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.
Ordinarily, the peculiar pains of dysentery first proclaim the
character of the disease. The severe grinding, twisting pains, tormina,
are more or less localized in the course of the colon, and hence
surround or traverse the entire abdomen, the pains at the epigastrium
being due to spasmodic contractions of the transverse colon. The
patient in vain adopts various postures in relief or sits with his
hands firmly compressing the abdominal walls. The tormina are more or
less intermittent or remittent, and are usually experienced in greatest
severity toward evening. During their acme the face wears the aspect of
the intense suffering, which is expressed in outcries and groans. At
the same time there is upon pressure over the whole abdomen more or
less tenderness, which soon comes to be especially localized at the
cæcum or sigmoid flexure.
The tenesmus (cupiditas egerendi) is a more distressing, and certainly
more distinctive, sign of dysentery. It is the feeling of heavy weight
or oppression, of the presence of a foreign body in the rectum, which
demands instant relief. At the same time intense heat is felt in the
rectum, which the patient likens sometimes to the passage of a red-hot
iron. The desire of evacuation becomes as frequent as urgent. In
well-marked cases the patient sits at stool half an hour or an hour at
a time, straining until faint {803} and exhausted, leaving the commode
with reluctance, only immediately or very soon to use it again.
Great depression is felt at the stomach at the same time, with nausea,
occasionally with vomiting; and strangury, with the discharge of only a
few drops of scalding urine or blood from the bladder, adds additional
suffering to the disease. Retraction of the testicle and prolapsus ani,
especially in children, are prone to occur in severe cases.
But neither the pain nor the prostration is so characteristic of
dysentery as the stools, which, though of very varied nature, are
nevertheless distinctive. After the discharge of the intestinal
contents the first evacuations consist of mucus in the form of glairy,
stringy matter, like the white of an egg, expressed as the result of
the violent efforts at straining. The mucus may be pure or tinged with
blood, but it is usually very scant in quantity, and stands in this
regard in marked contrast with the violence of the efforts to secure
its extrusion. It is the frequency of its discharge which constitutes
an especial distress. Twenty to forty, even two hundred, times in the
twenty-four hours the patient must go to stool. In the worst cases the
patient sits at stool or lies upon the bed-pan the most of the day.
The mucus is sooner or later mingled with pus or stained with blood.
The presence of pus by no means necessarily implies the existence of
ulceration, as the apparently pure mucus always shows occasional white
blood-corpuscles under the microscope, and even extensive suppurations
occur without apparent solutions of continuity.
The presence of blood is equally characteristic of dysenteric stools.
Usually it is intimately commingled with the mucus or pus or forms the
chief element of the copious so-called bilious discharge. The
evacuation of pure blood indicates erosion of vessels low in the colon,
often in the rectum itself, though enormous quantities of blood are
sometimes voided from unbroken surfaces. Thus Lécard reports the case
of a soldier who "while sitting restless at stool lost one and a half
quarts of blood." The patient died on the fifth day of the disease, and
at the autopsy there was found "apoplectiform congestion from the
ileo-cæcal valve to the anus, but no ulcers anywhere, nor any broken
vessels."
Besides the mucus, pus, and blood, the dysenteric stools contain the
sloughs which have been torn off by violent peristalsis in cases of the
diphtheritic form. Usually they are separated in shreds and fragments,
but occasionally large sheets, even casts of a section of the colon,
are voided en masse. These were the cases considered by the older
authors to be detachments of the mucous membrane itself. As already
observed, these fragments consist for the most part of inspissated
mucus, pus, blood, and tissue-débris; but there is no doubt that in
some cases partially necrosed mucosa also enters into their
construction. One enormous tubular cast fourteen inches long, preserved
in our Army Medical Museum, was found to be "composed of
pseudo-membranous lymph in which no traces of the structure of the
mucous membrane could be detected" (Woodward).
There still remains to be mentioned the boiled-sago or frogs'-spawn
matter whose origin has given rise to such a curious mistake. Not
infrequently these vitreous-looking bodies compose the bulk of the
sediment in the stools of dysentery, and even some of our modern
authors, {804} unacquainted with the more searching investigations of
Virchow, have regarded them as expressed contents of intestinal
follicles. Virchow found that under the application of iodine they
always assumed a blue color, whereupon he ironically remarks that the
sago-like mucus is really mucus-like sago. They are simply granules of
starch ingested as food, to remain partially or wholly undigested.
The scybalæ, the composite matter known as the lotura carnea, and the
micro-organisms found in the stools have already received mention
elsewhere.
Although the stools of dysentery are scant, as a rule, they are so
frequent as to discharge during the entire twenty-four hours a very
large quantity of albuminous matter. Oesterlen has made the curious
calculation to show that the mean daily loss of albuminates in
dysentery of moderate intensity is from 50 to 60 grammes during the
first fourteen days, and on an average about 20 grammes during the next
eight days. The total loss experienced in an attack of three weeks'
duration thus amounts to about 1000 grammes--in rough figures, two
pounds avoirdupois. The rapidity with which emaciation, hydrops, and
marasmus occur in severe cases is thus easily accounted for. Nägele
speaks of cases where patients were reduced to skeletons in eight to
fourteen days, so that the convalescence extended over six weeks to
eight months.
The alteration in the character of the secretion in dysentery is not
confined to the mucous membrane of the large intestine. On the
contrary, all the digestive juices are changed, in some cases entirely
checked. In the graver cases the saliva takes on an acid reaction and
loses its glycogenic properties; the gastric juice in the same cases
becomes alkaline and loses its peptonizing properties; while the
secretion of the bile is wholly arrested. Uffelmann, who had the rare
opportunity of studying the secretion of bile in a case of biliary
fistula, relates that during an attack of dysentery the bile ceased
entirely to flow, and only began to show itself again, at first
greenish, then greenish-brown, finally brown, during the process of
resolution on the ninth day of the disease. The anorexia, nausea, and
vomiting which so often mark the access or attend the course of
dysentery find thus easy explanation.
Should the disease continue, the general strength of the patient
becomes so profoundly reduced as to resemble the status typhosus. The
tongue, which has been hitherto thickly coated, now becomes black,
shows fissures, and bleeds, while the gums are covered with sordes. The
pulse becomes feeble, thready, or barely perceptible. The skin is dry
and harsh or scaly. The abdomen is tumid or collapsed, the anus
paralyzed, and the discharges continuously ooze out to excoriate the
perineum. While the brain is usually clear throughout the disease,
insomnia, stupor, or coma develop in the gravest cases from absorption
of disease-products (Senator), or death suddenly ensues from heart-clot
or from thrombus of the venous sinuses of the dura mater (Busey).