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.
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 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. 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.
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. 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.
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.
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.
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. 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.
{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.
(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. 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.
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 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.
(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. 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.
A System of Practical Medicine. by American Authors. Vol. 2 · The Wunder Library — complete classics, free to read, with narration.