Chapter XLIII: Front Matter (43)

Alum is not often prescribed. Sulphate of copper is fitted for cases in danger of passing into the chronic stage. Sulphate of zinc might be more generally ordered than is the case. The sulphate of iron and the fluid preparations of iron--tincture of the chloride, solution of the pernitrite, and persulphate--are astringents, and could be tried if other remedies fail. The effect of nitrate of silver is to constrict vessels, to coagulate and disinfect excretions, and to form an adherent protecting membrane (Phillips). It occupies the next place to lead, and is suited to a subacute stage when acute symptoms have subsided. It is warmly recommended by William Pepper and others.[63] The oxide of silver has been preferred by some writers.[64] For the protracted diarrhoea of children, in whom follicular ulcers form so rapidly, the nitrate of silver is of special value. To adults it is administered in a pill freshly made in doses of one-eighth to one grain. A solution in distilled water with syrup answers well for children, the dose varying from one-twentieth to one-fourth of a grain.

[Footnote 63: J. Maggregor, "On the Internal Use of Nitrate of Silver in Inflammation of the Intestines," _Lancet_, 1841, vol. ii. p. 937.]

[Footnote 64: Lane, _Med.-Chir. Rev._, July, 1840, p. 289 _et seq._; Eyre, _The Stomach and its Difficulties_, London, 1852.]

The theory of the germ origin of diarrhoea has naturally brought into notice antiseptic remedies. Carbolic acid,[65] creasote,[66] naphtha,[67] sulpho-carbolate of calcium,[68] salicylic acid,[69] and chlorine-water have each been advocated. Practice does not support their claim to be considered remedies for intestinal inflammation.

[Footnote 65: Habershon, _Lancet_, London, 1868, vol. i. p. 7; C. G. Rothe, _Berliner klin. Wochenschrift_, 1871, p. 527.]

[Footnote 66: _Southern Med. and Surg. Journ._, vol. ii., 1846, p. 583; _ibid._, vol. iii., 1847, p. 147; _London Med. Gaz._, vol. ix., 1849, p. 254; _ibid._, vol. xii., 1851, p. 235.]

[Footnote 67: _Gaz. des Hôpitaux_, 1849, p. 46.]

[Footnote 68: _Tr. Obstet. Soc. Lond._, vol. xii., 1870, p. 12.]

[Footnote 69: W. Wagner, _Kolbe's Journ. für prakt. Chemie_, Bd. xi., 1875, S. 60.]

{697} Treatment by the rectum may be employed when medicines are rejected by the stomach or when it is desired to bring the drugs into more direct contact with the inflamed colon. Opiates, astringents, and alteratives are employed in this way. Laudanum in two to four ounces of warm water or in warm milk or starch-water can be thrown into the rectum, the fluid being allowed to remain. The injections are to be given often enough to relieve pain and lessen the number of discharges. With the laudanum, or without it, the mineral astringents can be used by enema. Acetate of lead or sulphate of zinc is to be preferred. The objection that but a small portion of the inflamed surface is reached by the fluid is a valid one, and therefore those cases are most benefited where the catarrh is in the lower colon and rectum. Ringer[70] says that it is not at all necessary for the fluid to reach that part of the intestine which is the seat of the catarrh; the impression made on one part is communicated to the other by sympathy. It was the practice with O'Beirne,[71] Hare,[72] and others to inject fluid by a long flexible tube passed beyond the sigmoid flexure. This method is advocated and employed in Europe by Mosler, Winterinz, and Monti. Quite recently Dulles has drawn attention to irrigation of the large intestine as a means of treating inflammation of the colon, according to the plan of Alois Monti of Vienna.[73] Henoch has tried with partial success in children the throwing into the rectum of a large quantity of water holding in solution acetate of lead, alum, or tannin. His method contemplates medication above the sigmoid flexure; a part of the fluid escapes, while the rest remains five or ten minutes in the bowel.[74] Monti says as much as two pints can be injected into the bowel of a nursing child--for older children twice this quantity.

[Footnote 70: _Therapeutics_, New York, 1882, p. 99.]

[Footnote 71: _New Views of the Process of Defecation_, Washington, 1834, p. 85.]

[Footnote 72: E. Hare, "On the Treatment of Tropical Dysentery by means of Enemata of Tepid Water," _Edin. Med. and Surg. Journ._, vol. lxxii., 1849, p. 40.]

[Footnote 73: Dulles, "Irrigation of the Colon," _Philada. Med. News_, Aug. 19, 1882, p. 199. The patient is placed on the side, back, or on belly, with the hips elevated. A large flexible catheter if a child, a stomach-tube if an adult, is inserted into the rectum. The tube is connected with a reservoir of water elevated above the patient. The rectum is first distended with water, and the tube is gradually made to follow the course of the bowel until it finds its way into the descending colon. Thus the water may be made to distend the whole of the colon to the cæcum. The fluid remains from a few minutes to half an hour.]

[Footnote 74: Henoch, _Diseases of Children_, Am. ed., New York, 1882, p. 206.]

Messemer[75] reported three cases (one child and two adults) treated in this way with the most striking success. His object at first was to cleanse the rectum, but warm water did not check the diarrhoea. Cold water was tried, and (probably by reflex influences) diminished rapidly the number of the discharges. And Ewald[76] has imitated Messemer's method with results which are surprisingly good. He injected 200 and 300 cc. of cold water, which was expelled by pressure on the abdomen; 50 cc. were then thrown in and allowed to remain. He has used the treatment in a large number of cases in children. The question as to the ability to force water thrown into the rectum through the sigmoid flexure and distend the colon has been settled by the experiment of Mosler in a case where there was a cæcal fistula. Water injected into the {698} rectum traversed the colon and escaped through the fistula in two minutes.[77]

[Footnote 75: J. B. Messemer, "Cold-Water Enemata as a Therapeutic Agent in Chronic Diarrhoea," _American Journal of the Med. Sci._, vol. lxxvi., 1878, p. 133.]

[Footnote 76: _Lectures on Digestion_, New York, 1881, p. 149.]

[Footnote 77: _Berlin. klin. Woch._, No. 45, 1873, p. 533. Woodward, in discussing the claims of Battey of Georgia to priority in the discovery of the permeability of the entire alimentary canal by enema (see paper by Battey in _Virginia Med. Monthly_, vol. v., 1878, p. 551), quotes from A. Guaynerius, who lived in the fifteenth century, from J. M. de Gradibus (1502), Sennertus (1626), and from others among the older writers to show that it was well known that suppositories and enemata introduced into the rectum are sometimes thrown up by the mouth. He mentions experiments by Alfred Hall (1845), G. Simon (1873), and F. Köster (1874) which demonstrated that large quantities of water may be forced from the rectum into the stomach. (See Woodward, _op. cit._, foot-note, p. 836.)]

When ulcers are thought to be present, the remedies of particular value are nitrate of silver, bismuth or turpentine, and the mineral acids, given in conjunction with a rigid system of diet.

In hemorrhagic diarrhoea ice externally or ice-water injections, opium, acetate of lead in large doses (ten to fifteen grains), gallic or tannic acid, and ergot are the appropriate remedies.

Some modifications of treatment are required for the choleraic form (in children, cholera infantum); the danger here is imminent from the drain of water and collapse. For the vomiting of the early stages, pounded ice eaten freely, potassium or sodium bromide in ice-water, and counter-irritants over the abdomen, with cold sponging or cold baths and ice to the head if there is much body-heat. Brandy, whiskey, or coffee in full doses is called for early. Iced coffee can be given to children. Spirit of camphor in five-drop doses every ten minutes aids in averting collapse. Small doses of calomel every hour or two may benefit nausea and vomiting. Arsenic is said to do well for vomiting and profuse watery diarrhoea. For adults, morphia hypodermically is perhaps the best remedy for the vomiting and purging; even for children, minute doses given in this way are best for alarming illness. Hypodermic injections of ether have also been suggested.

For the relief of duodenitis means are used to relieve the digestion of the want of the biliary and pancreatic secretions. Nitrogenous food is to be taken, but no fats or starch. Counter-irritation over the epigastrium and right hypochondrium by a blister or iodine is of direct service. If icterus accompany duodenitis and catarrh of the bile-ducts, all treatment must be directed to the duodenum. For ileo-colitis and colitis the rules already given apply.

{699}

CHRONIC INTESTINAL CATARRH.

BY W. W. JOHNSTON, M.D.

ETIOLOGY.--Chronic intestinal catarrh has many of the same causes as the acute form; it is the expression of a large number of different pathological states and complicates many general and local diseases.

It is very common in children under two years of age, and is associated with change in diet in weaning and with the irritability of all the tissues during dentition. It is also a frequent disease in old persons, being due to imperfect mastication, the weakness of digestion, portal congestion, the gouty diathesis, and other causes.[1] Men have the disease more frequently than women. Hereditary influence and idiosyncrasy predispose to chronic catarrh of the bowel as to catarrh of the bronchi. Bad hygiene, want of cleanliness with an unhealthy condition of the skin, constant breathing of foul air due to want of proper ventilation, animal decomposition, or overcrowding predisposes to chronic diarrhoea. The chronic diarrhoeas among soldiers in camps,[2] among the inmates of prisons, workhouses, and asylums, are examples of these influences. Overwork, especially mental overwork with anxiety, and privation of sleep act in the same direction. In the chronic constitutional diseases and in many chronic diseases of organs diarrhoea sooner or later appears, and very generally is the immediate cause of death. In phthisis pulmonum, whether tubercular or not, simple catarrh of the bowel is nearly always present.

[Footnote 1: _La Diarrhée chez les Viellards_, Paris, Thèsis, 1865, No. 112. See also works of Durand-Fardel and Charcot and Loomis.]

[Footnote 2: According to the statistics prepared in 1871 by T. B. Hood of the U.S. Pension Office, chronic diarrhoea was the disease for which a pension was granted in 20 per cent. of all cases of disability from disease and in 75 per cent. of all the diseases of the digestive system (_Report of Commissioner of Pensions_, 1871).]

During the course of chronic Bright's disease, more frequently in the cirrhotic form, lesions are developed in the intestine which cause obstinate diarrhoea. The discharge of urea into the intestine, and its conversion into carbonate of ammonium, which acts as an irritant to the mucous membrane, is the reason of the diarrhoea in this disease, according to Luton and Treitz;[3] and in so far as the discharge represents the escape of urea by the bowel, it may be regarded as salutary. In gout, especially in old persons, periodical diarrhoea gives relief. Chronic gouty subjects assert that they are not benefited by colchicum until it has purged them. The {700} lithic-acid diathesis, pyæmia, septicæmia, scurvy,[4] diabetes, leucocythæmia, Addison's disease, and syphilis[5] have diarrhoea during some part of their progress. The malarial cachexia is often attended with a diarrhoea which quinia alone will relieve; this symptom may occur periodically or be constant.

[Footnote 3: A. Luton, _Des Séries morbides, Affections urémiques de l'Intestin_, Paris, Thèsis, 1859, No. 38, p. 45; also, Treitz, "Ueber urämische Darmaffectionen," _Prager Vierteljahrschrift_, Bd. 64, 1859, S. 143.]

[Footnote 4: See testimony as to the influence of scurvy in promoting diarrhoea (Woodward, _Med. and Surg. History of the War_, Part 2, Medical Volume, p. 638).]

[Footnote 5: A. Trousseau, "Comments on a Case of Syphilitic Diarrhoea cured by Mercury," _Clinique méd._, Paris, 1868, t. iii. p. 123.]

Disease of the liver, heart, or lungs, by retarding the circulation in the portal system, causes venous stasis and catarrh in the gastro-intestinal mucous membrane. The chief conditions which bring this about are tumors compressing the mesenteric veins, cirrhosis of the liver, tumors pressing on the ascending vena cava, valvular disease of the right and left heart, fatty degeneration or dilatation of the heart, cardiac debility from chronic exhausting diseases, fibroid phthisis, chronic pneumonic phthisis, chronic pleurisy, and pulmonary emphysema.

An unsuitable diet may not set up an acute catarrh, but may slowly induce changes of a chronic nature in the mucous membrane. This is the case in infants fed upon artificial food instead of breast-milk, or when the digestion is overtaxed after weaning. In adults food difficult of digestion and over-eating bring about the same result. Alcohol, spices, and condiments, if taken in excess, and the habitual use of purgatives, lead to chronic inflammation of the intestine.

Foreign bodies, such as fecal concretions, gall-stones, stones of fruit, bones, coins, and pins, by remaining in contact with the mucous membrane for a length of time, determine inflammation and ulceration.[6]

[Footnote 6: Lothrop, "Case of a Child in whom seventeen plum-stones, three cherry-stones, and seven small bones were impacted In the cæcum and ileum for a year. Inflammation, ulceration, and perforation of the bowel resulted" (_Buffalo Med. and Surg. Journ._, March, 1882, p. 346).]

Neglect in the treatment of acute catarrh, the prolongation of an acute attack, from its intensity and the incurability of the lesions, establish chronic disease.

All chronic lesions of the bowel are complicated with chronic catarrh, as chronic tubercular ulcer, neoplasms in the wall, pressure of a tumor from without, etc.

PATHOLOGICAL ANATOMY.--The alterations in the intestines in chronic catarrh involve the walls to a much greater extent than in the acute form.

The intestinal tube is dilated, contracted, or irregularly dilated and contracted. When the calibre is increased the walls are thinned. Hypertrophy and hardening of the tunics, chiefly of the muscular and submucous tissue, are accompanied by a narrowing of the canal, and this change, most common in the rectum and sigmoid flexure, sometimes involves a very considerable extent of the colon. Lebert records the case of a woman who had diarrhoea for six weeks; constipation and vomiting with abdominal tenderness ensued. There was hypertrophy of all the coats of the stomach and of the ascending colon and rectum. The rectum was so narrowed by the thickening of its wall that a female catheter could not be passed through it.[7] In chronic catarrh the mucous membrane {701} of the colon and of the lower part of the ileum is the seat of the most characteristic lesions. The colon was alone the seat of disease in 9 out of 99 cases analyzed by Woodward; in the remaining 90 the two were involved together. In these the lesions in the colon (especially in the rectum and sigmoid flexure) were always more advanced and more serious than in the small intestine.

[Footnote 7: Lebert, _Path. Anat._, t. ii. pp. 247, 248; another case, Laboulbène, _Anat. path._, Paris, 1879, p. 194.]

Gastric catarrh may by extension become duodenal catarrh, and from the duodenum the disease may extend into the common bile-duct and its branches. The duodenitis and catarrh of the ducts may persist, and become chronic after the stomach lesion is gone.

The mucous lining of the intestine is changed in color, form, thickness, consistence, and in the appearance of its glandular structures. The shades of color in chronic inflammation are dark red, livid, brown, drab, or slate-color, light blue, and greenish. The coloration is not uniform. Dark-red and gray spots are seen on a pale and uniform red ground; grayish streaks and patches are mingled with red or whitish areas, giving rise to a mottled or marbled appearance.[8] In some cases red predominates, in others the slate-color.[9] Dark-brown, almost black, patches are also seen. These different tints depend upon the intensity and character of the inflammation and the stage which it has reached. Diffused bright-red discolorations belong to acute inflammation, and are rarely seen in the chronic form. Acute hyperæmic patches appearing in the midst of a slate-colored membrane indicate intercurrent acute attacks. Dark-red streaks or spots are caused by extravasations. Brown and slate-colored areas represent the changes in old extravasations or pigment-deposits where inflammation or ulceration has existed. Where the inflammation is progressing toward the destruction of tissue the membrane is dark-purplish or black in color, mottled with patches of dull reddish hue and minute spots of bright red. Black dots are seen in the small and large intestine isolated or in close proximity. They are due to minute specks of black pigment deposited in the apices of the villi, in the centres of solitary glands, in rings around them, or in the glands of a Peyer's patch. The juxtaposition of pinhead black points gives rise to the shaven-beard appearance[10] of the mucous membrane. Dark streaks or wavy lines of pigment are also seen.[11]

[Footnote 8: For illustration of color of mucous membrane in chronic inflammation see the following illustrations in color: _Med. and Surg. Hist. of the War_, Part 2, Medical Volume--plates facing pp. 308, 518, and 520; also, _Illustrations of Morbid Anatomy_, J. Hope, London, 1834, figs. 128, 129.]

[Footnote 9: For an excellent illustration of slate-color of chronic inflammation, with supervening acute inflammation and hemorrhagic patches, see Carswell, _Path. Anat._, Plate ii. fig. 4; also, Lebert, _Path. Anat._, t. ii. Pl. cxiv. fig. 7.]

[Footnote 10: For an excellent illustration of this change see _Med. and Surg. Hist. of the War_, volume cited, plates facing pp. 298, 304; also, _Atlas d'Anatomie path._, Lancereaux, Paris, 1871, Pl. iii. figs. 3 and 4.]

[Footnote 11: See colored plates _Med. and Surg. History of the War_, volume cited, facing p. 308.]

In the ileum the mucous folds are obliterated or swollen and thickened. Obliteration of the folds occurs in connection with a dilated intestine; when the intestine is contracted they are elevated, tortuous, and close together. The villi are hypertrophied, looking often like minute polypi. The mucous coat is usually thickened, measuring from one-fifth to one-fourth of an inch. It is softened, and more easily scraped off,[12] but quite {702} frequently there is induration instead of softening. The solitary glands of the ileum are hypertrophied and appear scattered over the mucous surface as small rounded elevations. They are quite numerous or a few only may be seen. A ring of vascular injection usually surrounds each enlarged follicle. Peyer's patches may be unchanged or from swelling of the follicles are more prominent than is normal, but relatively the enlargement of the solitary glands is greater. In chronic catarrh the follicles acquire greater size than in the acute form. The apices of the solitary glands in the small intestine may be broken down, leaving small follicular ulcers, with swollen rings around them formed of the undestroyed and hypertrophied gland-structure. Here and there one or two of the follicles in the Peyer's patch may have its centre indented by ulceration. These changes are usually in the lower part of the ileum near the cæcum.

[Footnote 12: The mucous membrane is often tumefied and softened in cases where there are thickening and contraction of the intestine with great reduction of its calibre (Elliot Coues, _Med. and Surg. Rep._, Philada., 1863, vol. x. p. 207).]

In the colon the enlarged solitary glands are in greater number, and are dotted about more closely in the descending colon and sigmoid flexure.[13] When there is ulceration the large intestine has many more ulcers than the ileum, and they are more numerous in the lower part of the colon. They appear as sharply-punched openings, and give to the mucous surface a honeycombed look; their diameter varies from one-tenth to one-fourth of an inch. Large ulcers formed by the confluence of smaller ones measure from one-fourth to one inch in diameter; they may be so deep as to have the muscular tunic for their base, and quite often the bottom of the ulcers is black. A ragged or uneven appearance is given to the surface by the ulcers being close together. Such extensive destruction sometimes takes place that no normal mucous membrane seems to be left. Perforating ulcers are occasionally seen in the large intestine or ileum. Perforation occurred in two of Woodward's ninety-nine cases. Healing ulcers[14] are found by the side of others which are growing. Healed follicular ulcers are known by a puckered, stellated appearance[15] of the mucous membrane, which is pigmented and of a slate-gray or marbled-brown color[16] if the process has been long completed. Larger dense cicatrices, pigmented also, mark the site of more extensive ulcerations.

[Footnote 13: Illustration, _Kupfertafeln zu_ DR. LESSER _über die Entzündung und Verschwärung du Schleimhaut des Verdauungskanales_, Berlin, 1830, Bei Enslin, Tab. ii. fig. 4.]

[Footnote 14: Illustration, J. Hope, _Illustrations of Morbid Anatomy_, figs. 168, 169.]

[Footnote 15: Illustration, _Med. and Surg. Hist. of the War_, _tom. cit._, p. 528.]

[Footnote 16: Illustration, Cruveilhier, _Anat. path._, xxx. livraison, Pl. iii.; also, J. Hope, _Illustrations of Morbid Anatomy_, figs. 128, 129.]

Besides follicular ulcers the mucous membrane is disorganized by ulcers which have their origin in a loss of epithelium and superficial erosion. These deepen and may attain considerable size.

In addition to the lesions already described, the inflamed and ulcerated surface is sometimes covered with a pseudo-membranous layer of greenish-yellow color.

Chronic catarrh of the duodenum is the cause of dilatation of the vessels and thickening of the coats. A varicose condition of the veins may give rise to hemorrhage without ulceration.[17] The orifice of the common bile-duct and the ducts for some distance are narrowed by swelling of their lining membrane.[18] Ulcer of the upper part of the duodenum {703} is found rarely in connection with external burns and chronic Bright's disease. It is more common in men between thirty and forty years of age. An embolized artery is the starting-point of the lesion. The mucous layer, deprived of its nutrition in a limited area, dies or is destroyed by the acid gastric juice; a round ulcer with terraced edges is left, its base being the muscular or serous coat. Adhesions may form between the peritoneum near the ulcer and the liver, gall-bladder, or pancreas, or an opening may take place posteriorly in the right seventh intercostal space or into the peritoneal cavity. Cicatrization of the ulcer may lead to narrowing of the canal of the bowel or of the pancreatic and common bile-ducts.[19]

[Footnote 17: G. Coulon, _Bull. de la Soc. Anat. de Paris_, 1879, p. 690.]

[Footnote 18: Duodenitis was made much of by Broussais and his followers, and a great deal has been written about it. (See Boudin, Paris, Thèsis, 1837, No. 76, _Essai sur la Duodenite chronique_.)]

[Footnote 19: _Ziemssen's Cyclopædia_, Amer. ed., vol. vii. p. 404.]

Suppuration in the wall of the duodenum is still rarer. One case only is on record of pus being found in the intestinal wall.[20]

[Footnote 20: Picard, _Bull. de la Soc. Anat. Paris_, t. xv., 1840-41, p. 393. See also microscopic view of suppuration in wall of duodenum, Thierfelder, _Atlas d. path. Histologie_, 2 lief., Tab. x. fig. 6.]

Chronic proctitis or inflammation of the rectum may exist by itself. The mucous membrane is swollen, hyperæmic, and the walls may be indurated and thickened so as to reduce the calibre of the tube. Superficial erosions or deep ulcers and perforation are due to the retention of hard fecal matter in the distended pouches of the rectum. Inflammation in the tissue around the rectum (periproctitis) is excited by inflammation of the wall without perforation; abscesses form and burst externally or into the bowel, thus establishing fistulæ.

PATHOLOGICAL HISTOLOGY.--The essential primary feature of chronic catarrh is the increase and persistence of cell-accumulation in the reticular connective tissue of the mucous and submucous layer. After an acute or subacute attack some time elapses before the large number of cell-elements are disintegrated or absorbed. By remaining they offer a constant invitation to causes of irritation, hence the necessity for prolonged care in diet after acute attacks. Fresh causes--imprudence in eating, etc.--induce additions to the number of cells, and the tissue becomes overcharged with active elements of growth. Hypertrophy of tissues results, the mucous and submucous tissues thicken, and the glandular structures are stimulated to a condition of morbid activity. The glands of Lieberkühn elongate, the number of acini increases, and the contained cells multiply. Accidental closure of the gland-openings from outside pressure or over-accumulation of the contents leads to cyst-formations. The lymph-cells in the reticular tissue of the closed follicles undergo rapid increase; the follicle is over-distended, projects above the surface, bursts, and a small ulcerating cavity is left. This is now enlarged by the breaking down of the remaining tissue of the follicle, then of the submucosa. The overhanging roof of mucous membrane, deprived of its nutrition, sloughs off at the edges and the exposed ulcerated surface is increased. By the confluence of two or more burrowing ulcers more extensive destruction of the mucous and submucous layers is brought about. The large deepened ulcers have the mucous layer for their base. Cicatrization of the ulcers takes place by the formation of cicatricial tissue at their base; the excavation is filled up partially, by contraction the edges are brought together, and the tissue solidifies. No villi or epithelium covers these cicatrices.

{704} There are rarer pathological changes. In catarrh of long duration cysts are found, especially in the large intestine. They are about the size of a small pea, projecting above the mucous surface. They have a yellow or amber color, and contain a jelly-like yellow fluid which can be pressed out. They originate in the distension of the dilating glands of Lieberkühn; according to Woodward, they find a favorable nidus for their growth in the softening tissue of the solitary glands; hence the cystic forms are seen occupying the interior of follicles undergoing disintegration.[21] The presence of the glands of Lieberkühn in the interior of the closed follicles has been observed by other pathologists, some of whom are unable to explain so remarkable a lesion.[22] Around the edges or in the midst of healing ulcers in the intestine granulation-like excrescences or polypoid growths are observed as a rare lesion. These seem to be projections from undestroyed islands of mucous membrane, being surrounded by the ulcerated surface. The minute polypi originate in a process of growth of the undestroyed mucous tissue. Cicatricial contractions around their bases give them peculiar forms; they are club-shaped, simple, or branched. This lesion has been described by Johann Wagner,[23] Carl Rokitansky,[24] and J. J. Woodward[25] from original specimens. According to Woodward, the growths (pseudo-polypi he calls them) are composed of a central portion of connective tissue continuous with the submucous connective tissue of the intestine and a peripheral portion of diseased mucous membrane. The central connective tissue was filled with large and numerous cells, and the glands of Lieberkühn in the mucous covering were elongated and branched and showed evidences of an active hyperplasia.

[Footnote 21: J. J. Woodward, _op. cit._, pp. 570, 571.]

[Footnote 22: A. Laboulbène, _Anat. path._, Paris, 1879, p. 186.]

[Footnote 23: "Einige Formen von Darmgeschwüren; iii., die Dysenterische Darmverschwärung," _Med. Jahrb. des k. k. öst. Staates_, Bd. xi., 1832, S. 274.]

[Footnote 24: "Der dysenterische Prozess auf dem Dickdarme und der ihm gleiche am Uterus, vom anatomischen Gesichtspuncte, beleuchtet," _ibid._, Bd. xxix., 1839, S. 88.]

[Footnote 25: "Pseudo-polypi of the Colon," _Am. Journ. Med. Sci._, Jan., 1881, p. 142.]

Polypi of the colon have been seen and figured by other pathologists, but they were not connected with ulceration and cicatrization of ulcers. Luschka[26] saw the mucous membrane from the ileo-cæcal valve to the end of the rectum covered with polypi, club-shaped, the size of a hempseed or bean, and made up of glandular tubes simple or branched. Other cases have been described by Lebert, Heuriet, and others,[27] in which polypi were distributed in the rectum, colon, cæcum, or about the ileo-cæcal valve. This is the condition described by Virchow as colitis polyposa.

[Footnote 26: _Virchow's Archiv_, vol. xx. p. 133.]

[Footnote 27: Heuriet, _Bull. de la Soc. Anat. Paris_, t. xlviii., 1873, p. 250; _Tr. N.Y. Path. Soc._, vol. ii., 1877, p. 172. For illustration of multiple polypi of colon and rectum, Lebert, _Path. Anat._, tome ii., Pl. cxxii. figs. 1 and 2; granular elevations in ileum, _idem_, Pl. cxxi. fig. 1. Also, mucous polypi of rectum, Thierfelder, Tab. xiii. figs. 3, 3_a_, 3_c_; also, intestinal polypi of rectum, Lancereaux, _Atlas Path. anat._, 1871, Paris, Pl. iv. fig. 4. Polypi are rarely seen in the small intestine; see Böttcher, "Polypöses Myom des Ileums," _Archiv der Heilkunde_, xi. Jahrgang, 1870, p. 125.]

Atrophy of the wall of the intestine, chiefly of the mucous layer, supervenes upon catarrh. It is confined to certain areas, the rest being normal or in a state of chronic catarrh. It is found in 80 per cent. of the cases examined either in the large or small intestine. The cæcum is the most frequent seat; next in the order of frequency it is seen in the ascending {705} colon, the lower part of the ileum, the other parts of the colon, and is least common in the upper part of the ileum. In children the lesion is more common in the small intestine than in adults. The changes in the mucous membrane of the colon are a diminution in its thickness and disappearance of the glands of Lieberkühn. The mucous layer is reduced to one-fifth of its normal size, and no trace of the glands may be left; a layer of connective tissue with imbedded round cells is all that remains. The surface of the membrane is irregular and colored with yellowish pigment. In the ileum the villi are shrunken, with few cells; in some cases they disappear altogether. The muscular tunic may share in the atrophy.[28]

[Footnote 28: Nothnägel, "Zur Klinik der Darmkrankheiten," iii. Abtheilung, Darmatrophie, _Zeitschr. f. klin. Med._, Berlin, 1882, iv. p. 422; Virchow, "Ueber den Gang der amyloiden Degenerationen," _Virchow's Archiv_, Bd. viii. S. 364; E. Neumann, "Neue Beobachtungen über amyloide Degeneration," _Deutsche Klinik_, Bd. xii., 1860, S. 337, 353, and 373; Lambl, "Ueber amyloide und colloide Degeneration im Allgemeinen und die des Darmsinsbesondere," _Beob. und Studien_ (_aus dem Prager Kinder-Spitale_), Prag., 1860, S. 319; Frerichs, "Diseases of the Liver," New York, 1879 (_Wood's Library_), vol. ii. p. 180; M. G. Hayem, "Note sur la Dégénérescence amyloide du Tube digestif," _Compte Rend. des Séances de la Soc. de Biologie_, Nov., 1865, 4me Série, t. ii. p. 191; also, _Gaz. méd. de Paris_, t. xxi. p. 99.]

Lardaceous (amyloid or waxy) degeneration of the intestinal mucous membrane is met with in chronic catarrh. The small arteries of the villi and submucous layer, the muscular and other tissues, are infiltrated with a new material allied to fibrin. The membrane to the eye is paler than normal. When iodine is applied, a characteristic red staining of the infiltrated parts is noticed. This lesion is a cause of diarrhoea and of hemorrhage,[29] from the greater permeability and greater fragility of the arteries. It is also associated with follicular ulceration, and is probably a cause of disintegration of the mucous membrane.[30]

[Footnote 29: T. Grainger Stewart, "On Hemorrhage from Waxy or Amyloid Degeneration," _Br. and Foreign Med.-Chir. Rev._, vol. xli. p. 201.]

[Footnote 30: Frerichs, "Diseases of the Liver," New York, 1859 (_Wood's Library_), vol. ii. p. 180; also, E. Aufrecht, _Berl. klin. Woch._, 1869, p. 315.]

The abdominal organs present other lesions in chronic intestinal catarrh, few of which have any distinctive character. The peritoneum shows signs of old or recent inflammation. The former is subacute or chronic, and is recognized by the adhesions of opposed surfaces in a limited area, frequently corresponding to the seat of intense intestinal inflammation. Fatal perforations are delayed or prevented by these adhesions. General peritonitis with soft lymph or sero-purulent effusion is found with perforation. The mesenteric glands may be enlarged. The liver is larger or sometimes smaller than normal, and its tissue is softened and may be fatty. Abscess of the liver[31] is a very rare result of chronic intestinal catarrh, with ulceration. The gall-bladder is usually filled with bile. The spleen is small and firm in texture; less commonly it is soft and friable. The pancreas is healthy. The kidneys are large and pale; the cortical substance is relatively increased and the tubules contain granular epithelium.

[Footnote 31: It occurred in 4 per cent. of Woodward's cases of chronic follicular ulceration. See case reported by the writer in which the ulcers healed before the death of the patient from hepatic abscess (_Maryland Med. Journ._, March 15, 1883, p. 562).]

In the thorax the heart is flabby, pale, and small; clots are found in the right and left side extending into the pulmonary artery and aorta. Sudden death has been attributed to cardiac thrombosis. That coagula {706} do form in the heart during life is shown by the sudden occurrence of cerebral embolism with aphasia.[32]

[Footnote 32: The writer has seen one case of this kind occurring during the effort at stool in a patient who was very feeble and very anæmic from chronic intestinal inflammation with ulceration.]

Pneumonia is the most frequent pulmonary lesion; it may be single or double. It was found in 18 of the 99 cases of Woodward, and in 21 out of H. A. Allen's 41 cases. Inflammation of the pleura is not infrequent. The brain and its membranes may be congested, and fluid is found in the subarachnoid space, in some instances in cases which have had a sudden termination. The cornea is ulcerated, and the eye destroyed by opening of the anterior chamber in a small proportion of cases. The sloughing process begins in the lower part of the cornea and in the sclerotic.

SYMPTOMS.--When chronic intestinal catarrh succeeds the acute form, the transition is marked by the disappearance of fever and an amelioration of all the symptoms, with apparent recovery. The patient begins to go about, but diarrhoea returns whenever there is any unusual fatigue or excess in eating. In some cases there is no improvement in the diarrhoea, but in the general symptoms only. When the malady is chronic from the beginning, the onset is characterized by symptoms of indigestion and occasional diarrhoea, which become more and more pronounced according to the severity of the illness.

Mild forms of catarrh have constipation, or diarrhoea alternates with a normal or constipated state of the bowels. The form in which constipation is continuous is associated with mechanical stasis from liver and heart lesions and with the gouty and uric-acid diathesis. The mucous membrane is in a state of passive hyperæmia, an excess of mucus being the product of the inflammatory process. Mucus coats the lining tunic, lessens its irritability, interferes with digestion and absorption, and acts as a ferment, exciting decomposition in the food. The bowel is atonic and is distended with contained gas; there is great feebleness of peristaltic contractions.

Intestinal indigestion and constipation are therefore the symptoms of this form. The signs of indigestion occur one to three hours after eating, according to the location of the maximum of catarrh and the time taken by the food to reach this point. They are a sense of fulness or distress in the abdomen from gaseous distension, slight colicky pains, and a rumbling of gas, which may be prolonged during several hours after a meal. The constipation is indicated by the spontaneous passage of dry masses or scybalæ coated with layers of mucus which are clear or cloudy, or the mucus may be intimately mixed with solid matter. Pure mucus is also expelled without fecal matter. There may be no stool without a purgative, and then softened matter with scybalæ and mucus is passed. Altered mucus in the form of membraniform shreds or cylinders occasionally pass in the so-called membranous enteritis.

The abdomen is full and not sensitive to pressure. The tongue is coated and usually pale and flabby. In appearance the patient exhibits a general want of tone; the skin is white or muddy, the muscles are soft, and the expression indicates the depression of spirits, the lassitude, and the inertia which he feels. Hemorrhoids are very likely to {707} exist. Such a condition may last for months or years without much change. Under proper treatment recovery may take place, but if entirely neglected or improperly treated the disease inevitably becomes worse.

In a second mild form there is no permanent disease, only an impressionability of the mucous membrane of the bowel to causes which induce hyperæmia and excessive secretion ending in diarrhoea. Exposure to cold, fatigue, or slight indiscretions in diet may bring it on; even an emotional cause may do it. The attacks last one or several days, and may at times assume some gravity. This predisposition to diarrhoea lasting through a lifetime is analogous to the tendency to inflammation of the nasal and other mucous membranes.

In severer and typical forms the symptoms point to permanent lesions. The tongue is smooth, shining, or glazed, sometimes with a central brown streak, but it may be also pale and covered with a white coat. The appetite is diminished or lost, or it is capricious, craving unsuitable food. If there is no gastric catarrh, the chief distress does not come until some hours after eating, but the taking of food sometimes excites pain and brings on an evacuation of the bowels through reflex influence.

There may be slight tympanites or a retracted abdomen. The imperfect digestion of food and the fermentation of the intestinal contents develop gas which keeps the abdomen distended and causes slight pains and borborygmi. Pain may, however, be entirely absent. A feeling of abdominal soreness is not unusual; it is increased by coughing, sneezing, or any sudden movement. Sensibility to pressure is usually wanting; when it exists it is found along the line of the colon in most cases.

The diarrhoea is the characteristic symptom. The number of the stools varies from one to eight in twenty-four hours; four is about the average number. They occur usually in the early morning hours, from two to six o'clock, but food may at any time bring on peristaltic contraction, so that a motion after every meal is not uncommon. In quantity there is much variability; two to four ounces of fluid matter is the rule perhaps, but a very much larger amount than this is often passed with each evacuation. As a rule, the larger the quantity of fluid the more extensive is the catarrh and the more advanced are the lesions. The matters passed are composed chiefly of fecal matter varying in consistence from a solid or semi-solid mass to a watery fluid. In the soft stool, like thickened gruel, the consistence is due to the presence of mucus; in the thinner evacuation water is the chief element. Liquid stools are sometimes frothy. In color the dejecta are brown, yellow, red, green, slate-color, or white. They may be colored dark by medicines, as iron or bismuth, or by blood. The presence of blood gives a pinkish, bright-red, dark-brown, or black color, depending upon the amount of blood and the changes it has undergone in the bowel from a longer or shorter retention. Blood, when it comes from the rectum, is in bright-red streaks or small coagula. When its source is higher up, it is much altered, being dark and granular. Coffee-ground sediment in a fluid stool is blood from the upper part of the intestine or stomach. The spreading of an ulcer may open a vessel of some size, and a fatal hemorrhage follow. A yellow tint like that of a child's movement may arise from a mixture of pus and fecal matter. Pus, as a milky or creamy fluid which may be {708} streaked with blood, is a frequent appearance in disease of the rectum and sigmoid flexure. The odor of the stools is fecal, sour, or sickening from fermentation or offensive from decomposition. In bad forms of chronic diarrhoea in children the black watery stools have a most offensive odor.

Mucus is the most constant ingredient of the diarrhoeal stool, and is in itself a sufficient evidence of catarrh, as it is not seen in normal stools except as a temporary phenomenon. It is present in flakes in watery evacuations, giving a jelly-like character to the fluid if it is in excess, or it is mixed with semi-solid feces. Pure mucus may be passed, if the catarrh is low down, in clear, glairy, or opaque masses. The frog's-egg or boiled-sago particles supposed by Niemeyer and others to point to follicular ulceration, and by Traube to be the swallowed bronchial secretion, are said by Virchow to be partly-digested starch, and also by Nothnägel to be of vegetable nature.[33] The stools may contain small yellow or brownish masses which are mucoid in nature, being yellow from bile-staining. Pavement epithelial cells are found in the coating of mucus around a hard fecal lump. Cylindrical epithelium is passed uncolored or stained with bile. These cells are separated, and are deformed and shrunken, with a granular protoplasm and indistinct nucleus. Goblet-cells are also seen. Round cells in the form of mucus-corpuscles or giant-cells are mixed with shreds of mucus or float in the thin stools. Crystals of triple phosphate, of neutral phosphate, oxalate of lime, and other lime salts, and of cholesterin, are also seen.

[Footnote 33: _Virchow's Archiv_, v. S. 329; Nothnägel, "Zur Klinik der Darmkrankheiten," _Zeitschrift für klin. Med._, iii., 1881, p. 241.]

Micrococci and bacteria have no pathological importance; they are seen in different diseases and in health.

Unaltered food may be expelled (lientery) by rapid peristaltic movements. But the microscope will detect what cannot be seen by the eye--unaltered starch-granules, filaments of meat-fibre, or fat in drops or in needle-shaped or feathery crystals.

The nervous system is disturbed after a certain time. There is languor, with depression of spirits, mental weariness, and inaptitude for work of any kind. The patient is querulous, morose; his sleep is restless, but sometimes profound until disturbed by the demand to empty the bowel. Melancholia is attributed to this as to other diseases of the abdomen, but their influence in producing insanity is doubtful.[34]

[Footnote 34: Griesinger, _Mental Path. and Therap._, Am. ed., New York, 1882, pp. 137, 138.]

No decided symptoms are exhibited in the respiratory and circulatory systems. Even slight exertion will cause shortness of breath and increased frequency or palpitation of the heart. This irritability of the heart is a marked feature of the disease.[35]

[Footnote 35: DaCosta found that of 200 cases of irritable heart, 61 were in patients who had suffered from or still had diarrhoea (_Am. Journ. Med. Sci._, vol. lxi., 1871, p. 37).]

The appearance of the urine is normal; it may be abundant, with phosphatic deposit, or it is scanty and high-colored. In bad cases albumen and casts have been found.[36]

[Footnote 36: Alonzo Clark, "Proc. of New York Path. Soc.," _Med. and Surg. Reports_, vol. ix., 1862-63, p. 312.]

The symptom indicative of atrophy of the mucous membrane is believed by Nothnägel to be the persistent passage of one soft, unformed stool daily. Mucus and fat, which diminish the consistence of the stool, are {709} excluded by microscopical examination. One stool daily shows that there is no exaggerated peristalsis which hurries the food along so rapidly that water cannot be absorbed.[37]

[Footnote 37: Nothnägel, "Zur Klinik der Darmkrankheiten," _Zeitschrift für klin. Med._, iv., 1882, p. 422.]

PROGRESS AND TERMINATION.--As the disease advances it is marked by progressive emaciation and debility. The skin gradually acquires great pallor, indicating profound anæmia. The loss of flesh is very rapid. An exacerbation of the disease will in a few days cause the cheeks to grow hollow, the eyes to appear sunken with dark rings around them. In all cases of long duration the progress is intermittent; frequent relapses occur from which the patient may rally and regain a moderate degree of flesh. Recovery may take place in weeks or months--eighteen months is the average duration[38]--but in most instances a tendency to a recurrence of the diarrhoea from cold, fatigue, or indiscretions in diet will continue throughout life. An incomplete recovery may take place by the cessation of the diarrhoea and formation of a stricture from the healing of an intestinal ulcer. In the worst cases there is no rule as to the rapidity or regularity of the march of the disease.

[Footnote 38: C. H. Ralfe, Seamen's Hospital, London: see Aitken's _Handbook of Treatment_, New York, 1882, p. 116.]

When the advance is toward a fatal issue the emaciation progresses until it becomes extreme; nothing but skin and bone are left. The cuticle is hard and dry, pale or brownish in color. The muscular strength is so reduced that the patient is unable to move from bed. The voice may sink to a whisper. The nervous depression and moroseness assumes a more marked character. Among the soldiers during the Civil War who had undergone great privations with insufficient or improper diet the mental phenomena were those of dementia.[39] In them the disease was modified also by the symptoms of scurvy and malarial poisoning.

[Footnote 39: W. Kempler, "Entero-Colitis," _Am. Journ. of Med. Sci._, vol. lii., 1866, p. 337.]

Fever is seen in the late stages; it is nocturnal at first, and later assumes the features of hectic. The pulse grows more frequent and thready; aphthous deposits appear on the inside of the mouth and pharynx. Toward the end the discharges may become more frequent and very abundant; they are more fluid, lighter colored or black, with floating particles of blood and mucus. There may be a loss of odor or they may have a cadaveric smell.

Death takes place in a few weeks or after years of alternate suffering and relief. The immediate causes of death are exhaustion, marasmus from starvation, collapse from perforation of an intestinal ulcer and consecutive peritonitis, syncope from sudden exertion, pneumonia, or acute pulmonary congestion, pleurisy, or subarachnoid effusion in the brain, with coma and convulsions.

COMPLICATIONS.--General dropsy results from the hydræmia and languid circulation of the late period of the disease. Other causes of this symptom are coincident diseases of the liver, kidney, or the malarial cachexia. Oedema of one extremity follows a thrombus in the crural vein. Chronic bronchitis and pulmonary phthisis are sometimes met with. Acute pneumonia[40] and acute pulmonary congestion are occasional {710} causes of death. Peritonitis may occur with and without perforation. The latter variety begins as a local inflammation of subacute or chronic nature, and spreads slowly until it becomes general. Extensive adhesions and abundant accumulations of serous, sero-purulent, or purulent fluid in the abdominal cavity result.

[Footnote 40: Pneumonia (8 double and 12 single) occurred in 20 out of 41 fatal cases reported by Harrison Allen, _Tr. Path. Soc. Philada._, 1867, vol. ii. p. 161.]

The causal conditions which have been enumerated may be considered as complications. They are tuberculosis, Bright's disease, cirrhosis of the liver, abdominal tumors, scurvy, tubercular and other neoplasms in the wall of the intestine; attacks of intercurrent, intermittent, or remittent fever arise from the malarial influence to which the intestinal catarrh is due. These fevers and rheumatism and pseudo-rheumatism are complications in soldiers from the exposure to malarial influences and to cold and dampness.[41]

[Footnote 41: Woodward, _op. cit._, p. 495.]

Ulceration of the cornea, escape of the aqueous humor, and collapse of the eye were observed in quite a number of cases occurring among soldiers.[42]

[Footnote 42: Elliot Coues, _Med. and Surg. Reporter_, Philada., 1863, vol. x. p. 207, and H. Allen, _Tr. Path. Soc. Philada._, 1867, vol. ii. p. 161.]

SEQUELÆ.--The alteration of structure from long-standing inflammation leaves the mucous membrane prone to recurrence of inflammation. Chronic intestinal indigestion and permanent malnutrition come from the same cause. The glandular and lymphatic structures of the intestine and the mesenteric glands are so changed by disease that they imperfectly perform their function. Tabes mesenterica is the ultimate phase of this change. Constipation succeeds chronic diarrhoea, and is due to atony of the muscular wall from long-continued distension, and probably from degeneration of the muscular structure. A more serious cause of constipation, and sometimes of intestinal obstruction, is found in stenosis of the bowel from the healing of the ulcers of long-standing chronic catarrh. Stricture is more common in the colon, sigmoid flexure, and rectum. How frequently such a result follows the cicatrization of intestinal ulcers is not definitely known. Woodward concludes from a careful search of books and pathological museums that stenosis from this cause is very rare.[43] Syphilis is the most common cause of ulcer. Local or general peritonitis leads to the formation of adhesions or fibrous bands uniting neighboring links of intestine. By the contracting of these narrowing of the intestinal canal may result. Paralysis, hemiplegia, paraplegia, etc. have been found to follow upon diarrhoea of long standing.[44]

[Footnote 43: Woodward, _op. cit._, p. 504.]

[Footnote 44: Potain, "Parésie des Membres inférieurs ayant succedé à un Catarrhe gastro-intestinal," _Rev. de thérap. Med.-Chir._, Paris, 1880, xlvii. p. 562; "Paralysis spinale sécondaire à une Diarrhée chronique," _Journ. des Conn. méd. Prat._, Paris, 1880, 3, S. ii. p. 57.]

DIAGNOSIS.--The mild form of chronic catarrh of the intestines associated with constipation has been confounded with hepatic disorders, and the obscure symptoms attending it have been attributed to excess or diminution of bile, and medicines to regulate the liver have been given accordingly. In the absence of lesions in the liver, in cases where symptoms such as have been described have preceded death, the opinion is not justified that disease of this organ has existed. On the contrary, alteration in the mucous membrane is almost always found, which points to the true nature of the disease. The diagnosis is based upon the accompanying {711} gastric catarrh and upon the symptoms of intestinal indigestion and malnutrition. Greater sensibility to pressure over the right hypochondrium and along the line of the colon, pain one to two hours after eating, with distension of the abdomen, the passage of well-formed and somewhat indurated feces mixed or coated with mucus, are symptoms peculiar to these mild forms.

The tendency to diarrhoea from cold, indigestible food, etc. which marks the second form of mild catarrh is easily recognized.

The characteristic symptom of the severe form is the persistent diarrhoea. Paroxysmal pains, tympanites and rumbling of gas, tenderness on pressure over the colon, the alternate periods of improvement and relapse, with the constitutional signs of impaired nutrition and progressive anæmia and debility, point out the nature and the seat of the lesion with sufficient clearness. It is futile to attempt to distinguish chronic intestinal diarrhoea from chronic dysentery. The lesions of the two conditions are essentially the same; it depends upon the fancy as to which name is given to the lesions described here under the title chronic intestinal catarrh. A greater amount of blood and mucus in the stool with tenesmus would more properly be called dysenteric, but the same case may present at one time diarrhoeal, at another dysenteric, symptoms.

Primary must be distinguished from secondary diarrhoea. Therefore the liver, heart, and lungs must be examined to discover diseases which might cause portal congestion. Any constitutional malady may be a cause and an explanation: tuberculosis or pulmonary phthisis stands first in its influence; next, chronic Bright's disease, septicæmia, scurvy, syphilis, and gout are attended by intercurrent diarrhoea. If all general disease can be excluded and the morbid process be located in the intestine alone, its cause may be known by studying the habits, occupation, and diet of the patient. Foreign bodies--hardened feces, gall-stones, fruit-stones, etc.--are possible causes which the history of the case may point to.

Having located the disease in the intestine and decided upon its primary or secondary nature, it remains to determine more precisely (_a_) the locality of the lesion, and (_b_) the stage of the inflammatory process.

(_a_) In what part of the intestinal canal is the disease located? It must be remembered that in typical and fatal cases the large intestine is the home par excellence of the lesions of chronic catarrh, and that the lower part of the ileum is often associated in the morbid processes, but limited areas of the small or large intestine are affected in mild forms which yield readily to treatment.

Icterus, clay-colored stools, and bile in the urine show that the catarrh is in the duodenum and involves the opening of the common bile-duct. The absence of diarrhoea, with flatulence and colics, limits the area of inflammation to the duodenum. Symptoms of duodenal indigestion accompany this form of catarrh; the failure of bile to neutralize the acid chyme impairs the effect of the pancreatic secretion. Fats are not digested and there is fatty diarrhoea. To this may be added tenderness in the right hypochondrium, and pain and oppression in the epigastrium and to the right one hour after eating. There may be wasting and hypochondriasis.