indigestion and constipation, brings on diarrhoea. Constipation impairs
the muscular tone of the bowel, and hardened fecal accumulations act as
irritants which sometimes provoke acute catarrhal processes--diarrhoea
and dysentery. Insufficient clothing in children and in adults makes
the skin more susceptible to changes of temperature and conduces to
intestinal congestion. Smoking in excess and the use of narcotics and
stimulants are mentioned as debilitating causes which pave the way for
disease in the intestine; the habitual use of the stronger liquors, by
keeping up chronic engorgement of the mucous membrane, is undoubtedly a
potent cause. Occupations which involve deprivation of fresh air and
sunlight, and all trades which enfeeble the individual, make him liable
to all digestive disorders. A feeble constitution, debility from
disease, from over-fatigue, or from loss of sleep, or any perturbing
influence, puts the body in a state favorable to indigestion and
diarrhoea.
The eruptive fevers are accompanied more or less by gastro-enteric
catarrh. In scarlet fever, measles, and variola there is a state of
equilibrium between the skin and the intestinal mucous membrane. When
the morbid manifestation does not normally appear upon the skin there
is a transference of irritation to the intestine. The administration of
purgatives in the early periods of scarlet fever and measles delays,
sometimes prevents, the outburst of the eruption on the skin. The
intestinal catarrh of the eruptive fevers has sometimes the
significance of an exanthem and sometimes of a secondary complication.
In measles it is more frequently the former; in scarlatina and variola
it comes later as a complication.
Uræmia, malarial infection, chronic suppuration, pyæmia and septicæmia,
cancerous and strumous disease of the mesenteric glands, scurvy,
tuberculosis, Bright's disease, and chronic wasting diseases in
general, are conditions in which diarrhoea appears as a result of the
defective nutrition of the vessels of the intestinal wall and their
liability to dilatation and hyperæmia, or from the presence in the
blood of septic matter.[10]
[Footnote 10: For experiments relating to the production of intestinal
catarrh by injections of irritating or putrid matter into the blood
consult _Traité clinique et expérimentelle des Fièvres dites
essentielles_, Gaspard et Bouillaud; also, _Path. anat._, Lebert, tome
ii., Texte, Paris, 1861, p. 205.]
The ingestion of a larger quantity of food than the stomach and
intestines are able to soften, and the taking of food essentially
indigestible or improperly prepared by cooking, are causes of the
passage of masses of food more or less unaltered along the intestinal
tract. Hyperæmia {672} follows the mechanical irritation of the mucous
surface. When articles of food are in a partial state of putrefaction,
so that the antiseptic properties of the gastric juice cannot be
quickly enough brought into play, there is a rapid fermentation in the
stomach, with the development of symptoms of gastric and subsequently
of intestinal catarrh. Unripe fruit, vegetables composed of hard
tissue, as early potatoes, cucumbers, pineapples, and cherries, by
their indigestible nature, are frequent causes. Oysters, crabs, fish,
and lobsters often occasion acute diarrhoea in consequence of being in
an unfit condition for food. Cheese has been known to produce violent
illness with symptoms of intense intestinal irritation; these effects
are due to some poisonous substance, hitherto undiscovered, developed
in the course of putrefaction. New coffee causes diarrhoea; six months
is usually the time before coffee grown in Ceylon reaches the European
and American markets; by this time it does not have this effect.[11]
[Footnote 11: J. Stevenson, "Medical Notes from Ceylon," _Edin. Med.
Journ._, Feb., 1862, p. 693.]
The irritant and caustic poisons, as mineral acids, caustic alkalies,
corrosive sublimate, arsenic, oxalic acid, tartar emetic, and carbolic
acid, kindle an intense inflammation of the mucous membrane of the
stomach, duodenum, and of the lower portion of the intestinal canal.
Softening of the coats of the intestines from corrosion, with
perforation, is not an infrequent result.
Drastic purgatives act as irritant poisons in producing acute hyperæmia
of the mucous coat with excessive transudation of serum; or, in other
words, an acute catarrh. A discharge of vitiated bile or an excess of
bile is given by recent[12] as well as by older writers as a provoking
cause of diarrhoea. The proper relationship is the reverse of this: an
intestinal catarrh the result of irritant action upon the mucous
surface entails a more active outflow of bile, just as some cathartics
by irritating the duodenum excite the gall-bladder to empty itself.[13]
Impacted fecal masses are direct irritants, exciting inflammation
(typhlitis, dysentery); putrefactive changes in long-retained fecal
collections have an additional power of irritation. Foreign bodies
accidentally or purposely swallowed, intestinal parasites, the pus from
an abscess which bursts into the intestine, likewise are excitants of
disease. Tubercle nodules, typhoid ulcers, cancer, or other neoplasms
in the wall are surrounded by areas of inflammation.
[Footnote 12: Roberts, _Th. and Pract. Medicine_, Am. ed., Philada.,
1880, p. 160.]
[Footnote 13: "The propositions which are the foundation of the whole
theory that bile can cause diarrhoea, and that its absence leads to
costiveness, cannot be looked upon as proved" (J. Wickham Legg, _On the
Bile, Jaundice, and Bilious Diseases_, New York, 1880, p. 661).]
Alcohol taken in excess, as in a debauch, leads to acute
gastro-intestinal catarrh. The stomach symptoms are the earliest to
develop and are the most prominent. Habitual alcoholic indulgence is a
more common source of chronic than of acute intestinal catarrh.
The influence of unwholesome drinking-water as a cause of diarrhoea has
been carefully examined by Woodward.[14] Turbid or muddy water holding
inorganic matters in suspension, he concludes from the evidence, is not
a source of disease, and the injurious effects of such waters have been
grossly exaggerated. Water containing inorganic substances in solution
produce diarrhoea, and are purgative if the dissolved matters have
purgative properties. Limestone-water may produce {673} temporary
disturbance of the bowels, but is wholesome. Carbonate and sulphate of
lime and magnesium in solution are more cathartic, but not as much so
as selenitic waters which contain an excess of sulphate of lime. The
salts of sodium and potassium in the waters of Colorado, New Mexico,
and Utah are still more liable to produce diarrhoea.
[Footnote 14: _Med. and Surg. History of the War_, Part 2, Medical
Volume, p. 599 _et seq._]
Water contaminated with organic matters of vegetable origin, which are
found in states of decomposition in marshes and stagnant pools, does
not, in the opinion of Woodward and Parkes, have very great influence
in the production of diarrhoea or dysentery. Impurities from
decomposition of animal matters are unhealthful. This is especially
true of water impregnated with soakage from privies and sewers; and yet
epidemics of diarrhoea cannot as often be clearly traced to this source
as can outbreaks of typhoid fever. Parkes says water contaminated with
three to ten grains per gallon of putrescent animal matter may be
hurtful.
Contusions and injuries of the bowel by sudden pressure or shock to the
abdominal wall may lead to intestinal inflammation. The large intestine
is more exposed from its size and position to such injuries. Pressure
upon the bowel by a tumor, as an enlarged or retroverted uterus, may
cause diarrhoea, the source of which may be overlooked. Early-morning
diarrhoea from a displaced womb is of frequent occurrence.
Emotional influence, as sudden fright or grief, will produce sudden
diarrhoea. Lesions of nerve-centres--corona radiata, optic thalamus, or
corpus callosum--induce hyperæmia, softening, and ulceration of the
mucous membrane of the small intestine.[15]
[Footnote 15: Rosenthal, "Diseases of the Nervous System," _Wood's
Library_, New York, 1879, vol. ii. p. 266.]
Minute organisms (bacteria) are thought by some observers to be the
cause of diarrhoea, especially of a zymotic form, which prevails in the
summer months. In accordance with this theory, the dejecta from
infected persons are the vehicle of the contagious poison which by air-
and water-contamination infects others.[16]
[Footnote 16: Wm. Johnston, _Lancet_, London, 1878, vol. ii. p. 397;
also, _Brit. Med. Journ._, London, 1879, p. 81; also, G. E. Paget, "On
the Etiology of Zymotic Diarrhoea," _Brit. Med. Journ._, Nov. 19, 1881,
p. 819.]
PATHOLOGICAL ANATOMY.--A description of the morbid anatomy of acute
intestinal catarrh includes the changes which are observed (1) in the
exterior appearances of the intestines, (2) in their contents, and (3)
in the condition of their mucous lining.
1. The external appearances of the intestines depend upon the degree of
distension of the tube, the character of the contents, and the presence
or absence of inflammation of the serous coat. Great distension of the
colon, of the cæcum, and of the small intestines is met with in acute
intestinal catarrh of some duration, and is due to relaxation of the
muscular coat. The colon usually presents the greatest distension. The
calibre of the tube may be lessened by strong contraction of the
muscular layer in acute intestinal inflammation of great intensity with
early and fatal termination. The color of the exterior varies with the
tension of the wall, the color of the contents, and the amount of
vascular injection. If the bowel is much distended with gas, the color
is pale; the mingling of bile with the feces causes a yellowish or
brownish color; if blood is in the tube a dull red hue is given to the
walls. If the intestine is congested or inflamed, the vessels are
outlined distinctly and can be seen in {674} different layers. The
areas of external redness generally correspond to internal hyperæmic
patches. The serous membrane shows arborescent congestion at the
mesenteric attachment or is inflamed from perforation; the signs of
peritonitis are most marked in the neighborhood of the
irregularly-shaped, round, oval, or pin-point openings in the gut. The
abdominal cavity may contain fecal matter, food, medicines, or worms
which have passed through the perforation.
2. The intestinal contents, instead of being homogeneous, of
pale-yellow color, and pea-soup-like appearance in the small intestine,
brown and more condensed in the lower part of the large intestine, may
present various changes. The fluid is usually increased in quantity,
and is thinner than normal in the colon: the color is greenish from the
bile, very pale from the closure of the bile-duct, red or black from
blood. The odor is absent from excess of serum, or very offensive from
decomposition due sometimes to the closure of the common bile-duct and
the want of bile. Shreds or masses of mucus may float in the liquid.
Undissolved pills or drugs, as bismuth, accumulated seeds, skins of
fruits or vegetables, parasites, or foreign bodies are seen. Epithelial
cells, the débris of digestion, micrococci, and bacteria are visible
under the microscope.
3. Inflammation involving the mucous membrane of the whole intestinal
canal is rarely or never met with. The nearest approach to generalized
catarrh of the bowel is found in eruptive fevers, especially measles.
Inflammation extending throughout the whole length of either the small
or large intestine alone, and affecting all parts equally, is also
rare. The ileum is the part of the small intestine most frequently the
seat of disease, but the ileum is rarely affected alone. Inflammation
is more frequently limited to the colon than to the small intestine.
The most common form of intestinal inflammation is ileo-colitis, where
the lower part of the ileum and a part of the colon, sometimes of
considerable extent, are inflamed. The duodenum is sometimes the seat
of a local inflammation, but this rarely happens except in the case of
external burns; duodenitis is most frequently an extension of catarrh
from the stomach, but the pathological anatomy of the duodenum presents
some peculiarities which will be described hereafter.
(_a_) Hyperæmia of the intestinal mucous membrane may exist without
inflammation. The engorgement of the veins by mechanical retardation in
disease of the liver, heart, or lungs does not constitute catarrh,
although it is sooner or later followed by catarrhal processes, usually
of a chronic nature. Gravitation of blood to the most dependent parts
in cases of long illness distends the vessels, and post-mortem
hypostasis leads to the passage of serum and coloring matter into the
meshes of the mucous and submucous tissue. In fatal cases of acute
diarrhoea sometimes no lesion has been observed. The hyperæmic membrane
pales after death, as does the skin in scarlatina and erysipelas.[17]
The presence or absence of hyperæmia is therefore no positive proof of
the previous existence or non-existence of inflammation. To constitute
inflammation there must be other changes besides hyperæmia, as oedema,
softening, and infiltration with cell-elements.
[Footnote 17: It is difficult to recognize post-mortem hyperæmia in the
mucous membrane of the mouth or throat where intense inflammation has
been seen in life.]
{675} A degree of vascular turgescence visible to the naked eye is
nearly always present in the mucous and submucous tissues which have
been the seat of catarrh. It is usually found in the lower part of the
ileum, the cæcum, sigmoid flexure, and other parts of the colon. The
redness is diffused over a surface of several feet in length or is
circumscribed in patches of varying size. When vessels of small size
are distended with blood, red branching lines are seen (arborescent or
ramiform injection) which have their starting-point in the insertion of
the mesentery. When the capillary system is engorged a fine interlacing
network can be discovered, which gives to the membrane a more uniform
red color. Parallel lines or bands of redness extend in a transverse
direction across the axis of the canal corresponding to the folds of
mucous membrane in the small and large intestine.
The shades of color depend upon the intensity and duration of the
congestion. In acute mild forms the color is light red; in more intense
grades the membrane is more vivid or purplish. Brown and slate-colored
tints show a passage into the chronic stage. A black hue occurs in
gangrenous inflammation. Minute dots (speckled redness) are due to
minute extravasations, and ecchymotic irregular patches are sometimes
seen.
Bile-staining of the mucous surface is met with; this cannot be removed
by washing. In metallic poisoning the redness is more vivid and the
mucous membrane is eroded.[18]
[Footnote 18: For colored plates illustrating hyperæmia and
inflammation of the intestines see Carswell, _Path. Anat._, London,
1838, plate ii. figs. 1 and 2. These are beautiful representations of
(1) ramiform vascular injection passing into (2) capilliform injection,
which becomes (3) uniformly red, or from its intensity (4) ecchymotic
or hemorrhagic. See also Annesley, _Morbid Anatomy_, London, 1828,
plates x. (Fig. 2), xiii., xxii., xxiv., and xxv. Many of these are
illustrations of peritonitis as a complication of enteritis. See also
Kupferlafelnzer, Lesser, _Ueber die entzundung und Verschwarung der
Schleimhaut des Verdauungskals_, Berlin, 1830, tab. iv. fr. 3; also J.
Hope, _Illustrations of Morbid Anatomy_, London, 1834, figs. 116, 118,
124, and 125. These plates are wonderful in their truthfulness and
execution.]
(_b_) Acute oedema and increase in the cell-elements in the inflamed
parts give rise to swelling and to softening, so that the mucous
membrane seems to be easily scraped off. This is not always the case,
as no loss of firmness of the reddened tissue is often found. In the
small intestine the villi, which in health are not seen, become
enlarged, giving a "plush-like" or velvety appearance to the mucous
membrane; they are sometimes club-shaped from epithelial accumulations
on their free extremities.
(_c_) When the small intestine is examined the solitary glands, which
in the normal state are barely visible, are so enlarged that they
appear as rounded prominences. They are described as looking like
grains of mustard-seed on a red ground, and are the size of pinheads.
When they are distinctly seen it may be concluded that they are
enlarged. In children the glands are enlarged when there has been
slight or no diarrhoea.
Peyer's patches are also tumefied, and are more distinct from being
elevated above the surface, but they have not in intestinal catarrh as
great a relative enlargement when compared with the solitary glands as
in typhoid fever. The interfollicular substance of the patch may
hypertrophy without any increase in the size of the follicles; a
reticulated {676} appearance is then given to the gland. The color of
the swollen follicles in recent inflammation is translucent from
oedema; later they are gray and opaque. These changes are more marked
at the lower end of the ileum, because the isolated follicles and
Peyer's patches are more numerous there.
(_d_) Catarrhal ulcers--erosions--are produced by the loss of
epithelium or from a process of vesicle-forming and rupture, as in
stomatitis. They may enlarge, undermine, and coalesce, thus reaching
quite a large size. They may deepen and perforate the wall of the
bowel, causing peritonitis, or they may heal, forming cicatrices which
in contracting may narrow the canal.
Small follicular ulcers are found on the mucous surface. They result
from the breaking down of the exposed wall of the closed follicle from
over-distension. The ulcer is either on the apex of the dome of an
isolated follicle or is within the area of a Peyer's patch. Sometimes
several ulcers may be seen on the surface of the swollen patch.[19] The
ulcerative process is sometimes very rapid. In the case of a child aged
eight years, with no previous intestinal disease, who died in the
Children's Hospital, Washington, in June, 1882, after a two days'
illness with watery discharges and rapid prostration, the solitary
glands throughout the ileum were many of them enlarged. As many as a
dozen small ulcers were seen at the apices of the enlarged follicles.
[Footnote 19: See photograph facing page 302 of _Med. and Surg. History
of the War_.]
In the large intestine the same lesions are found, but in a more
advanced stage, especially in the cæcum and descending colon. Enlarged
solitary glands of the size of a pinhead or small bird-shot are
scattered along the canal.
Follicular ulcers[20] are found in the large intestine, occupying the
summit of the enlarged follicles and involving a large extent of mucous
surface. Pigment-deposits are seen which give rise to the appearances
described as occurring in chronic intestinal catarrh.
[Footnote 20: For description of the mode of formation and growth of
follicular ulcers see article on CHRONIC INTESTINAL CATARRH.]
(_e_) The mucous surface is covered, especially in the areas of
redness, with an adhesive, opaque mucus of neutral or alkaline reaction
and of yellow, red, or brown hue, depending upon the relative amount of
bile or blood. It is composed of mucus-corpuscles, epithelium-cells of
cylindrical and prismatic form, pus-cells, and sometimes
blood-corpuscles. Vibrios and bacteria also are seen.
The chief distinction between the lesions of acute intestinal catarrh
and typhoid fever are these: In typhoid fever the number of Peyer's
patches involved is larger; there will be a chain of enlarged glands
from the ileo-cæcal valve throughout the ileum, those nearest the ileum
being the most altered. Near the valve there is usually some
ulceration, so that the gland acquires a ragged appearance. In catarrh
of the bowel there is a more irregular distribution of enlarged glands;
they project less above the surface, and if ulcerated have one or two
spots of erosion. In typhoid fever the Peyer's patch has the most
prominence. In catarrh of the bowel the solitary glands are the most
enlarged. In catarrh the large intestine may be the seat of the most
advanced lesion; in typhoid fever, except with rare exceptions, the
lesions in the ileum are most advanced.
{677} (_f_) The mesenteric glands are enlarged, but not so uniformly so
or to the same extent as in typhoid fever. The stomach is sometimes
found inflamed, the mucous membrane being reddened, thickened, or
softened. The liver, spleen, and kidneys are normal or present
accidental conditions of disease. In the respiratory organs pulmonary
congestion, pleurisy, and pneumonia are found. The heart contains clots
which are fibrinous or soft and red; they are found on both sides, but
when one cavity alone is filled the right is the common seat. The brain
is usually normal; fluid may be in the subarachnoid space, and thrombi
in the cerebral sinuses.
PATHOLOGICAL HISTOLOGY.--In the genesis of catarrh of the intestinal
mucous membrane the first effect of the exciting cause is an
over-distension of the capillaries and small vessels; this congestion
is most marked in the meshwork of vessels around the closed follicles.
A transudation of serum takes place into the mucous layer, and in more
marked congestion into the submucous layer also; these tissues become
more or less oedematous and swollen. Transudation of serum into the
intestinal tube follows. From over-stretching the walls of minute
vessels may rupture and small extravasations take place, staining the
tissue red. These subsequently become black pigment-spots. Post-mortem
extravasations are due to decomposition of the wall of the vessel.
Rupture of vessels on the surface leads to escape of blood into the
bowel, which is mixed with the transuded serum. The proper secretion,
intestinal juice, is diminished as a result of these changes, but an
excess of the mucus with which the mucous membrane is always coated
immediately follows. The origin of the mucus is not to be sought for in
the activity of the glands alone, but in the transformation of the
protoplasm of the epithelial cells.[21] The varying proportions of
serum, mucus, and blood cause the stools to be serous, mucous, slimy,
or bloody, hence the terms serous, mucous, and bloody diarrhoea.
[Footnote 21: Rindfleisch, _Path. Histology_, Sydenham ed., vol. i. p.
412.]
Hypernutrition, swift life of the mucous membrane, the result of
continued excess of blood, entails the increase of the cell-elements.
Lymphoid cells accumulate in the submucous layer, especially where
these cells are normally most numerous. There is a saturation of the
membrane with an excess of plasma. Cells also appear in increasing
numbers in the interfibrillary spaces of the mucous membrane, which
increase its bulk, and the follicles of Lieberkühn appear as if pushed
apart. Lymph-corpuscles accumulate in the meshes of the closed
follicles, which are distended and project above the surface as
described. Multiplication of the cells within the follicle (follicular
suppuration) causes over-stretching and the wall bursts, forming the
first stage of the follicular ulcer. The appearance upon the epithelial
surface of an increased number of loosened cells, which are sometimes
epithelial in character and at other times resembling pus-cells
(epithelial and purulent catarrh), is believed to be due to a rapid
manufacture and exfoliation of epithelial elements, and to constitute
one of the essential features of catarrh. Desquamation of the
epithelium in catarrh of the bowel, even in that of Asiatic cholera,
has been called in question by Woodward, who thinks that the stripping
off of epithelium is cadaveric.
SYMPTOMS.--Owing to the difference in the intensity and extent of {678}
the catarrhal process there is every possible variation in the symptoms
of intestinal inflammation. No one symptomatic picture will properly
represent all cases, and with a view to greater convenience and
exactitude of illustration a division may be made into mild and severer
forms.