time. Under the irritative changes resulting from an altered circulation the connective tissue undergoes marked hyperplasia, so that the wall of the intestine becomes at times enormously thickened, and its calibre is often correspondingly diminished. Cornil observes that acute or subacute dysentery is characterized by infiltration of the submucous connective tissue, followed by destruction, while in chronic dysentery the predominant lesion is essentially a proliferation and thickening of the connective tissue of the large intestine. The muscular tissue also undergoes hypertrophy, and the peritoneum becomes thickened and opaque. Sometimes the peritoneum is covered with patches of false membrane, or agglutination occurs with other portions of the intestine to give rise to contortions or occlusions.
Ulceration shows itself in chronic dysentery in every grade and stage of the process, from the first denudations to old cicatrizations. In bad cases the whole course of the colon from the ileo-cæcal valve to the rectum may constitute one vast tract of suppuration. Blood-vessels may be opened by the necrotic process, and copious, even fatal, hemorrhage may ensue. When pure blood is discharged, the hemorrhage usually occurs in this way per rhexem, but the quantities of blood evacuated with other elements usually escape per diapedesem.
The cicatrization which results puckers the edges of the ulcers, and may in cases of extensive or circular ulceration lead to more or less stenosis of the intestinal tube. According to Rindfleisch, the scars of dysenteric ulcers are very prone to contract, so that "the liability of a subsequent stricture is directly proportionate to the extent of the previous ulceration." The danger in these cases may be immediate from entire, or more remote from partial, occlusion. Thus, Bamberger records a case of typhlitis due to impaction of feces above a stenosis gradually developed from a dysenteric ulcer.
Although dysentery is a disease of the large intestine, its lesions are not exclusively limited to this structure. It is always a purely local disease at first, and, strictly speaking, continues so throughout its course, yet it produces in severe or chronic cases widespread and general effects. Rapid emaciation sets in, and anæmia is soon pronounced in all the internal organs. The mesenteric glands show signs of irritation or of absorption of specific products in hyperæmic pigmentation and hyperplasia. The kidneys in acute cases exhibit venous stasis, and in chronic cases may undergo parenchymatous change. The joints are peculiarly liable to suffer in certain cases, and the nervous system may exhibit lesions—points to be described in the symptomatology of the disease. Should pyæmia occur, it superimposes its own particular lesions in the serous membranes and internal organs. All of these affections are to be regarded, however, rather as complications than essential effects.
But the liver is found affected so frequently in dysentery as to constitute more than a mere coincidence. Schneider has recently (1873) reported of the results of his observations on 1400 cases of tropical dysentery that in the 395 post-mortem examinations the liver was found normal in but 10 cases. The abnormalities were as follows: hyperæmia of various grades, 160; fatty degeneration, 62; abscess, 57; nutmeg liver, 47; perihepatitis, 25; granular atrophy, 19; syphilitic atrophy, 8; cicatrices, 6; excavation with helminth, 1. Bérenger-Féraud (1883) reports of 411 fatal cases of dysentery observed at Senegal that the liver appeared sound to the naked eye 98 times (23 per cent.) and diseased "undeniably" 313 times (77 per cent.). Of the 313 cases of hepatic affection there were found—hypertrophy, softening, or hyperæmia, 123 times (39 per cent.); abscess, 143 times (46 per cent.); simple discoloration, 29 times (9 per cent.); atrophy or cirrhosis, 18 times (6 per cent.). Annesley found abscess of the liver 21 times in 29 cases of dysentery; Hospel, 13 times in 25 cases; and Budd found ulceration of the large intestine 10 times in 17 cases of hepatic abscess. Gluck had the opportunity of making 28 post-mortem examinations in 151 cases of dysentery in Bucharest, finding abscess of the liver 16 times. All these authors adopt the explanation first offered by Budd of direct transfer of diseased products through the mesenteric and portal veins.