Part 134

So that at the present time dysentery must be regarded as a malady which stands in closer relation to, or finds a better analogue in, cholera than typhoid fever; for cholera is a disease which has the same geography, has likewise nearly uniform symptoms and lesions, so far as it leaves any, and certainly has two distinct forms of origin--one clearly specific, cholera Asiatica, and the other catarrhal, cholera morbus.

PATHOLOGY.--Dysentery is a local malady, but, like every local malady if sufficiently severe, it may show constitutional effects. It is usually gradually ushered in from a lighter form of gastro-intestinal catarrh. After a stage of incubation which lasts from a few hours to a few days symptoms of dyspepsia and diarrhoea set in or increase, attended with anorexia, heartburn, nausea, eructation or borborygmi, pain in the abdomen, and copious fluid discharges. Hereupon ensue the pains and the discharges characteristic of the disease. Violent griping and colicky pains (tormina) traverse the abdomen, with sickening sensations of depression. The desire of evacuation of the bowels (tenesmus) becomes intense and more or less constant, and the discharge itself is attended with little or no relief. At the same time the region of the rectum, intensely inflamed, is the seat of intolerable burning pain, which becomes excruciating with the introduction of a speculum or the finger.

The discharges may be copious, dark-brown, thin, and highly offensive (bilious dysentery), may contain occasional hard round fecal casts of intestinal sacculi (scybalæ), or may become more and more scant, until with the most violent efforts only the minutest quantity is extruded of mucus, generally streaked or tinged with blood (rose mucus) like the rusty sputum of pneumonia. Later, all effort at emptying the alimentary canal may be futile (dysenteria sicca), or the mucus may be pure or commingled with pus to remain perfectly colorless (dysenteria alba), or with blood in larger quantity (dysenteria rubra). In other cases, or at other periods in the same case, the discharges consist of fleshy masses composed of inspissated mucus or pus, blood, and tissue-débris (lotura carnea). Sometimes, though rarely, the discharges consist of pure blood, but oftener of a copious turbid fluid, which on standing separates into a clear upper layer of serum and a sediment of disintegrated lotura carnea. Or, lastly, the sediment is composed of small round vitreous masses, evidently swollen by maceration to look like sago-grains, which have been erroneously supposed to represent the liberated contents of the intestinal follicles.

The general condition of the patient suffers correspondingly. There may be fever or there may be none throughout the whole course of the disease, but the pain and discharges quickly exhaust the strength of the patient, and in severe or long-continued cases lead to emaciation and profound prostration.

The skin is hot and dry; the tongue is heavily coated; the face wears an anxious expression. The abdomen is tumid with gases, or in more advanced cases sunken, discolored, and tender, especially in the course {797} of the colon, whose thickened walls may often be felt beneath the emaciated surface. The anus is spasmodically constricted, or in the worst cases paralyzed, patulous, and livid or blue. Prolapse of the rectum is common in children, and excoriation of the perineum by the acrid discharges is not infrequent.

Finally, a typhoid state may set in or a pyæmia occur, when the discharges may become involuntary or unconscious, and brain symptoms--insomnia, stupor, delirium, and coma--supervene; or the patient may linger long enough to perish by simple exhaustion or marasmus.

Under favorable hygiene the great majority of cases of catarrhal dysentery recover without special treatment in the course of from three to ten days, but specific dysentery has no definite duration and but little tendency to spontaneous cure. The worst cases are often quickly controlled by appropriate interference, and the most surprising results may be sometimes obtained in cases of even years' duration. On the other hand, a certain percentage of cases is characterized by a defiance to every kind of treatment, including the last resort, a change of climate.

An acute case of catarrhal dysentery generally subsides without lesions, and the natural duration of the attack may be much abbreviated by proper treatment. Specific or epidemic dysentery lasts from two to four weeks, or, becoming chronic, continues for years or for life, with exacerbations and remissions.

Various complications are liable to occur in the course of the disease. Three deserve especial mention--viz. affection of the joints (rheumatism), paralysis, and abscess of the liver. Perforation and peritonitis, always possibilities, and deformities of the colon, thickenings, and constrictions, are not infrequently left.

MORBID ANATOMY.--The lesions of dysentery are the ordinary signs of inflammation of a mucous membrane and its subjacent structures. They do not differ in any essential way from those of any mucous surface in a state of inflammation, the minor variations being due to differences in the anatomy and physiology of the part affected. Thus, a description of the pathological process in inflammation of the pharynx, bronchi, or uterus would answer upon the post-mortem table for the same process in the large intestine, and the finer microscopic lesions could be differentiated in any case only by the histology of the part affected.

A slight lesion of any mucous membrane constitutes what is known as a catarrhal process; a more grave affection, a diphtheritic process; a more chronic inflammation, a hypertrophic or hyperplastic process. Hence an easy distinction between sporadic and epidemic cases might be based upon the character of the lesion found. But, as has been stated already, it is impossible to draw a line between catarrhal and specific cases, the same lesions being found in either form. The difference, so far as the morbid anatomy is concerned, is wholly in degree or stage, and not at all in kind, the specific (epidemic) form presenting the graver lesion as a rule. So most cases of sporadic dysentery show only catarrhal lesions, while most cases of epidemic dysentery show diphtheritic lesions.

Catarrhal dysentery shows as its first obvious alteration a hyperæmia of the mucous surface. It is limited exclusively to the large intestine in the vast majority of cases, and only in rare exceptions affects the small intestine, though cases have been mentioned as curiosities in which the {798} process has reached the stomach in its upmost prolongation. The hyperæmia is most marked, as a rule, in the lowest parts of the large intestine, the rectum and descending colon, but there is, as Virchow has pointed out, a peculiar predisposition to affection at the seat of all the flexures, the iliac, hepatic, splenic, sigmoid, where the additional element of fecal arrest or impaction is superadded to the cause of the disease.

The catarrhal process occurs first in detached spots or streaks upon the projecting folds or duplicatures of the mucous membrane; which spots coalesce to form extensive surfaces. Examined by transmitted light, these surfaces show a distinct arborescence of the vessels. Or the disease may commence in the follicles in distinct areas of the large intestine, and may remain confined to these structures to constitute the variety known as follicular dysentery.

The hyperæmia of inflammation is attended with dilatation and paresis of the vessel-walls and retardation of the circulation. The whole process may be arrested at this stage, so that there escapes from the vessels, at most, only serum to develop the oedema which, with the defective nutrition from arrest of the circulation, gives rise to the softening of the epithelial cells. These cells may be thus lifted from their bed to constitute the process of desquamation, the fundamental anatomical characteristic of acute dysentery, by which process the submucous connective tissue is laid bare and the so-called catarrhal ulcer results. Or the epithelium, but partially detached, may remain upon the surface, "either raised in the shape of small vesicles which contain clear serum, or it forms a grayish-white layer resembling the mealy scurf of the epidermis--an appearance which probably induced Linnæus to term dysentery scabies intestinorum interna" (Rokitansky).

Kelsch maintains that the inflammatory process in dysentery commences in the delicate connective tissue between the follicles, the network of small spindle-shaped cells with multiple nuclei becoming speedily penetrated by a number of very small, newly-formed vessels. Where the epithelium is desquamated the surface is covered with granulations as after a wound. The disposition of the follicles is soon deranged, for, instead of standing in rows like gun-barrels, they are pushed asunder and uplifted, so as to remain at different heights. Their interior becomes blocked with mucus or their orifices occluded, so that retention-cysts are formed to give rise to the appearance of the bead necklace. Soon the walls of neighboring follicles coalesce, dissolve away, and communication is established between them. The interior of these communicating tubes or canals is filled with vitreous mucus; the walls are stripped of their lining cells, but their "blind extremities contain still adherent colossal epithelial cells." Moreover, the follicles break into each other under the proliferative budding process, so that the end of a distorted tube may be found in the interior of another. Where follicles are destroyed the mucous membrane above them or in their vicinity collapses--a condition observed and described by Colin as effrondement. The mucosa in these regions may appear perfectly uninjured, but by "blowing upon it with a tube it is lifted up like an ampulla to show an opening in its centre," though more frequently the mucous membrane collapses or sinks in at the region of destruction. The inner surface of the mucosa is rendered additionally uneven by the elevations or protuberances caused by the {799} proliferations in the submucous connective tissue. The older writers (Pringle, Hewson) regarded these projections as tumors of the mucosa, and Rokitansky, who describes their true nature, speaks of them as warty, tubercular (nodular) swellings or fungoid excrescences--constituting a condition, he says, which Gély has termed hypertrophie mamelonné. The alternate elevations and depressions thus produced have been likened to the representations of bird's-eye views of mountain-chains.

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 {800} 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 {801} 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.

But more extensive observation has developed the fact that the frequency of abscess of the liver in connection with dysentery is a peculiarity of tropical climates. In the temperate and colder regions of the North this complication is not by any means so frequent. Frerichs declares that of 16 observations collected by Louis and Andral, "ulcers were present in only 3, and in 2 of these cases the ulcers were tubercular; of his own 8 cases, there was intestinal affection in none." Gluck believes that the liver is more prone to show suppuration when already predisposed to it by a preceding amyloid or cirrhotic change of malarial origin. Eichhorst calls attention to the well-known fact that abscess of the liver is especially a disease of the tropics independently of dysentery, and the frequency of its occurrence here may be a mere coincidence. But it must be remembered that opportunity for post-mortem examination, upon the {802} results of which these statistics are based, does not occur in the great majority of cases of dysentery, and abscess of the liver is very often overlooked. Thus, Schneider cites cases where persons with abscess of the liver of the size of the head were considered simulants up to twenty-four hours before death. Since the diagnosis of hepatic abscess has been made so easy by aspiration, cases begin to multiply; and it is doubtless the experience of most practitioners, in the temperate zone at least, that the decided majority of cases of hepatic abscess acknowledge an existing or previous attack of dysentery. Certainly, few authors would now venture to subscribe to the view of Annesley, that the abscess of the liver was the primary malady and was the cause of the dysentery.

SYMPTOMATOLOGY.--Dysentery, as stated, begins, as a rule, with the general signs of a gastro-intestinal catarrh. So frequent is this mode of inception, and so few are the exceptions, that it is impossible to resist the conclusion that the disease is caused by the introduction of a noxious element into the alimentary canal. The irritation thus induced begins at the stomach, and is rapidly propagated throughout the whole tract of the intestine. In the course of a few days the cause of the disease becomes strictly localized to the large intestine, whose greater capacity and more sluggish movement fit it for the easier reception and longer retention of noxious matter.

But specific dysentery and the more intense forms of catarrhal dysentery occasionally exhibit distinctive symptoms from the start, and in rarer cases the disease is suddenly announced with such tempestuous signs as to excite the suspicion of poisoning. Thus, a case (one of five lighter cases) is reported from the Rudolfstiftung in Vienna (1878) where the disease closely simulated Asiatic cholera, and where it rapidly ran a fatal course, in spite of laudanum, soda-water, ice pills, mustard plasters, injections of amyl nitrite, camphor, and ether, and faradization of the phrenic nerve to stimulate the failing respiration. Finger reports similar cases from the hospital at Prague.