Persons subject to attacks of colic may diminish the intensity, or even prevent the recurrence, of the disease by employing during the intervals such remedies as would be indicated in their individual cases. Phosphate of sodium has been highly recommended for preventing the recurrence of attacks of colic. R. N. Taylor states25 that his experience with the use of the drug is quite extensive, and he found the treatment uniformly successful. Thirty grains dissolved in a glassful of water may be taken three times a day—preferably before meals—and this quantity should be reduced if it causes any irritation of the stomach. The bowels should be regulated and strict attention given to diet. A milk diet is of course best in obstinate cases. Any article of food known to disagree must be excluded, and tea, coffee, and alcoholic drinks should also be prohibited.
25 Med. Herald, Louisville, 1880-81, ii. p. 348.
SYNONYMS.—Enteritis, Catarrhal enteritis, Mucous enteritis, Endo-enteritis, Ileo-colitis, Entero-colitis, Diarrhoea. Older synonyms: Chordapsus, Cauma enteritis, Enterophlogia, Enterophlogosis, Colica acuta seu inflammatoria, Ileus inflammatorius, Enteralgia inflammatoria, Febris intestinorum seu Iliaca inflammatoria, Colique inflammatoire.
HISTORY.—It is interesting to start at the fountain-head of the two streams of inquiry—the clinical and the anatomical—and to follow each in its widely-diverging wanderings until they unite to give to the phenomena of intestinal inflammation a just interpretation.
The symptom diarrhoea was fully described by the earliest writers in medicine.1 The symptomatic differences between diarrhoea, dysentery, and lientery and the different forms of diarrhoea (bilious, watery, etc.) were given in detail by the Greek and Roman physicians. The Arabians had a much more elaborate classification of the fluxes. Avicenna made seven varieties of simple diarrhoea. European writers followed closely in these footsteps. Sennert made twelve and Sauvages twenty-one varieties of diarrhoea, depending upon as many different causes, as undigested food, worms, the bile, etc. Many recent writers have adhered closely to the older authors in their method of treating of diarrhoea, regarding it as a disease and dividing it into varieties based on the causes or on the appearances of the stools. Among them may be mentioned Cullen (1789), Good (1825), Tweedie (1841), G. B. Wood (1852), Trousseau (1865), and Habershon (1879).
1 J. J. Woodward, Med. and Surg. Hist. of the War, Part 2, Medical Volume, foot-note, p. 273 et seq.
It was only after many years of laborious investigation that the appropriate lesion was affixed to a symptom so well understood and described in its clinical aspects. The first conception of abdominal and intestinal inflammation had no relation to diarrhoea. Under the name [Greek: eileos], Hippocrates described abdominal symptoms of intestinal obstruction and inflammation. For Sennert (1641) inflammation of the intestines meant peritonitis. Bonet (1679), Hoffman (1710), and Boerhaave (1758) included under this head peritonitis, ileus, and all febrile and painful abdominal affections. Sauvages (1763) and Morgagni (1779) gave in detail the symptoms of peritonitis and called the disease intestinal inflammation—enteritis. In 1784, Cullen made an advance in subdividing enteritis into e. phlegmonodoea and e. erythematica—the one involving the entire wall of the intestine and the peritoneum, the other the mucous membrane lining the intestine. John Hunter (1794) first fixed the place of peritonitis as a distinct affection from inflammation of the mucous membrane of the intestines.2
2 J. Hunter, A Treatise on the Blood, Inflammation, and Gun-shot Wounds, London, 1794, p. 284.
Up to this time constipation was the chief symptom of enteritis. The meeting of the streams, the affixing the symptom diarrhoea to its appropriate lesion, was brought about hypothetically at first by J. Carmichael Smith in these words: "I think it is probable (for we can have no positive evidence of the fact) that in diarrhoeas from catching cold the villous or interior coat of the stomach is sometimes slightly inflamed."3
3 Paper read Jan. 8, 1788, Med. Communications, London, vol. ii., 1790, p. 168.
On the Continent enteritis soon after this was limited in its meaning by Pinel (1798) to inflammation of the mucous membrane of any part of the intestines. He gave the name catarrhal diarrhoea to the same condition. A still further restriction of its meaning was made by Broussais (1821), who defined enteritis to be an inflammation of the mucous membrane of the small intestine; he gave the name colitis to the same disease in the colon. This distinction was adopted by Rostan (1826), Andral (1836), C. H. Fuchs (1846), G. B. Wood (1852), Wunderlich (1856), Grisolle (1865), Flint (1866), and Aitkin (1868). According to the views of some authors, chiefly English, as Copland (1844), Bristowe (1871), Roberts (1874), Habershon (1879), enteritis includes inflammation of the serous as well as of the mucous coat of the intestines.
Niemeyer (1864), Jaccoud (1869), Leube (1875), Bartholow (1880), and most German and French authors prefer the name intestinal catarrh as applied to inflammation of the mucous coat; inflammation of the serous coat is peritonitis; the word enteritis is abandoned as involving a pathological error.
NATURE AND CLASSIFICATION.—Catarrh of the intestines is an inflammation of the mucous membrane of the intestinal tract. There are various peculiarities of the catarrhal process due to the anatomical structure of the parts involved, the presence of open glands, lymphatic follicles, etc. This disease is to be distinguished from inflammation of the serous coat of the intestine (peritonitis). The two are quite distinct in their etiology, pathological anatomy, and symptomatology, although they have been often confounded under the same name, enteritis.4 As so much confusion prevails as to the proper meaning of enteritis, it is best to abandon the word altogether.
4 For cases called enteritis in which the lesions of peritonitis were found, see Hamilton, Edin. Med. Journ., vol. ii., 1857, p. 304; also Breed, Chicago Med. Examiner, Oct., 1869, p. 579.
Diarrhoea is still regarded by some authors (J. J. Woodward) as synonymous with intestinal catarrh; by others it is considered separately as a disease distinct from catarrh. Habershon describes the lesions of catarrhal diarrhoea and mucous enteritis almost in the same words.5 It is an unscientific method to take one symptom of a pathological state, to erect it into a disease, subdividing it into varieties which are but differences in the intensity of its manifestation, and to assign to it no fixed lesion. Diarrhoea is in reality but a sequence and symptom of hyperæmia or inflammation of the intestinal mucous membrane.
5 Such a method of treating the subject involves a repetition, with an inversion, of the same description. Thus, catarrhal diarrhoea has as its lesion mucous enteritis; mucous enteritis has for its symptom (catarrhal) diarrhoea.
ETIOLOGY.—Intestinal inflammation is more prevalent in the Northern, Middle, and Western than in the Southern States. There is no relation between the distribution of malarial and intestinal diseases: in some regions where malarial disease is rife there is very little disease of the intestines. Limited areas in Lower Mississippi, Eastern Kentucky, Eastern North Carolina, etc. have a special predisposition to diseases of this class.6
6 F. A. Walker, Statistical Atlas, 1874, table v. p. 3; also plates xlii. and xlv.
During the Civil War diarrhoea and dysentery were more frequent and fatal in the central region than in the Atlantic and Pacific regions.
It is difficult to compare the relative liabilibity of the native and foreign-born populations in the United States to intestinal disease. Inasmuch as children, among whom the bulk of such cases occur, bear such a small proportion to the adult foreign population, allowing for differences due to this cause, statistics show that the foreign-born race has a very distinct predisposition to these forms of disease.7 The Swedes, Norwegians, and Danes have a marked susceptibility to intestinal diseases; the English and Welsh have the same tendency; but the Irish have a comparative immunity. The colored race is more prone to intestinal than to malarial diseases in the Middle States, but there is the reverse susceptibility in the Northern and Southern States.
7 The number of children under ten to 1000 native population is 306; number of children under ten in 1000 foreign population, 47 (F. A. Walker, "Relations of Race and Nationality to Mortality in the United States," Statistical Atlas, 1874, p. 213).
Under ten years more males than females have enteritis, in the proportion represented by the figures 362 and 299. After ten the predisposition of the two sexes is about the same.
The summer is the season when diarrhoea is most prevalent and most fatal. June, July, and August are the months in which the greatest number of cases occur and in which there is the highest mortality. The extraordinary death-rate in these months in cities is of course due to the influence of summer heat on children, and the death-rate from diarrhoea and entero-colitis is chiefly among infants under one year. But among adults the same rule holds. The highest monthly mortality from acute diarrhoea among the U.S. troops (white) between 1861 and 1866 was 147, in July, 1862; the next highest was 114, in August, 1862. June and September were after these the most fatal months. According to the census of 1870, the most fatal month is August.
Elevation of temperature in the summer months is the cause of the prevalence of intestinal catarrh and of its great mortality among infants and children. The number of deaths bears a direct ratio to the degree of heat, the highest death-rate occurring in seasons of unusual high temperature.8 The effect of excessive or prolonged heat is to arrest or weaken the digestive processes; undigested masses in the stomach or the intestines act as foreign bodies and produce inflammation.
8 Among the numerous publications bearing on this subject, those contained in The Sanitary Care and Treatment of Children and their Diseases (Boston, 1881) are of especial value. S. C. Busey's article contains much valuable matter on the relation of summer heat to illness and mortality among children.
Sudden changes of temperature from cold to heat or from heat to cold develop diarrhoea. If the air is at the same time saturated with moisture, the effect of a change in temperature is greatly intensified. In the first hot days of June there is on the Atlantic coast, especially in cities, a rapid increase in the number of cases of gastro-intestinal disturbance. A larger number of children are taken ill in June than in August. The child in time becomes habituated to heat, and if not attacked early runs less risk of illness in the later months. A sudden or unusual exposure to low temperature, as in lying on damp ground, leads to the same result. The check to perspiration after violent exercise is especially provocative of diarrhoea. In these instances the congestion and consequent inflammation of the mucous membrane are brought about through the effect of heat or cold upon the peripheral nervous system. Cold may act more directly by the driving of suddenly-cooled blood from the surface of the body to the interior. External burns belong to the same category, as they lead to extensive inflammation, sometimes to ulceration, of the duodenal mucous membrane through reflex influence. A case is reported of a boy aged twelve years who after an external superficial burn of the left thigh was taken with profuse diarrhoea which ended fatally in three hours (Ziemssen).
Contamination of the atmosphere with emanations the result of the overcrowding of many human beings together, as in prisons, camps, or asylums, especially where decomposition of organic matter is going on, is of great influence in causing diarrhoea. Persons living in badly-ventilated houses, or in houses improperly drained where the air is vitiated by escaping gas from sewer-pipes, are especially prone to be attacked. But sewer-gas, per se, does not cause diarrhoea any more than it causes diphtheria or scarlatina.9 It is a step backward to hang upon this ready explanation all our doubts and our ignorance of the origin of disease. The specific germ of the zymotic diseases may be conveyed in the gases from sewers, but there are other and more direct modes of communication which should receive equal attention.
9 Longstaff (Brit. Med. Journ., London, 1880, vol. i. p. 519) believes that summer diarrhoea has a specific poison which is intimately connected with the process of putrefaction, and that the infective material has its source in the public sewers.
Children are much more liable to intestinal inflammation than adults. This is due to the greater susceptibility of the mucous membrane in them to congestion and catarrh from external influences and from direct irritation. In infants fed upon an unsuitable diet—cow's milk or other substitutes for mother's milk—this susceptibility is much increased. The age most liable to attack is under one year, or from the first to the second year, when, in consequence of dentition, weaning, and a change from a diet chiefly or almost wholly liquid to one of solids, there is a great liability to a disturbance of the normal equilibrium. Intestinal catarrh forms almost one-third of the total number of the affections of childhood. According to the census of 1870, 761 out of every 1000 deaths from diarrhoea, dysentery, and enteritis occurred under the tenth year. In old age a similar predisposition exists, and a mild attack will in old persons induce more serious symptoms than in middle life. Epidemics of diarrhoea among the aged in asylums and hospitals are not uncommon.
Temperament and idiosyncrasy are causes of differences in predisposition. Many persons in consequence of taking cold invariably have diarrhoea, while others as invariably have nasal catarrh or bronchitis. Certain articles of food, as oysters and eggs, lead always in some persons to intestinal disturbance. An exaggerated sensibility of the mucous membrane to particular impressions is the cause of this peculiarity.
Previous attacks of intestinal inflammation render the individual liable to recurrences from very slight causes. The suppression of the menses and of hemorrhoidal discharges and the healing of eruptions are said to be followed by serious diarrhoea, but such an occurrence is probably more often a coincidence than a result.
Sedentary life, by enfeebling muscular movement and by inducing 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
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 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
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 recent12 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.
12 Roberts, Th. and Pract. Medicine, Am. ed., Philada., 1880, p. 160.
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 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.
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
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
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 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.
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.
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
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 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.
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 ulcers20 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.
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.
(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.
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 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.
Under the head of mild forms can be included all cases of intestinal catarrh which by their short duration and benignant character point to a mild degree of inflammation. They correspond to the following anatomical states: hyperæmia of the mucous membrane of parts of the small or large intestine, or of parts of both simultaneously; slight or moderate swelling of the membrane from serous saturation; transudation of serum into the canal; increase of lymphoid cells in the mucous and submucous tissues; and increased manufacture of epithelial cells, but without any marked tumefaction or ulceration of the closed follicles. The termination is by resolution, which is reached in a few days usually, and the membrane is rapidly and entirely restored to the normal state. Between the normal condition of the mucous membrane, with its recurring periods of physiological hyperæmia, and the hyperæmia with exaggerated secretion and peristalsis which leads to diarrhoea, there is no well-defined border-line. Diarrhoea may be regarded as the most certain sign of the catarrhal process. Whenever the frequency and fluidity of the stools are such as to be regarded as pathological, some stage or other of catarrhal inflammation may be assumed to exist.
In a large number of mild forms the onset is sudden. After a meal of indigestible food or an unusual excess pain will be felt in the abdomen, recurring in paroxysms, which start in the neighborhood of the umbilicus and radiate throughout the abdomen. The pain is accompanied by borborygmi, and is succeeded sooner or later by a desire to go to stool. The first one or two movements, which follow each other in quick succession, are more or less consistent or moulded, but in a short time diarrhoea is established by frequent discharges of watery fluid, containing perhaps some undigested fragments of food, which may have been the exciting cause of the illness by mechanical irritation. Each stool is preceded by colics, griping pains in the abdomen, which are relieved by the evacuation. An attack beginning in this way and from such causes may cease in a few hours, and be unattended by any general symptoms if proper precautions are taken. A slight dryness and coating of the tongue, with loss of appetite and occasional griping pains or a tendency to looseness of the stools, may continue for a day or two. Indiscretions in diet or other imprudences, as fatigue, may prolong the mildest attack during one or more weeks, but the character of the illness is here due not to the nature of the disease, but to the addition of fresh causes which delay the natural progress toward recovery.
Severer forms either begin suddenly, as in the milder forms just described, or are preceded for a time by symptoms of gastric or intestinal indigestion. The patient may have complained of distress after eating, flatulence, colicky pains, distension of the abdomen and tenderness on pressure, loss of appetite, with a general feeling of ill-health—symptoms which point to the existence of a condition of the mucous membrane of the gastro-intestinal canal favorable to the action of an exciting cause.
A feeling of chilliness ushers in the attack. This is accompanied by fever, which at first, and sometimes throughout, is of a marked remittent type. The griping pains, colics, which at first are infrequent and dull, now recur at short intervals and become sharper. They are sometimes attended with vomiting of food or of a greenish fluid. The intensity of suffering may be so great as to cause pallor of the countenance, a feeling of faintness, and coldness of the surface with sweating. The paroxysm usually precedes a movement. The more severe pains extend to the lower extremities and the scrotum.
Movement of gas in the intestines produces rumbling, gurgling, or splashing sounds, called borborygmi. They are paroxysmal, lasting a few moments, or are coincident with pain, and frequently are the immediate precursors of an evacuation. The cause for their production is the quick propulsion of the fluids by strong peristaltic action from one part of the bowel to the other or the rapid movement of gas within the bowel. Relief is obtained both from the pain and from the sense of distension by expulsion of flatus.
Tympanites is closely connected with the symptoms just described. An excess of gases within the bowel is not primarily a result of the inflammation of the mucous membrane, but is an early phenomenon due to the decomposition of indigestible food in its transit through the intestine. Later, the gases are developed very readily by the decomposition of even the most digestible articles of food, the mucus, which is the product of the catarrh, acting as a ferment.
The distension of the intestinal canal produces an intumescence of the abdomen which is commonly uniform, but may be greater in some portions of the tract than in others. Thus the transverse and descending colon are more projecting and more distinctly outlined than other portions of the canal.
Sensibility of the abdomen to pressure exists along the line of the colon or over a considerable area. But no defined limitation of the affected part can usually be made by the location of pain to the touch. If there is any local tenderness, it is over the descending colon. In one form of enteritis—typhlitis—the localization of the inflammation in the cæcum produces subjective pain and pain on pressure in a restricted region—a peculiarity which results no doubt from the early intensity of the inflammation and the implication of the connective tissue behind the bowel. But this is not true of inflammation of any other part of the intestinal canal.
A sensation of soreness on movement, as in turning in bed, standing, or walking, is not uncommon, even when the attack is of no great gravity. The patient on standing bends forward to relieve tension, and he may feel nervous when the bed is shaken.
Diarrhoea is the most important symptom, as it is directly related to catarrh. The number of evacuations varies from one or two to twenty or more in the day. In cases of medium intensity there are from six to ten in twenty-four hours, the interval between the movements being two to three hours during the day and somewhat longer at night. The matters passed in quantity range from two ounces to a pint; the average is about four fluidounces. This, however, is subject to great variations, depending upon the intensity of the disease; the more choleriform the attack the greater the amount of fluid passed. The weight of the evacuations varies from five ounces to forty pounds in twenty-four hours; this increase does not depend upon the greater quantity of water only, but the solid constituents are in greater amount.
The normal brown color, which is due to hydrobilirubin, changes as the movements become thinner to yellowish-brown or pale yellow from dilution of the fecal matter with water. An excess of serum or mucus renders them colorless. A greenish-brown, greenish-yellow, or green hue is due to the presence of bile. The rapid descent of the contents of the bowel delays or prevents the reabsorption of bile,22 or the fluid is expelled before the usual transformations in color take place.23 The bile-pigment is also absent in duodenal catarrh from closure of the opening of the ductus choledochus.
22 L. Brunton, "On the Action of Purgative Medicines," The Practitioner, London, June, 1874, p. 403.
23 The reaction of bile-pigment with nitric acid, which does not take place in the contents of the colon or in normal feces, is seen in the green stools of acute intestinal catarrh, especially in children.
The coloration of the stools further depends upon the character of the food and drink and upon the drugs given. From an exclusive milk diet the discharges are pale or contain undigested whitish lumps of casein. The preparations of bismuth and iron give a black color and the sulphate of copper a dark-green hue. A green or greenish-brown tint is observed after the use of calomel, and while the experiments of the Edinburgh committee demonstrated that no increase of bile follows its administration in dogs, yet the opinion is still general that the green stools contain an excess of bile.
Blood appears in three forms in the stools: as a coffee-ground or black powder from hemorrhage in the stomach or upper bowel; as a reddish fluid with small coagula in flakes, which come from intense congestion or ulceration of the intestine; or an abundant hemorrhage may result from deep ulceration in the duodenum or elsewhere.
The characteristic odor of the feces is altered in several ways. As the movements become less solid they acquire a nauseous or sour smell, due essentially to the volatile products formed in connection with the decomposition of fatty matters.24 When very thin and containing little or no feculent matter the discharges lose odor, as in cholera, or they become excessively offensive—cadaveric—in intense and fatal inflammation and in ulceration of the bowels. After exposure to the air the stools of diarrhoea undergo decomposition and develop offensive smells more rapidly than in health. The absence of bile, whether there is diarrhoea or not, gives rise to a peculiar and unpleasant odor, showing that this secretion is to some extent an antiseptic. The escape of fetid gas from the anus is rarely an accompaniment of a decomposed state of the rectal contents. In children the stools are more variable in quantity, color, and odor than in adults, and are more readily affected by the ingesta.
24 Guttmann, Physical Diagnosis, Sydenham Soc. ed., p. 404. The odor of normal feces is due to a substance isolated by Briequer, called scatol, which is a final product of the putrefaction of albumen (Ewald, Lectures on Digestion, New York, 1881, p. 106).
In the diarrhoea of old persons the discharges are thin, yellow, offensive, and often frothy.
The disorder of the digestive apparatus is attended with other symptoms. The tongue is normal in some cases; in others red at the point and edges with a central whitish coat, or the surface is red, polished, and dry. Marked change in the appearance of the tongue is due to a complicating gastric catarrh. There is thirst, with loss of appetite, and a tendency to nausea and vomiting in children and feeble persons. The breath has a peculiarly offensive odor (spoken of as fecal) in some instances.
Fever is not always present. In cases of moderate severity it occurs in the beginning of the illness, but declines rapidly under treatment by rest and diet. The course of fever does not conform to any type even in severe cases, although it so nearly resembles that of typhoid fever in its first week as to lead to mistakes in diagnosis. The height of the fever and its duration are measures of the extent of the lesions and their gravity. Sudden outbursts of fever point to some complication. In catarrh of the bowel due to cold the fever is higher than when indigestion is the cause. In very feeble persons, in children, and in any case from neglect and improper feeding the body-heat may be very high.
The urine is diminished and high-colored. Very little disturbance of the nervous system is seen except in young and old patients; some headache and restlessness are all that may be observed. Moderate delirium at night accompanies very acute attacks. In children convulsions are not unusual in the onset and at the end of the attack. In the aged exhaustion from the illness soon lapses into stupor or coma.
Paraplegia and contraction of the muscles of the extremities are referred by some observers to gastro-intestinal inflammation.25
25 Potain, Le Praticien, Paris, 1879-80, p. 88.
In uncomplicated mild cases of intestinal catarrh there is a movement toward recovery after a few days' illness. The stools become less frequent, smaller, and more consistent. In a week to ten days the tongue cleans, the thirst ceases, the appetite returns, the tympanites and pain diminish. The fever declines, and ceases before the diarrhoea is completely arrested. There are always more or less emaciation and loss of strength from the fever and arrest of nutrition. The liability to relapse is great, and the patient by indiscretions reproduces the same symptoms, thus prolonging the attack for several weeks. Acute intestinal catarrh may pass into the chronic form by a disappearance of fever and amelioration of all the abdominal symptoms. The patient begins to take solid food, gains strength and flesh, but complete recovery does not come. The diarrhoea recurs at variable intervals as the result of indulgences in a mixed diet, over-exercise, or exposure to cold, and in time we have some degree of chronic catarrh permanently established.
Very mild cases may be prolonged by the neglect of the patient to consider his painless diarrhoea of sufficient moment to need attention.
In inflammation of the more intense kind the picture is somewhat different. The prodromes are longer and the general symptoms more severe. Restlessness, a sense of prostration, delirium, and high fever mark the early stages and continue for a longer time. The patient loses flesh and strength quickly. The features express anxiety and illness, the skin is hot and dry, and the thirst great. Vomiting is repeated. Borborygmi, the tension of the abdomen, pain, and sensibility to pressure are all intensified. The stools are at first yellow and thin, but change much from day to day. They may be green or very thin and dark or grayish, and are sometimes very offensive in odor. Blood and mucus may be seen in them, being slimy or grumous and bloody. When the patient is very weak the discharges are involuntary; the tongue is coated white, with bright red tip and edges, and is often dry.
The severer forms last from three to six weeks. After a tedious period of alternate improvement and relapse the illness becomes chronic or the patient dies from asthenia, perforation and peritonitis, or some other complication.
In the most intense varieties which find examples among Europeans and Americans in intertropical countries, or result from acute mineral poisoning and from rapidly-progressing cases of acute ulceration of the intestinal wall, especially in children, there is a sharper and more violent invasion. The strength is reduced in a very short time, and there is rapid emaciation; the features assume an anxious expression; the complexion is leaden or livid; the skin is cold and clammy; the pulse is small, weak, and rapid; the breath comes quick and short, and is frequently complicated with hiccough. In the early stages vomiting occurs, due to a concurrent gastritis; in cases of poisoning vomiting is incessant.
The pain in the abdomen is intense, and less paroxysmal than in other forms. The abdomen is tympanitic and excessively tender to the touch, and the knees are drawn up to relieve the tension of the abdominal muscles. Thin, black, or reddish stools are passed every few moments. As the attack progresses the urine is suppressed, the voice becomes whispering, and collapse is developed. This is marked by cold extremities, dyspnoea, feeble and finally imperceptible pulse. Death may end the scene in a few hours or the patient may rally and recover slowly.
Choleriform diarrhoea occurs chiefly in children during hot weather.
VARIETIES DUE TO SEAT.—The symptoms and progress of acute catarrh of the intestines present numerous differences depending upon the seat of the inflammation. The symptomatology already given is that of the most common form (ileo-colitis), in which the lower part of the ileum and a considerable portion of the colon are simultaneously involved. Many cases no doubt occur in which the disease is limited and in which early recovery is the rule. The pathological anatomy of cases of generalized catarrh is better known, as they form the bulk of the fatal cases.
I. Acute Duodenitis.—The most common form of duodenitis is that in which the inflammation spreads by continuity of tissue from the stomach to the duodenum, as in acute gastric catarrh after a debauch. The prominence of the gastric symptoms disguises the intestinal lesion, unless the catarrh, as is frequently the case, extends into and obstructs the common bile-duct and its branches, and suddenly develops icterus with clayey stools and altered urine. Besides icterus, a careful isolation of symptoms will show that some cannot be attributed to the stomach: there is a dull pain seated in the right hypochondrium, extending to the right shoulder or shoulder-blade, which is increased by pressure upon the region of the duodenum. As the gastric symptoms improve there is no change in the icterus, which continues for some days or weeks longer. The connection between burns of the integument and ulcer of the duodenum is well known. Symptoms of perforation, with death, may be the first sign of this lesion, but vomiting of blood, icterus, purging of blood, indigestion, and cardialgia occur from duodenal ulcers.
The typical acute duodenitis described by authors as an independent affection is of rare occurrence. An epidemic of duodenitis26 has been reported where many persons were simultaneously attacked, all the cases having had the same traits—headache, pain in the line of the duodenum at the left edge of the right hypochondrium, pain in the first and second lumbar vertebræ, constipation, jaundice, slow pulse, and mental depression. Gangrenous inflammation of the duodenum27 has been once seen, and produced a chill, a severe sense of weight and pain in the epigastrium, retching and eructations of gas, tenderness on pressure, frequent pulse, and high temperature. There was obstinate constipation, with dyspnoea, death ensuing in a few days. At the autopsy gangrenous inflammation of the duodenum was found, which ended abruptly twelve inches from the pylorus. There was a large gall-stone in the gall-bladder.
26 McGaughey, Philada. Med. Times, Aug. 1, 1872, ii. p. 407; also, T. N. Reynolds, Detroit Clinic, June 7, 1882, p. 181.
27 Eskridge, Philada. Med. Times, Feb. 15, 1879, ix. p. 239.
A fatal case of duodenitis is recorded28 in which the following symptoms were observed: sudden and severe pain in the right hypochondrium, increased by pressure; rigors, vomiting and purging of a green flocculent fluid, and later of blood; jaundice, fever, delirium, collapse, and death. The pylorus and two-thirds of the duodenal mucous membrane were much inflamed and the orifice of the bile-duct closed.
28 Die Krankheiten des Duodenums, Mayer, quoted by Leube in Ziemssen's Cyclopædia, Am. ed., vol. vii. p. 373.
II. Acute Ileitis, Acute Jejunitis.—When the ileum, with or without the jejunum, is the seat of catarrh, diarrhoea may not be present, provided the inflammation is slight and there is no increase of colon peristalsis. The symptoms then are borborygmi, pain and fulness about and below the umbilicus or between it and the right ileum, especially after eating, and the general symptoms arising from indigestion and malnutrition. Fever is slight or absent; there are malaise and loss of strength. The feces give important indications. They contain unaltered bile and fragments of muscular fibre and starch-granules in excess of the quantity found in health. An increased quantity of mucus, diffused evenly in a fluid evacuation, or globules of mucus stained with bile, or bile-stained epithelium, denote inflammation confined to the small intestine. A larger amount of indican in the urine than is normally present is a sign of the same lesion.29
29 These conclusions are based upon the results of one thousand examinations of feces made by H. Nothnägel, and reported in Zur Klinik der Darmkrankheiten; Zeitschrift für klin. Medicin, iv., 1882, p. 223.
Intense inflammation of the small intestine may exist without diarrhoea or other symptoms betokening the real nature of the attack. Flint30 mentions having met with three such instances, and Goodhart31 records thirteen cases of enteritis with marked lesions in which no diagnosis had been made before death. Rilliet and Barthez report twenty-four autopsies in children with intestinal lesions in which no symptoms had been observed.32
30 Clinical Medicine, Philada., 1879, p. 280.
31 Guy's Hospital Gazette, Sept., 1878, p. 98 et seq.
32 Maladies des Enfants, Paris, 1861, tome i. p. 748.
III. Acute Colitis.—Fifty years ago colitis was synonymous with enteritis, and not with dysentery, as at a more recent date.33 The older signification expressed the fact that inflammation in the colon is essential to diarrhoea. Later the term was used synonymously with dysentery.34
33 Journal général de Médecine, Paris, 1825, t. xci. p. 18.
34 Tweedie, System of the Practice of Medicine, 1841.
The colon is a conducting tube; the contents are composed of matters unabsorbed in the small intestines. At first the mass entering the colon is fluid, but by the gradual absorption of its watery part it approaches solidity. The discharge from the rectum of a fluid shows that the propulsion through the large intestine is so rapid that the process of drying does not take place, or that from inflammation of the colon there is an excess of fluid transudation from the intestinal wall. The superficial position of the colon, its great size and length, expose it to the action of external cold, to blows, etc.
In catarrh limited to the colon there are essentially the same symptoms as in ileo-colitis, inasmuch as the inflammation of the colon gives to that form its characteristic features—borborygmi, diarrhoea, and tympanites. When the disease in the colon preponderates or exists alone, the pain and tenderness are more superficial and confined to the line of the large intestine. The distended colon projects and the abdominal swelling is not so uniform. If the attack is subacute or mild, the stools contain normal feces mixed with a great deal of mucus; when the inflammation is in the sigmoid flexure, pure mucus is passed. Blood mixed with mucus and tenesmus accompany inflammation low down. Blood may, however, come from intense inflammation of the ascending and transverse colon without disease of the lower bowel.35
35 In a case seen by the writer of colitis terminating fatally from perforation of the transverse colon this point was illustrated. A woman aged fifty was taken with diarrhoea in August, 1873. In November the symptoms became worse: tongue dry and red; abdominal pain; tympanites; frequent stools, ten to seventeen in twenty-four hours; quantity large, of a yellow or brownish-red color with floating flakes. General symptoms grew worse; blood in stools from time to time. November 24, sudden cessation of discharges from the bowels, and the following day sudden collapse and death. Autopsy: Descending colon and sigmoid flexure comparatively healthy. Transverse colon adherent to stomach; deposits of lymph on colon and small intestines; fluid and feces in the peritoneal cavity. The mucous membrane of the ascending and transverse colon in a state of black pulpy disintegration. In the transverse colon the walls were thinned by ulceration and easily torn; gangrenous appearance of mucous coat; perforation of the colon wall below greater curvature of the stomach.
IV. Proctitis.—The rectum may be the seat of simple catarrh, which differs in its symptoms from catarrh of other portions of the canal. By many this form is called simple, non-infective dysentery. But as it is a form of intestinal catarrh, it is right that it should be considered in connection with colitis. The first indication of its onset is a frequent desire to go to stool, with an unsatisfied feeling after each effort. Normal fecal matter is first expelled in solid form, coated with mucus which may be streaked with blood. Soon, however, the discharges consist of jelly-like mucus, alone or mixed with blood. A small quantity of this is passed with tenesmus at short intervals. The patient complains of a burning feeling in the rectum and a constant and irresistible desire to strain. The same spasmodic contraction may involve the bladder.