Enteritis

ENTERITIS, ENTEROCOLITIS (enteritis, enterocolitis), catarrh of the intestines, inflammation of the mucous membrane of the small and large intestines, occurring separately or, more frequently, as a generalized disease. This does not include isolated diseases of individual parts of the large intestine (colitis), especially its segmented forms (see Typhlitis, Sigmoiditis, Proctitis). In acute cases, the inflammatory process often arises simultaneously in the stomach as well, in which case it is a matter of gastroenteritis (see) or gastroenterocolitis. It is very difficult to distinguish catarrh of individual parts of the small intestine: the jejunum (jejunitis) and the ileum (ileitis); only from a pathological point of view can catarrhs of the ileum be distinguished as ileitis; here, lesions in typhoid fever are frequently localized and are then called ileotyphus. Clinically, acute and chronic forms of enterocolitis are distinguished. - Acute catarrh of the intestines (enteritis seu enterocolitis acuta) is etiologically connected primarily with infection and intestinal toxicoinfection. Most often, this involves a bacterial process with a greater or lesser participation of microbes grouped under the general name of paratyphoids, which also includes the permanent inhabitant of the intestine - Bacterium coli commune (see). Among paratyphoids, bacteria causing food poisoning (see Food infections, poisonings) and their toxins are of particular importance; these include Bacillus enteritidis Gaertner, Bacillus Breslau, Paratyphoid A and B, Bacillus suipestifer, and a number of other microorganisms of this group, as well as Bacillus proteus vulgaris. Although toxicoinfections are an important cause of acute enterocolitis, which is why intestinal catarrh as a rule comes to the forefront in food poisoning after the consumption of substandard food and especially in meat and fish poisonings, they are nevertheless not the only cause of acute intestinal catarrh. Overeating, especially with inadequate gastric digestion, consumption of very cold food and drink, as well as catching a chill, can cause enterocolitis. This also includes enterocolitis resulting from allergic and anaphylactic processes and frequent psychoneurotic affects in individuals with an irritable intestine (Enteric of German authors) (see Diarrhea). Pathological anatomy. Even macroscopically, marked hyperemia of the mucous membrane is visible, expressed mainly on the folds of the intestine and in the region of its follicular apparatus, at Peyer's patches, along with edema and petechial hemorrhages. The surface of the intestine is covered with inflammatory products—mucus, fibrinous exudate, and desquamated epithelium. In individual cases, there is a thickening of the muscular wall of the intestine and clouding of its serous cover involved in the process. Microscopically, there is dilation of the intestinal vessels, desquamation of the superficial layers of the epithelium over a considerable extent; the epithelium of the Lieberkühn glands is usually preserved, but the glands are shortened; from the side of the interstitial tissue, there is infiltration with a predominance of polymorphonuclear leukocytes and lymphocytes grouping around the follicular apparatus (enteritis granulosa, s. follicularis). Clinical picture. The onset of acute enterocolitis is most often rapid. Amidst complete health, frequent urges to stool appear, unpleasant sensations in the abdomen, quickly turning into sharp colicky pains that do not disappear even after defecation, usually accompanied initially by a significant amount of gases (see Gastroenteritis). After the first bowel movements, normal or mushy, frequent stools appear with mucous-watery discharges, greenish, foul-smelling. Over time, in very acute forms, the stool becomes watery, colorless, and odorless, sometimes resembling the rice-water stools of cholera patients (cholera nostras). The general condition of the patient varies in different cases, but is always more or less poor. As a result of hemodynamic changes (blood concentration with vascular spasm initially and paralysis of the vascular wall in the most acute cases), reaching the point of collapse in individual cases, and metabolic disorders with significant loss of chlorides, a number of very severe symptoms may occur. These include cramps in the lower extremities, especially the calf muscles, significant weakness, anuria, and sometimes cardiac failure. A febrile state joins in, and the temperature can hold at high figures (39°-40°) for 2-3 days, sometimes herpes labialis appears. Objectively: the tongue is coated, the abdomen is bloated, rumbling is felt, tenderness upon palpation, mostly in the middle of the abdomen; with thin abdominal walls, it is possible to see worm-like peristaltic movements of the small intestine, and spastically contracted loops of the intestine are palpated in places. Examination of the stool at first yields many remnants of undigested food, muscle fibers, and drops of neutral fat. The presence of mucus is especially significant, and the lower the process is localized along the intestine, the more mucus the stool contains; in individual cases, they also contain an admixture of blood. The fermentation test yields varying results—either phenomena of fermentative or putrefactive dyspepsia (see Dyspepsia). Bacteriological examination of the stool yields relatively little in acute enterocolitis; only in individual cases of food poisoning, if the excrements are examined in the very first days, is it possible to detect one or another type of paratyphoid; subsequently, they are displaced by the normal inhabitants of the intestine. The stomach takes part in the process in almost half of the cases; at the beginning of the disease, nausea and vomiting often appear, and subsequently a lack of appetite. In acute cases, there is not always a decrease in acidity; on the contrary, gastric irritation with increased secretion has been described (Noorden). The amount of urine decreases, it has a high specific gravity; albuminuria and cylindruria are observed, and in rare cases nephritis develops, running however in a mild form. There are indications of glycosuria (Funk and Reichard), indicating the involvement of the pancreas in the process. The prognosis in acute enterocolitis is favorable; only in children, the elderly, and individuals weakened by other diseases can acute enterocolitis be the direct cause of death. With a favorable course, acute enterocolitis can nevertheless be the cause of prolonged digestive disorders (see Dyspepsia, Diarrhea); on the other hand, acute enterocolitis is often the cause of diseases of the liver and biliary tract, e.g., cholecystitis, as well as often pyelitis due to hematogenous infection of Bacterium coli commune. Chronic enterocolitis arises either as a result of frequent repetitions of acute enterocolitis or independently, sometimes beginning in early childhood and being the result of children's intestinal dyspesias and toxicosis. In the anamnesis, it is necessary to keep in mind food poisoning, even if it proceeded easily and was short-term, which is connected with the prolonged change in the intestinal flora after poisoning and irritation of the intestine by the breakdown of protein bodies; in this case, an allergic state with a very threshold of irritation is obtained, which is why subsequently even simple overeating of completely benign food gives an exacerbation of the process and reveals latent forms of enterocolitis; these are the so-called "weak stomachs." In some cases, there is a constitutional decrease in the resistance of the intestinal epithelium, in others it is the result of toxicoinfections or other pathological factors. - Pathological-anatomically, the mucous membrane does not have the usual fresh red color, is slightly grayish, with a bluish tint as a result of stasis, and sometimes a brown coloration appears due to pigment deposition. The intestinal mucosa is most often thinned, sometimes there are cystic formations, proliferations are rare, most often in the distal sections of the intestine. Microscopically, there are changes analogous to acute enterocolitis, but small-cell infiltration is poorly expressed, and proliferations of interstitial tissue sometimes appear. It must be noted, however, that the evaluation of these pictures presents great difficulties. The clinical picture of chronic enterocolitis consists of a series of exacerbations and clear intervals. The general condition of patients usually does not change, in contrast to acute forms of enterocolitis. Subjectively: complaints of vague unpleasant sensations in the abdomen, not always having the character of pain. Constant unpleasant sensations in the abdominal cavity, a feeling of heat, transudation, distension, and pain, irregularity of bowel movements, diarrhea alternating with constipation—all this leads to vegetative and nervous disorders; patients become irritable, complain of decreased working capacity, especially when it comes to mental labor. From here, a special mental state, long known under the name of hypochondria et neurasthenia intestinalis, easily develops; the patient's attention is fixed on the stool, its consistency, character, and the presence of mucus. As a result, patients develop a number of phobias—fears of a particular food, often having no real basis in the function of the stomach and intestine and being the result of fixed ideas about the harm of food. To this are added phenomena of anemia, sometimes giving grounds to think of pernicious anemia. Objectively, there is a very indistinctly expressed picture of the disease.

Most often the abdomen is moderately distended; during periods of exacerbation, there is tenderness upon palpation in its middle parts, in the umbilical region, where gurgling is also felt. On the other hand, spastically contracted loops of the intestines and individual sections, especially of the ascending and descending colon, are easily palpated. Sometimes, along with gurgling and splashing in the ileocecal region, a spastically trapped fecal cylinder is palpated in the descending and sigmoid colon. The number and quality of stools depend on the site of the main localization of the process—in the small or large intestines (see Diarrhea, Constipation). Examination of the stools less often than in acute enterocolitis yields unchanged bile pigments, blood, and pus; if it is a matter of predominant lesion of the large intestines, there is a greater or lesser significant amount of mucus (see Colitis). During clear intervals, the examination of stools yields various results depending on one or another type of intestinal dyspepsia usually accompanying enterocolitis (see Dyspepsia); however, in contrast to pure dyspepsias, they contain more intestinal juice and inflammatory products, especially mucus. Mucus appears either in the form of individual clumps or even layers, or is diffusely distributed through the stools, giving them a shiny, lacquered appearance. When the process is localized predominantly in the small intestines, the mucus is colored yellow-green by bilirubin. With the Schmidt diet, it is easy to detect that the functional activity of the intestine is significantly reduced and that a number of food substances, especially muscle fibers and fats, are insufficiently digested. Thus, depending on the various combinations of inflammatory and functional changes in the intestine, objective data, and in particular the number and character of stools in chronic enterocolitis, create very diverse clinical pictures. The course of chronic enterocolitis is very prolonged; they sometimes drag on for years, which is why the prognosis for recovery is unfavorable. Sensitization of the intestine gives rise to exacerbations under the influence not only of dietary errors, but also of mild infections: influenza, tonsillitis, malaria, and even a common cold can become the cause of a prolonged exacerbation of the process. At the same time, on the basis of enterocolitis, segmental lesions of the intestine easily arise (typhlitis, sigmoiditis, and appendicitis). In the course of chronic enterocolitis, the state of gastric digestion is of great importance. The absence of free hydrochloric acid or a decrease in the secretory activity of the gastric glands (achylia gastrica, subacidity) has as its direct result an increase in the number of pathogenic microbes in the small intestines, which explains the extreme persistence of enterocolitis in these cases and its high tendency to relapses. This is of particularly great importance in the therapy of enterocolitis and for understanding a number of complications of this disease. Such a change in the bacterial flora of the intestine, especially in achylia, leads to irritation of the epithelial cover of the intestine with a disruption of the function of its cells, as a result of which cleavage products of protein bodies, which normally undergo further processing in the liver, can enter the bloodstream. As a result of the partial failure of the barrier function of the liver, over time these intestinal poisons can cause chronic endogenous intoxication. This autointoxication (Senator, Bouchard, Kraus, Mechnikov) causes a number of functional disorders on the part of the nervous system (irritability, depressions, hypochondriacal state, headaches, decreased working capacity, general malaise) and serves as a starting point for numerous diseases of individual organs and systems—the liver, pancreas, hematopoietic apparatus, avitaminoses (pellagra), joint diseases, and so on. The genetic connection of these pathological processes with chronic disorders of intestinal digestion as a result of the constant absorption of protein cleavage products is not always clear, but it deserves great attention when it comes to the disorder of intermediary metabolism as a result of enterocolitis. The diagnosis of chronic enterocolitis is based on the study of the etiology of the given disease, with infections suffered by the patients, and first of all bacterial food poisoning, being of particularly great importance. Functional disorders of intestinal activity, diarrhea alternating with constipation, the results of the Schmidt test, the study of the bacterial flora of the intestine by the method of determining its landscape (v. den Reis), X-ray examination, and rectomanoscopy make it possible to make a correct diagnosis. However, patients with chronic enterocolitis often go under various diagnoses for a long time, most often neuropathies, neurasthenia, hypochondria, solar plexus neuralgia, ganglionitis, intestinal adhesions, biliary dyskinesias, tuberculous peritonitis, and even abdominal angina (angina abdominalis). In individual cases, due to the lack of objective data, they are even considered malingerers. An isolated chronic lesion of the small intestines without the involvement of the large intestine, i.e., enteritis, undoubtedly exists, as evidenced by pathological-anatomical data, but it is very difficult to diagnose. Nothnagel considers typical for pure forms of enteritis the absence of diarrhea, minute lumps of mucus tightly bound to the stools lying inside the fecal masses, the presence of unchanged bile pigments tightly bound to the mucus ("gelbe Schleim-Körner"), undigested muscle fibers, and an increase in the amount of indican in the urine. So-called jejunal diarrhea must be distinguished from enteritis. Nothnagel described this rare disease, characterized by special properties of the stools resembling the contents of the small intestines; these are greenish-yellow, gelatinous masses with a high mucus content, odorless, containing unchanged bilirubin and a huge amount of residues of undigested food—meat, bread, potatoes, eggs, and so on; upon treatment with sublimate, these stools take on an intense green color. As an independent disease, jejunal diarrhea occurs very rarely; at times it appears during chronic enterocolitis as its exacerbation with localization in the small intestines (jejunitis). The differential diagnosis between pure forms of dyspepsia and chronic enterocolitis sometimes presents great difficulties. Some authors (Noorden) generally believe that there is no difference between these two groups of intestinal diseases (on the relationship between chronic enterocolitis and pernicious anemia, see Anemia). Treatment. In acute enterocolitis, the task of the physician is the fastest and most complete removal from the intestine of the infecting principle, its toxins, and decay products, and providing the intestine with the longest possible rest. Of the laxatives, castor oil (1-3 tablespoons), mineral salts—sodium sulfate, magnesium sulfate—one tablespoon in a glass of water, calomel either 0.3 twice over the course of an hour or 0.05 every hour until the appearance of characteristic greenish stools are especially indicated. Animal charcoal (Carbo animalis, 1 tablespoon in a glass of water or in a solution of magnesium sulfate) works excellently against bacterial processes in the intestine; charcoal resorb decay products. Against dehydration of the organism in sharply expressed forms of acute enterocolitis, the introduction of physiological saline solution by hot high enemas, subcutaneous and intravenous infusion of saline solution works excellently. This therapy is particularly indicated because, together with water, the organism loses large amounts of salt during acute diarrhea, and the decline in cardiac activity, convulsions, and a number of other symptoms are the consequence of chlorine starvation of the tissues—chloropenia. To raise the tone of the cardiovascular system, enemas and infusions of an isotonic glucose solution are indicated. Great benefit is brought in the first days by the apple diet, with the patient receiving only liquid tea and 1.5 kg of raw grated apples (preferably Antonovka) for two days in a row, with the exclusion of any other food. Of the medications, after thorough emptying of the intestine, Tinctura Opii simplex (5-10 drops) is given 1-2 times until the pain and diarrhea decrease. On the abdomen—heating pads, alcohol compresses. Very gradually, the patient is transferred to a normal diet (see Gastroenteritis, Diarrhea). The treatment of chronic enterocolitis presents a significantly more difficult task. At the basis of treatment lies the determination of the type of intestinal dyspepsia usually accompanying chronic enterocolitis. Therefore, the Schmidt-Strassburger functional test should precede the treatment of every enterocolitis. The diet at first, for 4-6 weeks, is sparing, constructed differently depending on what form of dyspepsia the functional examination of the intestines reveals (see Dyspepsias, Diarrhea, Gastroenteritis, Colitis). In any case, smoked preserves, game, fried fish, meat, pork, sauces, black bread, coarse varieties of vegetables, peas, beans, sauerkraut, and especially cold food and drink are forbidden for a long time. As a rule, patients tolerate whole milk poorly, as well as cream, cottage cheese, sour cream, and kefir. Medicinal treatment must take into account first of all the state of gastric digestion and, chiefly, the state of gastric secretion. In achylia and subacid gastritis, hydrochloric acid and pepsin or natural gastric juice are indicated (see Achylia gastrica, Gastritis).

Great benefit is provided by pancreon (Pancreon) and pancreatin (0.5 three times a day). In fermentative dyspepsia, calcium preparations (Calcium carbonicum, Calcium phosphoricum, Calcium lacticum, etc.) are prescribed for prolonged use, either alone or together with tannin preparations (tanalbinol, etc.). The use of disinfectants (Salol, Benzonaphtol, Naphthalinum) should be avoided; bismuth preparations work better (Bismutum salicylicum, Bismut. subnitricum, Bismut. subgallicum [Dermatol], Bismut. betanaphtholicum [Orthol], etc.). For pain and colic, atropine, bellafolin, and belladonna extract are indicated; opiates should be avoided. Among special methods, treatment with autogenous vaccines prepared from the patient's feces deserves attention (Wendt, Knorr, and others). Great benefit is provided by proper treatment with the parenteral administration of peptone (Luria, Umber, and many others). Physical methods of treatment consist chiefly of the systematic application of heat (warm wraps, heating pads, local light baths, Sitz baths) and diathermy. High intestinal lavage has been proposed in the form of so-called subaquaqueous intestinal baths (subaquale Bäder), performed with a specially designed apparatus. Treatment with ordinary enemas brings little benefit, especially enemas of tannin, which significantly worsen the inflammatory process in the intestine. Treatment with mineral springs gives good results both when prescribed in the form of bottled water and, especially, at health resorts. Depending on the form of enterocolitis, treatment is indicated in Essentuki, Zheleznovodsk, and abroad in Carlsbad, Kissingen, Homburg, Vichy, Neuenahr, and Tarasp (see respective articles). However, health resort treatment consists not only of drinking mineral water, but of a whole series of very powerful factors, such as climate, balneotherapy, mud therapy, diet therapy, and psychotherapy. The treatment of chronic colitis must take into account not only the direct effect on the diseased organ—the intestine—but the restructuring of the entire organism. Therefore, repeated treatment at health resorts often yields very favorable results in chronic enterocolitis.