Colitis

COLITIS. Contents: General etiology, pathogenesis and bacteriology of colitis 402; Pathological anatomy 404; Clinical forms of colitis 406; Diagnosis 418; Prophylaxis 419; Treatment 420; Colitis in children 423. Colitis (from Latin colon - large intestine), inflammation of the large intestine, regardless of its form, prevalence, and localization, characterized by pain along the course of the large intestine and functional disorders of the large intestine, in particular, disturbances in the number and properties of stools. Colitis can involve the entire tract of the large intestines—generalized colitis (pancolitis)—or be limited to individual sections—segmental colitis; the latter most often affects the cecum and ascending colon (typhlocolitis) or the sigmoid colon (S-Romanum), often together with the rectum (sigmoiditis, proctosigmoiditis), or predominantly one transverse colon, sometimes together with its flexures (transversitis, angulotransversitis). Widespread lesions of the large intestines (pancolitis), especially those proceeding acutely, are often encountered simultaneously with lesions of the small intestines and are known under the general name of intestinal catarrh, or enterocolitis. However, recently, thanks to the works mainly of the French (Mathieu, Roux, Cade, P. Carnot, Bensaude, Goiffon, and others) and the Germans (Nothnagel, Rosenheim, Strauss, and others), and in the USSR—Obraztsov and his school, clinical descriptions began to separately describe lesions of the small intestines under the name of enteritis, and of the large intestines under the name of colitis, in view of the sufficiently different etiology, pathogenesis, clinical symptomatology, course, and even therapy for them. Mayor (1893), Gaillard (1897), Dieulafoy (1898), and Obraztsov (1904) first mentioned segmental colitis. Both generalized and segmental colitis can proceed acutely and chronically, and the inflammatory process can involve not only the superficial layers of the mucous membrane (superficial colitis), but also infiltrate and destroy deeper layers of the intestinal wall with subsequent formation of ulcers of varying depth—ulcerative colitis, infiltrating colitis, and sometimes, having spread to the serous membrane, even cause inflammation of the peritoneum with subsequent formation of adhesions of the large intestines with surrounding organs (pericolitis). General etiology, pathogenesis, and bacteriology of colitis. An anatomically correctly constructed and physiologically normally functioning tract of the large intestines in a completely healthy individual remains normal as long as the entire chemistry of digestion remains normal, which depends on the correct and sufficient secretion of digestive juices, the number, composition, and virulence of the bacteria inhabiting the intestine, and the normal movement of the food mass along the gastrointestinal tract. Disturbance of the secretion of digestive glands, restructuring of the intestinal flora, migration of any group of bacteria to an improper place, mutation of microbes and strengthening of their virulence, as well as the entry of pathogenic bacteria and parasites into the intestinal lumen with food, through the lymph or blood, and the presence in the intestine of irritating chemical substances introduced with food or formed during fermentation or putrefaction of the latter, or finally poisons secreted by the mucous membrane of the large intestines (e.g., during poisoning with heavy metals, uremia)—all this causes irritation of the mucous membrane and its inflammation—colitis. Favorable moments for the occurrence of inflammation are, on the one hand, stasis of intestinal contents, and on the other—disturbance of the biochemical and immunobiological properties of the mucosa and disturbance of blood circulation in the mucosa. Stasis of contents depends either on a disorder of the physiological peristalsis of the intestines due to a lesion or functional disturbance of the neuro-hormonal apparatus regulating normal intestinal peristalsis (habitual constipation), or as a result of a mechanical obstacle as a result of an anatomical lesion of the intestine itself (stricture, tumors) or outside it (adhesions, tumors, etc.). Due to the fact that in some sections of the large intestines (cecum, sigmoid colon, rectum) the physiological intestinal contents remain for a fairly long time, and also due to the fact that due to anatomical features and peculiar function the normal movement of intestinal contents in them is easily disturbed, inflammation of their mucosa is encountered significantly more often than in the small intestines. The occurrence of colitis is also favored by frequently encountered congenital anomalies of the large intestines in the form of an excessively long large intestine (so-called dolichocolia) with various abnormal positions of its individual sections and their great mobility (caecum mobile, sigmoid colon mobile), which contributes to the disturbance of peristalsis (spasms) and the occurrence of a mechanical obstacle due to kinks and twisting, favoring the stasis of contents in these sections. Partial stasis of contents can also depend on the accumulation and retention of fecal masses in so-called diverticula. Anomaly of position and excessive length, as well as diverticula, are quite often encountered in the sigmoid colon, where, therefore, a primary inflammatory process easily arises (sigmoiditis and perisigmoiditis), which then often spreads upward and involves either the entire tract of the large intestine (pancolitis) or that section of it where physiologically the intestinal contents remain longer, namely—the cecum and ascending colon. Children, the elderly, and weakened subjects are especially predisposed to the disease of acute colitis, as well as cardiac and hepatic patients with disturbed blood circulation in the mucosa (heart decompensation, portal hypertension). Genotypic factors and constitution (anaphylactic colitis) also have a certain significance in the origin of colitis; segmental colitis often arises due to the transition of inflammation to the mucosa of the large intestine from an inflamed organ in the neighborhood (appendicitis, adnexitis, cholecystitis, etc.); pancolitis usually develops due to intoxication, autointoxication (toxic colitis), or infection (infectious colitis). Excessive overloading of the gastrointestinal tract with food, especially not entirely fresh and wholesome or spicy, in persons with weak digestive capacity gives rise to the disease of colitis. Sometimes colitis arises due to irritation of the mucosa of the large intestines by toxic substances introduced directly through the mouth (lead, phosphorus, etc.) or secreted by the intestinal mucosa during careless administration under the skin or into the blood for therapeutic purposes (mercury, arsenic). The most frequent cause of colitis is infection. In this regard, the group of Escherichia coli, especially together with streptococcus, plays a prominent role in the etiology of colitis. But streptococcus alone can also cause extremely severe inflammation of the mucosa of the large intestines. There is no doubt that staphylococcus and pneumococcus are also capable of causing the disease of colitis, since in persons who died from pyemia with symptoms of colitis, or pneumonia complicated by colitis, these microbes are found predominantly in the mucus removed from the surface of the intestine. Often colitis is caused by the typhoid bacillus, paratyphoid, dysentery bacilli, enterococcus, Bacillus perfringens, Proteus, or Bacillus pyocyaneus, putrefactive bacteria, etc. In general, it must be admitted that every pathogenic microbe entering the intestine is capable of causing colitis. However, in order to resolve the question of which specific microbe the disease is caused by, it is not enough to find this microbe in predominant quantity in the stools and lumps of mucus, but it is necessary to prove the presence of specific immune bodies for it in the patient's blood. In the etiology of colitis, especially in southern countries, protozoa (amoebae, lamblia, Balantidium coli, Bilharzia) also play a role. It must be noted that recently in the USSR, at least in Ukraine, one has to see more and more often colitis caused by lamblia and balantidia. One cannot deny a certain role of worms in the origin of colitis, especially whipworm and pinworm. Pathological anatomy. Inflammatory diseases of the small and large intestines have many common features, and very often both these sections of the digestive tract are affected simultaneously; the existing differences are conditioned partly by local features of the large intestines (denser consistency of the contents of the large intestines, tendency to stasis of fecal masses, especially in the cecum and rectum), partly by their relative local tissue insensitivity to some or, conversely, susceptibility to other viruses. According to the classification generally accepted for all mucous membranes, among inflammatory lesions of the large intestines, catarrhal, fibrinous, necrotizing (gangrenous), and ulcerative forms are distinguished, with further, more detailed subdivisions of each of them. The pathological-anatomical picture of non-specific catarrhal colitis can be quite diverse depending on the character of the catarrh, its duration, and also the age of the patient.

In ordinary acute mucoserous or mucopurulent catarrh, the mucous membrane appears swollen (from edema), unevenly hyperemic, turbid (due to abundant desquamation of the epithelium), and covered with numerous clumps of mucus or a semi-liquid mucopurulent mass, upon the removal of which a greater or lesser number of small extravasations are usually noticeable in the mucosa; often, there is also hyperplasia of the follicular apparatus. Such pictures can often be observed during the period of so-called summer diarrhea in children, in whom such diseases are of great importance, as they can be accompanied by fatal intoxication of the entire organism or lead to severe complications, such as, for example, septicemia or septicopyemia with the presence in the blood and secondary foci of the same bacteria as in the intestine (most often diplococcus and streptococcus colitis), or even to peritonitis due to the much easier penetration of bacteria through the loosened intestinal wall than in adults (Durchwanderungsperitonitis of German authors). In a prolonged process, the hyperemia gradually disappears, the intestinal wall becomes pale, somewhat less swollen, but denser due to the predominance of infiltrative, proliferative, and subsequently indurative processes over exudative ones. Since these changes take place mainly in the submucosal tissue, these forms are sometimes designated as colitis submucosa. Slate-gray pigment spots appear in the places of former hemorrhages. The secretion of mucus usually does not decrease, unless atrophy of the mucous membrane in general and its glands in particular finally sets in (colitis chronica atrophicans). The latter leads to thinning of the intestinal wall, sometimes all the more significant because the muscularis may also be involved in the atrophic process. In other cases, on the contrary, under the influence of prolonged inflammatory irritation, polypous outgrowths (so-called mucous polyps) arise on the intestinal mucosa, consisting of an overgrown adenoid base of the mucosa with hyperplastic and stretched glands. They are more common in children, and the rectum serves as the favorite site for their development. Special types of catarrhal colitis are 1) follicular colitis and 2) mucous or membranous (membranaceous) colitis. Follicular colitis is characterized by particularly strong involvement of the follicular apparatus in the process, which either simply becomes sharply hyperplastic (colitis follicularis simplex) or, in addition, undergoes necrosis and suppuration with subsequent formation of small ulcers at the site of the follicles (colitis follicularis apostematosa, ulcerosa). In most cases, such follicular ulcers are as if outlined by a dark red inflammatory hyperemic or hemorrhagic strip, due to which the entire surface of the intestine acquires an extremely characteristic appearance. In mucous colitis, it is mainly a matter of the formation of cysts in the mucous membrane—either superficial ones, developing at the site of ordinary intestinal glands due to increased production and stagnation of mucus, as well as narrowing or blockage of their outlet, due to inflammatory changes in the stroma, or deep ones, located already in the submucosal layer. The formation of the latter is associated with inflammatory growths of glands in the area of damaged or dead follicles, and since these growths sometimes reach the muscular layer, it is natural that the contents stagnate extremely easily in their cavities. With stronger contractions of the intestinal tube, thickened mucus from cystic cavities of both types can immediately enter the lumen in large quantities, where it takes on a ribbon-like or vermiform shape and in this form is expelled outward during defecation, often giving rise to its confusion with tapeworms or round intestinal worms (colitis mucosa s. mucomembranacea). In some cases, an excessive amount of thick mucus can apparently be secreted periodically into the intestinal lumen even from normal, non-distended glands under the influence of purely functional disorders. The etiology of catarrhal colitis is very diverse. Besides various bacterial pathogens, all kinds of toxic factors play a role here, either in the form of the direct effect of a toxin introduced from outside (e.g., in poisoning with ptomaines from spoiled meat, fish, etc.), or in the form of autointoxication (in uremia or children's so-called dyspeptic disorders), or finally in the form of infectious-toxic influences (in septicemia or diphtheritic intoxication). A significant part of chronic catarrhs also develops on the basis of general or local blood stasis (heart disease, liver disease, stasis in the area of the hemorrhoidal veins of the rectum). Fibrinous inflammation of the large intestine, which is divided into croupous and diphtheritic forms, essentially does not differ from fibrinous inflammation of other mucous membranes. Fibrinous and necrotic colitis are most often encountered in dysentery (see). Occasionally, their causative agent is the diphtheria bacillus (mainly in children when the process spreads from the anal area to the mucosa of the rectum). In addition, they can accompany certain poisonings (mercury, arsenic, uremia), and can also be caused by mechanical influences (decubital necroses during fecal stasis). In the further course, sloughing of the necrotic areas and the formation of ulcers occur. With the prolonged existence of ulcers in the corresponding area of the intestine, exacerbations of the process often occur in the form of new attacks of catarrhal or fibrinous inflammation. These repeated inflammatory irritations, in the presence of hyperplastic processes associated with the healing of ulcers, give rise to the development of mucous polyps even more often than simple catarrhal inflammation. Ulcerative colitis almost always develops secondarily from catarrhal, follicular, fibrinous, or necrotic forms. In addition, ulcers can form due to the breakdown of certain specific granulations arising in the intestines (e.g., in tuberculosis, syphilis, actinomycosis, typhoid, paratyphoid) or tumors (carcinomas, less often sarcomas) (see Intestine). Primarily, ulcers in the large intestine appear mainly under the influence of traumatic effects (e.g., damage to the rectal wall by enema tubes, ulceration of hemorrhoids during the passage of dense, voluminous fecal masses, etc.). In all these cases, as an outcome of the ulcerative process, more or less extensive cicatricial deformities and strictures, or various kinds of lesions of the surrounding parts, may arise. Regarding inflammation of the vermiform appendix, see Appendicitis.

N. Strazhesko, M. Skvortsov. Clinical forms of colitis. In view of the difficulty of often establishing the etiological factor in colitis disease, it is most rational to divide all forms encountered in practice according to the anat.-clinical principle. 1. Diffuse colitis (pancolitis): a) mild dyspeptic colitis (mucous enterocolitis) and b) severe colitis (ulcerative-infiltrating colitis). 2. Segmental colitis: a) typhlocolitis, b) transversitis, and c) proctosigmoiditis. 3. Membranous colitis (colica mucosa). The latter form constitutes a transitional group from neuroses to inflammatory disease of the large intestine. Often, developing on the basis of true colitis, it then acquires all the features of intestinal neurosis and vice versa (see Intestine--neuroses and Colica mucosa). All three indicated groups of colitis can be acute, subacute, and chronic in their course, and according to the character and degree of path.-anat. changes—superficial (catarrhal), infiltrating, ulcerative, ulcerative-gangrenous. Depending on the acuteness of the course and the seriousness of the anat. lesion, the clin. picture and course, while generally retaining the same characteristic features and symptomatology, differ only in the degree of severity of all phenomena, both local on the part of the affected section of the large intestine and stool, and general in the sense of the influence of the intestinal disease on the entire organism as a whole and on each organ individually. I. Acute diffuse colitis (pancolitis, enterocolitis). In the majority of cases, there simultaneously exists inflammation of the mucous membrane of the small intestine, with which acute colitis begins. Therefore, at the beginning of the disease, it is in most cases expressed by symptoms common to enteritis and colitis and even gastritis. Depending on which section of the large intestine is predominantly affected—proximal (cecum) or distal (sigmoid colon and rectum)—the syndrome of typhlocolitis or proctosigmoiditis may come to the fore (see below). A distinction is made between acute superficial colitis, when the inflammation involves only the superficial layers of the mucous membrane (colite muqueuse A. Mathieu), and severe acute colitis, in which the inflammation, having started on the mucosa, involves the remaining layers of the intestine (submucosal, muscular, and even serous). A. Acute mucous colitis (colitis mucosa) usually begins suddenly with gastric phenomena, which, however, do not last long, accompanied by general malaise, lack of appetite, nausea, and even vomiting, as well as an increase in temperature to 38.5-39°. Soon, colicky pains appear in the abdomen, rumbling, urges to defecate, and finally stools, at first semi-liquid and abundant with a large admixture of mucus, and later consisting almost exclusively of liquid mucus, sometimes with an admixture of a small amount of pus and blood. The pains are concentrated predominantly in the left half of the abdomen; patients complain of frequent tenesmus, pain, and burning in the rectum. Each time after a pain attack, there follows the discharge of mucous masses, and the number of stools can reach 10-15-20 or more per day. Often, colitis is accompanied by epigastric pains, nausea and urges to vomit, headache, dizziness, increased pulse rate, and urges to urinate. Soon the temperature decreases, while still remaining subfebrile, general well-being improves, appetite increases, and the patient, who willingly agreed at first to stay in bed, already strives to leave it. Diarrhea subsides, but periodically, attacks of abdominal pain still arise along the tract of the large intestine, sometimes accompanied by rumbling, belching, followed by a mucous stool, which now contains a significant admixture of fecal masses. After the stool, the pains do not subside immediately, and an unpleasant sensation in the left iliac region and rectum remains for some time. Physical examination of the abdomen reveals its slight distension, and palpation of the large intestine shows that the entire colon is irritated, contracts spastically under the hands, and is painful upon palpation. Such changes are noted mainly in the sigmoid colon and partly in the cecum. Rectosigmoidoscopic examination reveals edema, swelling, and redness of the mucous membrane, which is covered with mucopurulent masses throughout the entire distal segment of the large intestine. The introduction of the sigmoidoscope is painful and not always successful due to spasm of the sphincters. The character of the stools in acute colitis depends on the extent to which the colitis is accompanied by enteritis, how long the latter lasts, and which sections of the large intestine are predominantly affected. At first, the stools are liquid, foul-smelling, well-colored; only mucous threads and clumps are interspersed in them. They contain a large amount of undigested food residues, indole, phenol, ammonia, and dissolved protein. Stools of this character remain for a long time if the proximal segment (typhlocolitis) is mainly affected among the sections of the large intestine. In the case where colitis predominantly involves the distal segment (sigmoid colon), the liquid fecal masses soon disappear completely from the stool, and it consists of mucus, pus, and an admixture of blood, has almost no fecal odor, smells rather of dampness, and under the microscope, mucous clumps and strands are visible, among which are interspersed cells of shed intestinal epithelium, pus, red blood cells, and a mass of predominantly rod-shaped bacteria. The disease lasts a week or two. The temperature falls by the 3rd-4th-5th day, when the appetite is restored, the thirst observed at the beginning of the disease disappears, pains appear less frequently, diarrhea with mucus occurs less frequently, and little by little the stool, having passed the stages of mushy cow-like stool with mucus on the surface, becomes formed, but still with mucus. Acute mucous colitis lasts from a few days to 2-3 weeks. However, the disease easily recurs, especially in adults, and has a tendency to transition into a chronic state. Complications in the superficial form of colitis are comparatively rare and mainly concern the subsequently developing mild anemia, slight albuminuria, pyelitis, and rheumatoid phenomena. B. Severe acute colitis (colitis gravis) are encountered significantly less frequently than mucous benign colitis; they occur in severe poisonings (mercury, arsenic), in food intoxication (with putrid meat, spoiled sausage, fish, cheeses, etc.), and less frequently in uremic intoxication. Sometimes they arise during typhoid infection in various septic processes, in amoebic dysentery and giardiasis. The etiology of this form of acute colitis has not yet been clarified, since the Proteus, Pyocyaneus, streptococci, staphylococci, pseudodysentery bacilli, hemolytic species of Escherichia coli, Giardia, etc., found in the stools can also be considered as secondary microbes that have settled on the already diseased mucous membrane and only maintain the inflammation. The severe form of acute colitis is encountered most often in summer or early autumn, when fruits and raw vegetables are consumed in abundance and many cold drinks are consumed. Previously suffered dysentery, as well as superficial mucous colitis, predispose to the disease. Severe acute colitis manifests most often in the form of diphtheritic-ulcerative colitis (colite dysenteriforme Mathieu). Phlegmonous and gangrenous forms of severe colitis are encountered very rarely. Occasionally, the disease begins acutely, suddenly, mostly at night, with severe abdominal colic, which is then replaced by cutting pains, localized predominantly in the right and left parts of the abdomen and radiating to the lumbar region. Often, simultaneously with abdominal pains, there appear urges to urinate and pain during urination. In the majority of cases, however, the entire described picture unfolds gradually over 2-3 days and subsequently is replaced by periods of relative well-being and exacerbation. The general condition of the patient soon, sometimes quite rapidly, changes sharply. The patient complains of weakness, headache, pain in the limbs, sometimes cramps in the calf muscles, and general malaise. The temperature rapidly reaches high figures—up to 39-40°—and remains, having a remittent character, for several days at a fairly high level (38.5-39.5°), and then gradually decreases. The patient complains of dryness of the tongue, thirst, and periodically of severe abdominal pains, which have the character of either dull pains in the form of a painful band lying across the abdomen, or cutting pains in the lateral parts of the abdomen, or pains around the navel. To these constant painful sensations, periodically, 10-12-20 times a day, severe intestinal colics are added, accompanied by tenesmus. At the beginning of the disease, the stool is mushy, consisting of semi-liquid fecal masses with an admixture of glassy mucus; then it becomes purely mucous and finally dysenteric, consisting of mucus, pus, and blood (in the form of liquid raspberry jelly). In some cases, due to abundant serous exudate, the stool resembles meat washings, in which mucous films, mucous threads, and necrotic sections of the mucous membrane float (gangrenous form of severe acute colitis). Subsequently, during periods of relative calm, the stool again acquires the character of liquid-mushy with an admixture of inflammatory products: mucus, pus, and blood.

Its reaction can be either acidic or alkaline; under the microscope, there are many remnants of meat, starch, shed necrotic epithelium, a mass of bacteria, many of which are iodophilic, mucus, erythrocytes, purulent elements, among which quite a few eosinophils are found (Levy, Komarovsky), Charcot-Leyden crystals, and detritus. No specific bacteria or protozoa are found in the stool in this form of colitis, and bacteriological examination yields a negative result (Mathieu). It is possible that severe, especially gangrenous cases should be considered as a hyperergic form of inflammation of the colon. The abdomen, distended at the beginning of the disease, then retracts and sinks in; the abdominal wall is tense and painful; palpation of the colon causes pain, and the entire colon appears spastically contracted; this is especially pronounced in the sigmoid colon, which is hard, nodular, does not gurgle, and is sharply painful, and in case of complication with pericolitis, it loses its mobility. Sometimes a true plastic exudate forms around the sigmoid colon, located along the intestine and giving the impression of a sausage-shaped painful tumor upon palpation. During rectosigmoidoscopy, which is extremely painful and rarely successful, a strongly reddened, easily bleeding mucous membrane is visible, covered with a mucopurulent bloody coating; in many cases, ulcers of fairly large diameter are discovered, covered with the same dirty purulent-bloody masses and extending to various depths. Severe acute colitis has a varied course. In some cases, patients recover in 3-4 weeks; during this period, the temperature drops, pain disappears, and the stool gradually acquires normal properties. The recovered patient looks extremely emaciated, exhausted, and anemic. In other cases, relapses of the disease are observed, and the colitis acquires a chronic course. Finally, many die (50% according to Mühsam, 19.4% according to Schmidt) from exhaustion, recurrent intestinal hemorrhages, perforation of the colon and peritonitis, secondary sepsis, or heart failure. In general, the prognosis for this form is extremely serious, because even if the patient does not die, in many cases he remains incapacitated for a long time, and most importantly, he is left with chronic colitis or, at best, a colon tract that is extremely sensitive to inflammatory diseases. II. Chronic pancolitis most often develops from acute, especially in cases where the patient and the physician treating him lack sufficient patience during treatment and, most importantly, during the gradual expansion of the diet; but in some cases, even the most thorough treatment does not ensure complete healing of acute colitis, and it still transitions into a chronic form. This is often facilitated by dystonia in the autonomic nervous system, anomalies in the position of the colon, inflammatory adhesions around them, diseases of neighboring organs that reflexively affect the peristalsis of the colon, and anomalies in the secretion of digestive glands, in short, all those factors that distort the course of digestive processes and contribute to the stasis of intestinal contents. But still, chronic colitis is not always a consequence of acute; in some cases, it develops gradually and imperceptibly, without passing through an acute period. The usual form of chronic inflammation of the colon is chronic mucous colitis. It often originates in adults from childhood or develops in adulthood as a result of frequent dietary violations, especially in patients suffering from various forms of dyspepsia, and in patients with habitual constipation who abuse laxatives. Patients with chronic colitis complain of a bad taste, abdominal pain, bloating and colic, as well as variability in the frequency and properties of the stool; a characteristic feature of chronic colitis is the inconsistency of manifestations and the alternation of periods of relative well-being with periods of significant deterioration, during which not only are bowel movements and the character and properties of the stool often sharply altered, but the general condition of the patients also suffers significantly, and a mass of phenomena develops from other systems, such as, for example, the nervous, cardiovascular, liver, kidneys, etc., and often even small increases in temperature are observed. During periods of relative well-being, the general condition of chronic colitis patients is satisfactory, and individual manifestations from other organs are weakly expressed. The clinical picture of chronic pancolitis is extremely diverse and polymorphic and is determined, as in acute pancolitis, by many conditions: the state of the nervous system, disturbances in the secretion of digestive juices, the predominant involvement of one or another part of the colon—proximal (colotyphlon) or distal (sigmoid colon), which determines to a certain extent the course of bacterial processes and chemical disturbances in digestion, and the characteristics of the stool, etc. If chronic colitis predominantly affects the distal segment of the colon or is accompanied by local spasms in the colon, it often, especially in neuropathic patients, proceeds with symptoms of constipation or with symptoms of alternating constipation and diarrhea. Often in such cases, so-called "false diarrheas of Carnot-Bensaude, constipation diarrheas of Pevzner" are observed, when almost formed feces enter the sigmoid colon, dry out there, collect into lumps (scybala), are retained, and, by mechanically irritating the mucous membrane of the intestine, which responds by secreting an exudate containing mucus and an admixture of pus, cause false diarrhea. In these cases, several times a day, a peculiar stool occurs with pain and tenesmus, consisting of hard pellets of fecal masses and liquid mucus containing pus. But usually, in such colitis patients, periods of exacerbation are observed when the stool becomes liquid, cow-like (en tasse, en bouse de vache), which is characteristic of pancolitis with localization of the inflammatory process in the proximal segment and the involvement of the small intestine tract in the inflammatory process as well. In the latter type of pancolitis patients, suffering from a bad sour taste in the mouth, mild dyspepsia, abdominal bloating, dull pains, meteorism and gurgling in the abdomen, bad mood, dizziness, palpitations, and pseudo-anginal phenomena, the stool has an abnormal character. This is especially evident during periods of exacerbation, the cause of which is most often violations of the prescribed diet, emotional distress, or chilling of the abdomen. During periods of relative calm, the stool can be quite normal in both frequency and consistency, and only chemical and microscopic examination can detect the features characteristic of colitis in it. However, even in this period, patients do not cease to feel heaviness in the abdomen, painful gurgling (colica flatulenta), and sometimes even real painful spasms. In the period of exacerbation, due to increased peristalsis of the colon, bowel movements sometimes occur reflexively for insignificant reasons. Thus, often any introduction of food into the stomach causes lively peristalsis of the colon due to the gastrocolic reflex, accompanied by pain along the colon tract, belching, and the need to get up from the table in order to empty the bowels (diarrhée prandiale des colitiques Carnot). The stool occurring 6-7 hours after dinner also has such an imperative character in colitis patients, when liquid contents from the small intestines, especially with concomitant enteritis, pour into the cecum, which, being inflamed, responds with violent peristalsis, involving the entire tract of the colon in succession (diarrhée de la septième heure Carnot). In general, patients suffering from chronic pancolitis have a stool 3-4 times during the day, with the first time occurring early in the morning (intestin réveillé matin), which is explained by the fact that just by this time the irritated colon is filled with remnants of food eaten the night before. Each bowel movement is accompanied by gurgling, colic-like pains, and a mushy stool mixed with mucus, containing a large amount of water and often having a foul odor. The reaction of such stools can be alkaline, acidic, or neutral depending on the degree of predominance of processes of either putrefaction or fermentation; in the latter case, the fecal masses foam. The stools contain poorly digested muscle fibers, potatoes, casein, a significant amount of ammonia and organic acids, as well as indole, phenols, and dissolved protein. Mucus is contained either in the form of lumps or films or in the form of small, barely noticeable clumps, which under the microscope consist of gelatinous mucus, among which are enclosed desquamated epithelial cells, purulent elements, and clusters of bacteria (les amas mucoïdes of Goiffon). With the simultaneous presence of ulcers in the colon, especially in the distal segment, intestinal hemorrhages are sometimes observed in chronic colitis patients, reaching significant proportions in some cases. Objective examination of the patient in prolonged cases reveals a significant decline in nutrition. This is observed in colitis patients suffering from diarrhea; in colitis cases proceeding with constipation, nutrition may not be impaired. The tongue is coated, and a bad breath is often felt. The abdomen is in most cases distended, and tympanitis is noted upon percussion.

Palpation of the abdomen reveals a painful colon, easily peristalsing and contracting to the density of a rope, especially in the section of the descending colon and the sigmoid colon (corde colique). The cecum is either distended with gas and can be palpated in the form of a dense, painful pear with thickened walls, which gurgles dryly, or it has the form of a relaxed tube that produces loud gurgling. The physical properties of the large intestine tract are inconsistent and depend on the degree of its filling with contents and the properties of the latter; therefore, depending on whether the examination is performed before or after a bowel movement, or whether the colitis patient is suffering from constipation or diarrhea during the examination period, the results of the examination vary. In some cases, palpation provides quite definite indications of a prolonged spasm of one or another section of the large intestine; in others, a dense, constantly peristalsing terminal segment of the ileum is determined, which indicates a prolonged spasm of the Keith-Kellogg sphincter. X-ray examination of the intestine reveals a whole series of functional and anatomical disorders. In most cases, significant pneumatosis (accumulation of air bubbles) of the large intestine, high standing of the diaphragm, and compression of the stomach are detected. The contrast mass passes through the intestinal tract with large deviations from the norm, indicating significant dyskinesia. In some cases, it remains for a long time at the Bauhin's valve due to spasm of the sphincter (according to Kantor in 75%) and then, having broken through into the large intestine, passes through it quickly. In other cases, in the absence of a spasm of the Keith-Kellogg sphincter, it quickly passes through the entire intestinal tract and reaches the rectum after 9 hours (hyperperistalsis of the large intestine). Sometimes, at the site of the greatest manifestation of the inflammatory process, a local spasm is observed, and in the vicinity of these areas, there is atony of the large intestine. Finally, in the areas of the large intestine affected by the ulcerative process, the barium mixture does not linger, and interruptions are observed in the column of the contrast mass (Stierlin-Bensaud symptom). In other cases, in the intestine already emptied of the contrast mass, spots and strips of the contrast mass remain, surrounded by gas in the intestine. This is the settled contrast mass on the mucous membrane at the site of the ulcers. Upon romanoscopy, the mucosa of the sigmoid colon is sometimes pale and atrophic and covered with mucus, and sometimes red, congested, bleeds easily, and is sometimes covered with superficial ulcers. Examination of the secretory capacity of the stomach and pancreatic gland and examination of the bile give an extremely motley picture. In many chronic colitis patients, gastric achylia or hypochylia is observed (according to Strazhesko's statistics, achylia in 23%, hypochylia in 27%). In other cases, on the contrary, hypersecretion is noted. Pancreatic secretion is in most cases unchanged. In the bile from the gallbladder, a lot of mucus, purulent elements, bilirubin crystals, shed epithelium, Bact. coli, and streptococcus are often found, which indicates concomitant chronic cholecystitis. The liver, upon examination, turns out to be enlarged and painful. Chronic colitis patients often do not lose their appetite, easily violate prescriptions, and pay for this every time with an exacerbation of pain and increased diarrhea; others, on the contrary, lose their appetite and tolerate very little food. Any introduction of coarser food, and especially meat, acidic, spicy, and piquant food, causes a seizure of pain, and sometimes almost immediately after eating - belching, nausea. Such colitis patients refuse food, fearing to cause a seizure, avoid eating, lose weight, turn pale, and fall into a nervous state, which increases intestinal spasms and contributes to all kinds of reflex phenomena from the heart in the form of palpitations, pseudo-anginal seizures, and arrhythmia seizures; hypochondriacal mood, insomnia, dizziness, and rheumatoid pains often appear. The course of chronic colitis is extremely slow (years and decades). Violation of diet, nervous shocks that change the course of normal intestinal peristalsis and contribute to spasms, and consequently to stasis and the development of bacterial processes in the overlying sections with subsequent increase in fermentation and putrefaction, play a significant role in the course of colitis and its clinical manifestation. III. Segmental colitis. A. Typhlocolitis is the most frequently encountered form of segmental colitis. At one time, typhlocolitis was often confused with appendicitis, but thanks to the work of a number of authors (Dieulafoy, Hartmann, Mathieu, Guillaume, and others in France; Sonnenburg, Klose, Noorden, Fahr, and others in Germany; Obraztsov, Gausman, and others in the USSR), it has again entered clinical practice as a separate nosological form. A significant part of so-called "chronic appendicitis" is actually typhlocolitis. Confusion is easy due to the commonality of signs and the transition of inflammation with the participation of the serous membrane from one organ to another. The development of typhlocolitis is facilitated by the irregularity of the function of the ileocecal sphincter (spasm) (Gross in appendicitis, Kantor in colitis) and subsequent putrefaction in the small intestine, as well as insufficiency of the Keith-Kellogg valve (in anatomical processes in it and in appendicitis - Groedel and others); paresis of the sphincter in neuropathic patients can also play a certain role, as well as any stasis of normal contents in the proximal section, whatever its origin (ascending type of constipation), twisting, strangulation, adhesions in the region of the hepatic flexure, etc. Hematogenous infection in acute infectious diseases (influenza, typhoid, typhus, measles, scarlet fever, septic diseases, etc.) also plays a certain role, as well as lymphogenous infection of the intestinal wall in diseases of neighboring organs (adnexitis). Typhlocolitis manifests itself in the same clinical forms as other segmental colitides and pancolitides, since the same conditions for the development of an infectious process are present here as in other sections, with the only difference that due to the development of a wide network of lymph vessels, the proximity of the vermiform appendix, gallbladder, and appendages, the conditions for isolated inflammation are more favorable here; a favorable condition is sometimes a special network of films covering the proximal section (Jackson, Hofmeister, Rezanov, and others), as well as a frequently encountered anomaly of development and attachment of the cecum (caecum mobile, caecum elongatum); the prolonged stay of chyme in the cecum and the weakness of the musculature of the cecum compared to other sections. The development of an infiltrating form of typhlocolitis with subsequent narrowing is just as possible as in other sections of the colon, which, among other things, is often facilitated by the presence of diverticula in the proximal section. Perityphlitis is also observed, since the peritoneum is involved in the process more often than in other sections of the large intestine. The clinical picture of acute and chronic typhlocolitis differs only in the intensity of general phenomena, such as: increase in temperature, leukocytosis, the nature and intensity of pain, etc., as well as percussion and palpation data from the abdomen. In acute primary typhlocolitis caused by infection and stasis, there is usually bloating of the entire abdomen, bloating and tension of the wall of the entire lower section of the ascending and cecal colon, and sharp pain upon palpation. Sometimes the intestine reaches the volume of a newborn's head, and then it is visible through the abdominal walls, which are tense, but not as strongly as in appendicitis. Palpation in the area of the intestine is painful. However, isolated pain of the intestine persists only as long as there is no retroperitoneal lymphadenitis and perityphlitis, which often complicate typhlocolitis. As soon as they appear, the abdominal wall tenses more strongly, and the described signs that distinguish typhlocolitis from appendicitis become blurred. Stool is usually delayed during the period of stasis; when the contents, which have liquefied due to putrefaction and fermentation, break through the site of narrowing, caused mainly by spasm, into the transverse colon, a liquid-mushy, foul-smelling, cow-like stool follows several times, one after another, resembling the stool in putrefactive dyspepsia, but with a more obvious admixture of catarrhal products. After several foul-smelling bowel movements, the abdomen subsides, general phenomena improve, and the temperature drops. The pain at the beginning of the disease is dull, then becomes sharper and sharper; it can be accompanied by nausea and vomiting and radiates to the epigastric region, as in appendicitis, as well as to the lower back, the right leg, the groin, and if the process spreads to the right flexure, then to the IX-XI right nerve, to the right shoulder blade and shoulder, resembling the pain symptom complex in biliary colic. Among the frequently encountered complications, one should mention jaundice, acute hepatitis, and pyelonephritis. The course of acute typhlocolitis with adherence to diet, bed rest, and treatment is quite favorable; usually, complete recovery occurs within 5-7 days. But the tendency to relapses remains, and the process easily passes into a chronic state, especially if there are moments favoring stasis of contents in the cecum and ascending colon. In the event that the inflammation spreads to the serous covering and typhlocolitis is complicated by perityphlitis, the course is more prolonged.

In this case, a plastic exudate may form, and the condition may progress to suppuration, with the development of a perityphlitic process accompanied by temperature fluctuations, chills, leukocytosis, sweats, and often diarrhea. In this instance, the clinical picture resembles purulent appendicitis, and its diagnosis is very difficult. The picture of chronic typhlocolitis is somewhat different. Here, the symptoms change: constipation is often replaced by diarrhea. During constipation, there is stagnation of contents. The caecum is tense, its wall is thickened and painful upon palpation; loud rumbling and a splashing sound can be elicited in it. During the period of diarrhea, the typhlocolon is usually contracted, painful, and has thickened walls, but it does not produce significant tympanites upon percussion; however, we find liquid contents in the colon transversum during this period. Extremely characteristic is the irritability of the typhlon upon palpation, which a normal intestine does not exhibit at all. It is painful, and palpation causes it to contract. B. Proctosigmoiditis is observed in an acute or chronic form. Inflammation of the mucosa of the S-Romanum and the upper part of the rectum is facilitated by the stasis of solid fecal masses and often by infection of diverticula (diverticulitis—Graser, Suzuki, and others). The syndrome of proctosigmoiditis consists of pain, often accompanied by tenesmus, radiating to the lower back on the left, the left leg, the buttock, and the perineum, as well as dysuric phenomena. Corresponding to the innervation of this section (nervus splanchnicus minor, nervus pelvicus), the radiation of pain can also be higher—into the back, into the region of the IX-X intercostal nerves, when the colon descendens and flexura lienalis are involved in the process. The stool is usually hard with an admixture of mucus, pus, and blood, sometimes containing a large number of eosinophils and Charcot-Leyden crystals. Sometimes true intestinal hemorrhages occur. In some cases, during acute sigmoiditis or an exacerbation of chronic sigmoiditis, there is no fecal matter in the stool at all due to spasm of the colon descendens. In this case, the liquid stool (false diarrhea) consists only of exudate, which is a product of the inflammation of the mucous membrane. The rectoscopic picture is characteristic: superficial inflammation, ulcers (in infiltrating proctosigmoiditis, the formation of a stenosis). The abdomen is almost not distended.

in the acute form, and distends in the chronic form due to the development of narrowing from infiltration of the wall or perisigmoiditis. The sigmoid colon is painful upon palpation, dense, nodular, and hard; sometimes it loses its mobility due to perisigmoiditis, which in acute cases can manifest in the form of plastic local peritonitis with a characteristic distribution of exudate in the form of a distended urinary bladder (Obraztsov). Sometimes the plastic exudate can suppurate, and then an abscess is formed, descending into the small pelvis. Reflex phenomena from other digestive organs and other systems are expressed relatively little. General phenomena depend on intoxication; in the acute process, there is a high temperature up to 39°C, malaise, and joint pain. Complications observed in this form include stenosis, generalization of septic phenomena, and thrombophlebitis. In the chronic form of proctosigmoiditis, the development of polyps is observed on the mucous membrane, which, together with ulcers, give rise to periodic intestinal bleeding. Polyposis can involve a significant part of the distal section of the large intestine. Among other forms of segmental colitis, colitis of the transverse colon (transversitis) and colitis localized in the flexures—angulitis—are encountered less frequently; the symptomatology of the latter, if there is no pericolitis, differs so little in right-sided angulitis from typhlocolitis, and in left-sided localization from transversitis, that during life they are usually not diagnosed. Transversitis develops most often on the basis of stasis, on the basis of coloptosis, spasm in the region of the splenic flexure, Payr's disease; it is characterized by a painful mesogastric syndrome with radiation of pain to the back (region of the IX-XI ribs), dysphagia due to mechanical pressure on the diaphragm by the gas-distended intestine, and major reflex phenomena from the stomach, heart, and lungs, dizziness, and anginal-asthmatic attacks (Loeper-Baumann), as well as a lively reflex from the stomach to the colon, since the normal motor reflex (Hertz-Newton) is intensified after the introduction of food into the stomach; after filling the stomach, pains easily appear, especially when eating sour fruits, indigestible and coarse food, and coffee; they have a transverse direction in the form of a band (douleurs en barre). The pains are accompanied by belching and salivation, and sometimes by anginal and asthmatic phenomena. They have the character of a pain wave moving from right to left and sometimes accompanied by a dull rumbling. After several waves, the passage of gas or a call to stool often occurs. After several attacks of pain, painful spasms of the stomach appear. For this localization of colitis, the development of pneumatosis of the large intestines, depending on enteroneuritis and sensory-motor dyspepsia (Loeper), is characteristic in the chronic period. Upon examination of the abdomen, local distension in the region of the transverse colon, sharp tympanitis of the upper parts of the abdomen, tenderness upon palpation of the transverse colon, hardness and a spastic state of it during an acute process, and paresis and tympanitis of the intestine are more common in a more chronic process, especially with the existence of pericolitis. Stool in the presence of diarrhea resembles in character the putrefied or fermented contents of the cecum, but with an admixture of mucus and even blood. With constipation, it is in the form of hard masses covered with dense mucus. The development of an infiltrating process in the intestinal wall is possible, as is the formation of local exudate around the intestine (plastic pericolitis). The course is sometimes acute, accompanied by an increase in temperature and general intoxication, and sometimes more chronic with periods of exacerbation and remission. The pains described above are characteristic of periods of exacerbation of chronic transversitis and of acute transversitis. In the period of remission, the patient complains only of heaviness in the abdomen, pressure, bloating, and shortness of breath due to the high position of the diaphragm caused by the large intestine distended with gas. The clinical forms of segmental colitis described above are encountered in practice in their pure form relatively rarely. In the majority of cases, adjacent sections of the large intestine adjacent to the inflamed segment are also involved in the process; but here the degree of the inflammatory process is less, and therefore there are no characteristic symptoms allowing one to speak with certainty about the participation of the mucous membrane of these sections in the inflammation, and the entire clinical picture is characterized in typhlocolitis by the described syndrome of the right iliac region and the right lateral part of the abdomen, in transversitis by the mesogastric syndrome, and in proctosigmoiditis by the syndrome of the left iliac fossa and the left lateral part of the abdomen. For this reason, these clinical forms are given the specific name "segmental" colitis. The diagnosis of colitis is made on the basis of data from questioning the patient, objective examination of the abdominal cavity and intestines using physical methods of examination, by means of X-ray examination, rectoromanoscopy, and detailed examination of fecal masses. The task of diagnosis includes not only establishing the fact of the presence of colitis in the patient but also determining the form and localization of the colitic process, clarifying the causes of the onset of colitis and its transition into a chronic form, as well as determining the etiological factor and pathogenesis of the inflammation of the large intestines. With modern clinical methodology, which allows for the recognition of the above-described syndromes of pancolitis and segmental colitis, the diagnosis of colitis is generally easy. The most valuable data for recognition are provided by methodical palpation (Obraztsov, Hausmann, Strazhesko) and X-ray examination of the intestine, which allow not only to determine morphological changes in the tract of the large intestines (infiltration of the wall, ulcerative process, tumor, tubercular lesions, polyposis, pericolitis, change in the position of the intestine, disturbance of mobility) but also to determine functional disturbances in it (insufficiency of the ileocecal sphincter or its spasm, general and local hyperperistalsis, dyskinesia of the intestine, spasms, etc.). Thorough examination of stools with attention to their physical properties, to the digestibility of food products, examination for the presence of protein, mucus, pus, blood, study of the flora, and precise determination of the amount of acids, ammonia, and enzymes in them, as shown by Nothnagel, Guafon, Wichert, and others, also provide the clinician with those above-described characteristic coprological signs, on the basis of which one can not only diagnose the presence of colitis but also determine its localization. No less important data are obtained during rectoromanoscopy, especially for the recognition of proctosigmoiditis. It not only reveals the presence of a catarrhal, ulcerative, or even gangrenous process in the lower section and all possible complications, such as, for example, narrowing of the intestinal lumen, polyposis, but often establishes the nature of the disease, e.g., tuberculosis, syphilis, cancer, etc. The greatest diagnostic difficulties are encountered in the recognition of acute severe colitis, since they have to be differentiated from general infectious processes, which are often accompanied by damage to the intestinal tract, such as, for example, dysentery, typhoid fever, paratyphoid, colibacillosis, and sepsis. The prevention of colitis, especially for persons suffering from various forms of gastric dyspepsia, pancreatic and hepatic insufficiency, as well as those who have already suffered from intestinal diseases, consists in strict adherence to diet, labor hygiene, and sanitary conditions of life. The consumption of spoiled meat, putrefied and fermented dairy products, canned goods and all kinds of spicy substances, unripe vegetables and fruits, and unboiled water, especially in the summer, contributes to the onset of acute colitis. Washing hands, thorough washing and boiling of dishes, and the cleanliness of the table at which one eats and of napkins are of great importance in preventive terms, since pathogenic microbes and parasites enter the intestine mainly through the mouth with food, from hands, and from surrounding objects. Particular attention should be paid to this aspect in public canteens and dormitories, mainly in the summer. Since pathogenic microbes sometimes enter the intestine from neighboring organs, e.g., from the gallbladder in cholecystitis, from the vermiform appendix in appendicitis, and from inflamed female appendages, timely and thorough treatment of the latter is of great importance in preventing colitis. Even greater importance, especially for persons who have already suffered from colitis at some time, is the proper functioning of the intestine. Stasis of fecal masses, by irritating mechanically and contributing to the multiplication and strengthening of the virulence of the saprophytic microbes of the intestine, gives rise to the disease of colitis. Thorough regulation of bowel movements without abuse of laxatives, and primarily through diet, prevents the disease of colitis and contributes to the cure of colitis that has already developed. In the event that stasis is caused by narrowing of the intestines or adhesions, it must be eliminated surgically. And since bowel movement is subject to the nervous system, a normal lifestyle, avoiding overwork, and periodic rest and treatment with physical methods are of great importance in the prevention of colitis (especially in neuropathic individuals).

The treatment of chronic colitis can be started only after a comprehensive examination of the entire digestive apparatus, a study of the chemistry of digestion and the bacterial composition of the intestine, as well as an accurate determination of the nature of the pathological-anatomical process in the intestine, its localization, and the disturbance of intestinal functions. As for acute colitis, its treatment can be started even without a detailed examination of the entire digestive mechanism, especially if it is a case of infectious colitis. The prescription of a diet is made in accordance with the nature of the disturbance in the chemistry of digestion and the peculiarities of the changes in intestinal functions. Without paying attention to this circumstance, one can treat colitis for years without any success. It is desirable to periodically repeat the examination of the patient in this regard during treatment in order to timely change the diet upon noticing changes in the course of chemical processes in the intestine and a change in the intestinal 'landscape,' so as not to create conditions for the development of opposite processes in the intestine, e.g., not to turn fermentative dyspepsia into putrefactive and vice versa, which again will harmfully affect the course of chronic colitis. Thus, the treatment of colitis (see Intestinal Dyspepsia), especially its chronic forms, cannot be template-based; it is strictly individual and can be rationally conducted in any case in the first weeks only in a sanatorium-clinical setting. Subsequently, it can be conducted on an outpatient basis and at health resorts for patients not living in sanatoriums. The treatment of any colitis, whether it is acute or chronic, generalized and associated with enteritis or segmental, consists of prescribing a specific dietary regimen, drug treatment, the application of various physical procedures to the abdomen, local treatment of the mucous membrane of the colon itself, treatment of disorders in the nervous system, and in exceptional cases, the application of surgical treatment. In acute, favorably progressing colitis, bed rest is necessary, as well as the administration of a laxative at the very beginning of the disease (Olei Ricini 30.0; Natrii sulfurici 20.0) for the purpose of removing all food masses and pathogenic microbes from the intestine, and then the prescription of a strict diet and soothing therapy. It is extremely useful, if the patient's strength allows, to prescribe an absolutely fasting regimen and then very carefully add easily absorbable and digestible food. During fasting days, it is useful to inject subcutaneously or intravenously 2 times a day 250-300 cm³ of a 6-10% glucose solution in Ringer's solution. In the first days after 2 days of fasting, one can prescribe only tea with red wine, liquid mucous soups, and expand this diet only if there is no abdominal pain and diarrhea. Then one can add rusks, vegetables pureed in soup (potatoes, carrots, cauliflower), prescribe almond or protein milk, allow adding a little cream to tea, a little white rusks, and only with good stool and the absence of pain and phenomena of excessive putrefaction and fermentation in the intestine, gradually switch to minced varieties of white meat, boiled fish, boiled cottage cheese. Milk in its pure form, kefir, sour milk, eggs, beef, game, and coarse varieties of greens, lettuce, and fruits containing a large amount of fiber must be prohibited for a long time. When conducting a strict and semi-fasting regimen, the known emaciation, anemia, and weakness soon disappear upon the restoration of digestive processes, when the patient switches to a normal diet. Nothing can be worse than limiting oneself to dietary half-measures when treating acute colitis. This contributes to relapses and the transition of colitis into a chronic state. In severe forms of colitis, the regimen must be even stricter. After fasting, for a long time, only rice decoction, vegetable broth, and warm sugar solutions are given. The patient's nutrition should be maintained by glucose infusion and the subcutaneous administration of camphor oil. Hot compresses on the abdomen, a thermophore or heating pad, and the internal administration of opium and belladonna in the form of suppositories (in a dose of 0.02), as well as tincture of opium and valerian (Tincturae Opii 10.0 + Tincturae Valerianae 15.0, 25 drops 2-3-4 times a day) soothe pain and contribute to the cessation of diarrhea and tenesmus. The internal administration of ipecac root (Inf. Ipecacuanhae ex 1.0 : 200.0) with the addition of tannin and bismuth preparations (Bismuti salic. 0.5 three times a day), as well as disinfectants (Benzonaphtholi 0.5 x 3, Saloli 0.5 x 3, and simarouba) is quite rational. For details, see Dysentery. A good effect is provided by the simultaneous use of medications by infusion per rectum. A warm solution of gum arabic with the addition of opium, starch enemas, and irrigation with a warm infusion of chamomile with opium act in a soothing manner. Warm irrigations of the colon with Essentuki water No. 17 are also useful. The treatment of chronic colitis requires great patience from the patient and skill and endurance from the physician. As stated above, the treatment must be strictly individual. First of all, the physician must keep in mind the restoration of normal bowel function, e.g., the elimination of constipation, and moreover, mainly by prescribing an appropriate diet and medications (atropine for spastic constipation, 0.001 one-two-three times a day), the administration of Provence oil internally, paraffin oil (1 tablespoon 1/2 hour before meals twice a day), and by the systematic use of oil enemas. Water enemas, soap enemas, as well as herbal laxatives should be avoided if possible, as they can maintain irritation of the inflamed mucosa. In the case of colitis accompanied by diarrhea, the latter must be eliminated mainly by prescribing an individual dietary regimen. There is no regimen suitable for all colitis patients. When prescribing a regimen, it is necessary, guided by the nature of the disturbances in the chemistry of digestion, to restore the normal composition of the intestinal flora, to create an unfavorable environment in the intestine for the development and reproduction of pathogenic microbes that have entered from the outside or one's own saprophytic microbes that have strengthened and become pathogenic. It is necessary to change the composition of food in such a way that with the predominance of fermentative processes (enterocolitis) or putrefactive ones (pure pancolitis, typhlocolitis), the corresponding microbes would not find nutritional products for themselves and would die out (see Intestinal Dyspepsia). In both cases, fasting leads to the goal. Therefore, Noorden's suggestion to start the treatment of chronic colitis with 2-3 fasting days is quite rational. They need to be repeated every 20-30 days whenever a slight exacerbation of the colitic process is noticed. The strictest regimen should be conducted for colitis patients suffering from diarrhea. Beef, game, eggs, and milk are food unsuitable for the treatment of colitis patients. Mucous soups made from fine flour, broths from pureed vegetables, soup from pureed rice, pearl barley, potato puree (if there is no fermentative dyspepsia), fruit jelly, sugar in any quantity, tea with red wine are the most suitable food. Only after the cessation of diarrhea can one allow rusks, and then pureed and minced white chicken meat, a little boiled lean fish, a little pureed lean ham. Of dairy products, with normal stool in a colitis patient, one can add cream to tea, give boiled cottage cheese, allow 1-2 soft-boiled eggs. In the treatment of colitis accompanied by constipation, the regimen should not be so strict. Here, besides porridges, white meat, fresh fish, it is useful to give boiled pureed vegetables, boiled fruits, figs, honey, and sugar in large quantities. Such patients can be allowed a little good rye bread with butter. Drug treatment for diarrhea consists of prescribing bismuth salicylate (0.5x3), purified chalk (Calcium carbonicum pur. 1.0 three times a day), and tannalbin. Any exacerbation requires the prescription of the same medications as in the acute form of colitis. In case of intestinal spasms, atropine and Extr. Belladonnae (0.015 three times a day) are recommended. The systematic use of warm vodka compresses at night, flaxseed poultices in the morning and evening for 1 hour is quite rational. In case of insufficient secretion of gastric juice, natural gastric juice is prescribed (1 tablespoon 2-3 times a day in 1/2 glass of water 1/4 hour before meals), pancreon (0.5 three times a day). Local treatment for sigmoiditis by means of irrigating the colon with a warm solution of silver nitrate (0.1-0.2 per 1,000) is useful; likewise, irrigation with a solution of potassium permanganate (1 : 4,000-6,000) and calcium chloride (5 : 1,000) is useful. It is very useful to dust ulcers in the S-Romanum and rectum with dermatol during rectosigmoidoscopy. Surgical treatment of colitis was proposed in France by Folet and is highly recommended by Mathieu and Boas for severe forms of colitis that do not respond to conservative treatment. The goal is to create complete rest for the diseased mucous membrane and then directly treat the intestine from above by irrigation with disinfectant solutions. For this, in cases of moderate severity, appendicostomy is performed, and in more severe cases, an anus praeternaturalis in the ileum or cecum. By irrigating the entire colon through the created opening in the intestine with a physiological solution or a solution of silver nitrate, they contribute to the cure of colitis.

Quite a few cases of curing the most severe ulcerative colitis by surgical means have been described. The created opening may heal over time or require a secondary operation. Chronic colitis patients are sent in the summer to health resorts for treatment with diet, regimen, and mineral waters. The choice of resort depends on the general condition and nutrition of the patient, the nature of the disturbance in the secretion of digestive glands, and the peculiarities of the disturbance in the chemistry of the intestine and its functions. In the USSR, they are sent to Essentuki, Zheleznovodsk, and Mirgorod; in Germany, to Carlsbad, Marienbad, and Kissingen; in France, to Vichy, Chatel-Guyon, and Plombieres. At the resort, patients benefit from rest, climate, treatment, mineral waters, follow a regimen and diet, and are treated with baths, electricity, and mud compresses, and their colitis often subsides. In view of the influence of the nervous system on the functioning of the intestine, it is necessary to always include treatment of the nervous system according to the general rules for neurasthenics among the medical prescriptions for a colitis patient. To the question of whether it is possible to completely cure a chronic colitis patient, i.e., to ensure that he can eat everything like a healthy person, one should answer, together with Noorden, that a colitis patient can only be brought to a certain equilibrium, which varies individually, and he will always retain a certain sensitivity to dietary indiscretions, i.e., a tendency toward exacerbation of chronic colitis.

N. Strazhesko. Colitis in children is one of the most frequent forms of intestinal diseases and proceeds in an acute form with a tendency to transition into a subacute, and sometimes chronic course. Clinically, it is difficult to draw a line between colitis and dysentery. Colitis can be subdivided into primary and secondary. The causative agents of the former are various microorganisms, both of the type constantly living in the intestine—Bact. coli, perfringens, proteus—and exogenous ones—Streptococcus, Bac. pyocyaneus, Bact. pseudodysentericum, Pneumococcus, and others. Secondary colitis are complications of various infectious diseases, e.g., influenza, measles, malaria, etc., or sepsis (especially in infants). The source of the disease can be an intestinal infection from the consumption of spoiled, infected food (exogenous cause) or a dietary error of a qualitative-quantitative nature (crypto-endogenous cause). Colitis in children is most often encountered in summer, less often in winter and autumn in the form of epidemics, which once again confirms the predominantly infectious nature of the lesion of the large intestine. Pathologically, the large intestine is affected diffusely; the process rarely has a tendency to spread deep into the mucosa; the inflammation is characterized as diffuse serous-hemorrhagic or purulent-hemorrhagic with the involvement of the follicular apparatus. The follicles often necrose (small ulcers), and sometimes larger ulcers, resembling dysenteric ones, can also form. Inflammation of the large intestine in children, unlike in adults, is predominantly pancolitis. Clinically, colitis usually begins acutely. Three most frequent forms are noted: 1) a violently starting form with high temperature up to 39° and above, with the involvement of the nervous system in the form of vomiting, restlessness, sometimes convulsions, with frequent stools, indicating a lesion of the small and large intestines; 2) a form from the very beginning with typical colitic symptoms without sharply pronounced general symptoms at a high or moderate temperature; 3) a sluggish, latently proceeding form with symptoms of subacute dyspepsia. The first form often passes under the flag of toxic dyspepsia, especially in infants, in whom, in the case of a rapid lethal outcome, it is difficult to diagnose colitis due to the absence in the first days of typical colitic symptoms (tenesmus, mucous stool). In older children, after a few days, typical stools appear, clarifying the nature of the disease. An acute, violent rise in temperature usually lasts 2-3-5 days, then the temperature drops, but often remains high for one or two weeks. The second form is characterized by the early appearance of intestinal colitic symptoms and a relatively satisfactory general condition and well-being. The third form affects mainly children with sharply reduced nutritional disorders and weakened immunity; in them, colitis proceeds sluggishly with symptoms of subacute chronic dyspepsia, and only an autopsy often clarifies the true picture of the disease. During life, intestinal phenomena are sometimes completely absent. In typical cases, the characteristic intestinal symptoms in children are: 1) frequent, scanty, mucopurulent, often mucopurulent-bloody stool; the frequency of purulent-bloody stools gives a number of authors the right to classify colitis into the group of "bloody diarrhea," which, of course, is not entirely correct, since often, especially in infants, colitis occurs without the admixture of blood in the stools; 2) cramping abdominal pains (causing the so-called characteristic crying of infants); 3) tenesmus and 4) gaping of the anus, prolapse of the rectum—a symptom that is especially frequent and unfavorable in dysentery-like diseases. The involvement of the entire organism in a number of cases is expressed by symptoms of toxicosis. In cases of moderate severity and mild cases, along with the almost complete absence of general phenomena, there is some decrease in appetite, but sometimes it is even good. The course of the disease is different. There are cases (less frequent) that proceed violently, quickly leading to death; this especially includes colitis in infants, often proceeding as toxic dyspepsia (great loss of water, collapse); on the contrary, there are cases (more frequent) with a moderate and mild course of the disease, especially in older children, ending in recovery despite a long course. In general, a characteristic feature of colitis in children is the tendency to a subacute course of the disease, to frequent relapses after an apparent complete cure, and the cause of the relapse can be not only errors in diet, but more often infection, both enteral and parenteral (influenza), to which weakened children are especially prone. The differential diagnosis is not difficult in typical cases; but it is necessary to keep in mind the composite nature of the concept of "mucous-bloody diarrhea." The etiological moment is different; the presence of blood, especially in infants, does not at all predetermine the dysenteric nature of the disease; just the opposite, in infants, pseudodysenteric forms are more often encountered, caused by either Bact. coli, Bac. dysent. Flexner, or Bac. paratyphi, etc. Only a thorough bacteriological examination makes it possible to isolate true dysentery. In older children, dysentery is encountered more often, and therefore the presence of typical symptoms—bloody, mucous, very frequent stool, tenesmus, gaping of the anus—makes the diagnosis of dysentery probable even without bacteriological analysis. Due to the absence of typical stool and a violent onset with toxemia, it is easy to mistake colitis for the onset of toxic dyspepsia. It is important to pay attention to the influence of a starvation diet on temperature: the absence of a temperature drop speaks for the infectious nature of the intestinal disease (Finkelstein). The most frequent complications are, first of all, pyelocystitis, then nephritis, pneumonia. Pyelocystitis is especially frequent in infancy, more often in girls than in boys, proceeds acutely, but often also latently, and lasts, recurring, for years. It is necessary to especially emphasize the frequency of severe secondary nutritional disorders after colitis in infants, not only as a consequence of a long-lasting infectious disease, but also as a direct result of improper, one-sided (starchy) and scanty nutrition, or rather, starvation. The prognosis is generally favorable, with the exception of colitis in infants, especially with toxic symptoms. The older the children, the lower the mortality. The time of year has a great influence on mortality; in summer (especially in a hot summer) there is more colitis, and mortality is higher; along with this, the course is also longer; here, probably, the strength of the infection, and the decrease in the body's resistance (overheating), and the deterioration of nutritional conditions (poor quality of food) also play a role. The frequency of diseases in the hot season, the frequency of colitis in children fed artificially in a poor sanitary-domestic environment, also predetermines prevention: natural breastfeeding, prohibition of weaning in summer, proper artificial feeding, sufficient use of air and sunlight, appropriate food for older children, supervision of food products, hygiene of dwellings, fight against flies. In places of collective stay of children (infant homes, orphanages, kindergartens, boarding schools, etc.)—thorough sanitary supervision of the healthy, isolation of the sick, thorough disinfection of linen, disinfection of excreta, persistent ventilation of premises, etc. Treatment. In the first place, as with any gastrointestinal disease, is proper dietetics. The method of prolonged feeding with monotonous food, which is often essentially a starvation diet (starchy preparations, rice decoction, jelly, broth, rusks), which is unfortunately still widespread, must be abandoned and eradicated. The desire to "spare" the diseased organ very often leads to direct harm to the entire organism. In the vast majority of cases of colitis, where there are no general phenomena of toxicosis and where the appetite is only slightly weakened, and even more so if it is preserved, it is necessary to feed children guided not by the stool, but by the general condition of the child. Prolonged starvation, absolute and relative (one-sided), with inappropriate scanty starchy nutrition leads to severe exhaustion, weakening of immunity, and colitis acquires a severe or protracted course. In mild and moderate cases in infants, one should usually continue to give the same food as before the illness, reducing the quantity and adjusting to the state of the appetite. The transition to normal food should be gradual in accordance with the state of the intestine, better after 1-2 weeks of normal stool.

In severe cases resembling toxic dyspepsia, a short (6-12 hours) fast, a tea diet, decoctions, then a transition to the introduction of food, breast milk, buttermilk, protein milk; for older children, gradually starchy food, cottage cheese, clabber, kefir, vitamins, etc. It is necessary to emphasize the appropriateness of prescribing acidic dairy products (clabber, Mechnikov's lactobacillin, kefir) or milk mixtures acidified, for example, with lactic acid for colitis. Medicinal treatment to this day remains predominantly symptomatic. At the beginning of the disease, it is customary to administer Oleum Ricini (5-15.0) orally (repeated in the following days) or a solution of Natrium sulfuricum. For pain, heat is applied to the abdomen; belladonna suppositories or atropine orally; narcotics in a very limited number of cases. During the period of fecal diarrhea with a foul odor of the stools, disinfectants (salol, bismuth, etc.) are appropriate, as well as tannin preparations (tanalbin, tanismuth, etc.). In a later stage, various authors recommend enemas (1% Natrium benzoicum, 2-3% Natrium bicarbonicum, 1% Acidum tannicum, starch, etc.). Early use of enemas is in any case inexpedient. The use of specific sera and vaccine therapy, in view of the polymorphism of the microflora of colitis, has so far proven to be of little rational value. General treatment (anemia) and hygienic measures are of very great importance.

Colitis mucosa occurs in children over 4 years of age, more often in girls. The course of the disease is periodically recurring, very prolonged; it is characterized by the appearance of mucous-membranous clots, sometimes in the form of entire ribbons, often with a completely normal stool. Sometimes these phenomena follow some violation of the usual diet, and this violation is individually different: some do not tolerate dairy food, others meat, and still others, finally, certain fruits or vegetables. Filatov already pointed out the nervous nature of the disease. A number of authors currently view this colitis as a disorder of the autonomic nervous system. Treatment of this disease must be prolonged and persistent. The center of gravity is in the treatment of the nervous system. (See also Colica mucosa.)

V. Agionov.