Gastroenteritis

GASTROENTERITIS (from Greek gaster-stomach and enteron-intestine), inflammation of the mucous membrane of the stomach and small intestines or, as is often called, catarrh of the stomach and intestines. It is necessary, however, first of all to keep in mind that often, as will be seen below, functional diseases of the stomach and intestines proceed under the guise of G., not having at their base inflammation of the mucous membrane of the digestive tract. Although inflammatory processes of the mucous membrane of the stomach, small and large intestines can proceed completely independently and separately from each other, causing gastritis, enteritis, and colitis, it is practically correct to isolate from various combinations of these diseases gastroenteritis and colitis as diseases giving a distinctive clinical picture. It is expedient to consider separately acute and chronic G. as acute and as chronic diseases of the stomach and small intestines. At the same time, it is necessary to note that the symptomatology of G. as a nosological unit has much in common with some forms of pure gastritis (see), as well as with various intestinal dyspepsias and colitis (see), having a different patho-anatomical substrate and differing in their pathogenesis and course. Acute G. can result from a whole series of causes, among which infections and intoxications are in the first place. If we do not speak of such acute infectious diseases as cholera, where G. in acute form is a very frequent manifestation of the disease, then as causative agents of G. should be noted microorganisms united in the group Bact. coli and especially Bact. paratyphus B. It is very probable that in a number of cases of acute G., appearing when consuming poor-quality food, the disease owes its origin precisely to Bact. paratyphus B. To this same group of G. also belong diseases resulting from infection with Bact. enteritidis Gartner, Bact. enteritidis sporogenes Klein, the anaerobic Bac. botulinus van Ermengem, etc. Of course, the permanent inhabitants of the intestine Bact. coli can under certain conditions become pathogenic and cause acute G. With great probability it can be stated that the increase in acute G. in the summer months (diarrhea aestiva) is due to infection introduced into the stomach with spoiled food (milk) or contaminated fruits and vegetables. The activity of these same microorganisms must also be attributed to diseases of G., already having the character of mass poisonings from spoiled food (sausage products, fish products, pastries, ice cream) - a circumstance that forces special attention to be paid to sanitary supervision over food products, their preparation, and especially storage as a preventive measure against acute G. Along with microorganisms directly entering the stomach and intestines and causing G., a whole series of other infectious diseases with the character of bacteremia can be accompanied by acute G. These include influenza, septic processes, measles, pneumonia, malaria, etc.; here the matter is most likely not so much about direct acute catarrh of the stomach and intestines as about phenomena of anaphylaxis (see), clinically difficult to distinguish from G. Toxic G. can be of exo- and endogenous origin. G. as a result of exogenous intoxication appears as a result of poisoning with acids and alkalis, metals (mercury preparations), arsenic, phosphorus and abuse of laxatives, while it should be noted that G. can also arise with parenteral administration of medicinal substances (for example, mercury and arsenic and their preparations) and with intravenous administration (e.g., when injecting salvarsan). The most frequently occurring G.-due to overeating, when a large amount of taken, although quite wholesome food, is not digested by the stomach-can also be attributed to exogenous intoxication from products of improper breakdown of proteins and carbohydrates. - To endotoxic G. belong digestive disorders in violation of metabolism and in nephritis (in uremia), in gout, etc. Undoubtedly, in the origin of G., besides infection and intoxication, constitutional factors also play a certain role, in the form of low resistance of a given intestine (A. Schmidt, J. Bauer, von Noorden, etc.); these are people with so-called 'weak stomachs', easily subject to inflammatory processes under circumstances completely harmless to other persons. Düring (M. During) tends to see in this a manifestation of a decrease in the bactericidal force of the intestinal epithelium. It is difficult to explain the mechanism of the appearance of G. immediately after drinking cold water, after taking wholesome cold food (cellar food, ice cream), as well as after a cold. These G. undoubtedly occur and can be attributed to a decrease in the resistance of the cells of the epithelial covering of the stomach and intestines as a result of fine chemical-physical changes in the intestinal wall itself (Schade). Patho-anatomically in G. the matter concerns various changes depending on the severity of the disease. Macroscopically the mucous membrane of the stomach and intestines appears swollen and more or less hyperemic, especially at the tops of the folds and (in the intestine) in the area of follicles and Peyer's patches; in places small hemorrhages are visible, the surface of the mucous membrane is covered with a layer of mucus and desquamated epithelium, sometimes a more or less pronounced edema of the wall is noted. Often an increase and plethora of follicles are noticeable. In severe forms of G. on the tops of the folds (and sometimes over the entire mucous membrane), mainly of the ileum, an aphthous gray coating appears, and later losses of substance of the mucous membrane-small ulcers (gastroenteritis ulcerosa simplex)-are found, which serve as gates for the penetration of infection into the deeper layers of the wall; sometimes small ulcers are found only in the area of the intestinal follicles. Microscopically it is possible to see significant dilation of the vessels in the mucous and submucous layers; the surface epithelium is usually desquamated; in the deeper parts of the Lieberkühn glands the integrity of the cells is not violated, however, phenomena of parenchymatous degeneration of them are noted; the glands are somewhat shortened and club-shaped thickened at the blind end; there is infiltration, most often lymphocytic. The layers muscularis and serosa are involved in the inflammatory process very rarely (see also Enteritis and Colitis). The clinical picture of acute G. in adults is very diverse, starting with mild cases barely noticed by the patient himself and ending with severe cases requiring serious intervention and sometimes, for example, in old people, threatening life. The disease usually begins suddenly, most often with a sudden onset of diarrhea, which constitutes the main symptom of the disease. After the first mushy, with a sharp fecal odor, stools appear a series of abundant watery light yellow or greenish stools up to 5-8-12 times a day, rarely more; the stools contain a significant amount of water and a little mucus; large amounts of mucus in the form of shiny drops or strands and the lacquered appearance of the stools indicate that the large intestines are also involved in the process (see Colitis). The stools, especially at the beginning, contain a significant amount of residues of undigested food (meat, potatoes, vegetables). In the stools there is a significant amount of bile pigments, easily revealed by the corrosive sublimate test. Simultaneously with the appearance of diarrhea patients complain of nausea, often accompanied by single or double vomiting, usually containing residues of eaten food and a certain amount of mucus. Examination of the stomach contents is usually not performed in these cases; it shows a decrease or even complete absence of free HCl. At the same time in the patient not only does appetite disappear, but aversion to food appears, the tongue is sharply coated with a white sticky coating, there is an unpleasant taste in the mouth and a number of symptoms indicating gastric dyspepsia: eructation, empty or sour, much less often heartburn, meteorism (abundance of gases). Dyspeptic phenomena from the stomach and intestines are accompanied by unpleasant sensations in the abdomen, from a feeling of indefinite pulling pains to sharp colicky spasms. The abdomen is usually somewhat swollen and more or less painful on palpation in the epigastrium and in the area of the navel. In the intestine gurgling and splashing are felt. Depending on the severity of the case the general condition of the patient suffers more or less. If in mild cases the matter is limited to general malaise, then most patients with acute G. are nevertheless forced to leave work, and the ensuing general weakness forces the patient to go to bed. The temperature often rises, reaching 38-39°, the pulse significantly quickens in connection with the general toxemia and reflexes from the intestine. Urine excretion decreases, its specific gravity increases, occasionally albuminuria appears, accompanied by the excretion of granular cylinders, erythrocytes, i.e., the picture of acute nephropathy. From the skin, herpetic rashes, of the type herpes labialis, have been described in G.

The course of acute G. in adults varies greatly; from mild cases of gastro-intestinal dyspepsia (the French 'indigestion'), lasting 1-2 days, there is a whole series of transitional forms to the most severe G., resembling cholera-like diseases on the one hand, and typhoid-like on the other, when the duration of the disease reaches several weeks. The nature of the etiological factor and the individual peculiarities of the patient determine the course, complications, and outcome of the disease. Among complications, besides signs of cardiovascular weakness with symptoms of collapse, especially in elderly patients, one should keep in mind nephropathies and acute parenchymatous hepatitis, occurring under the guise of so-called 'catarrhal jaundice'. These complications often make the true recognition of the disease difficult, drawing the physician's attention to jaundice, albuminuria with cylindruria, cardiac weakness, etc., which come to the forefront. Bacteriological investigation is practically important in cases of epidemic occurrence of acute gastro-intestinal disorders (see Cholera, Paratyphoid), in mass poisonings, but in sporadic diseases it rarely clarifies the matter; however, in more severe cases it is necessary to resort to examination of feces in a well-equipped and competent bacteriological laboratory. In differential diagnosis of acute G., besides acute infections, one should keep in mind the appearance of nervous diarrhea, endocrine diarrhea, and a special type of diarrhea, which should be classified as allergic diseases resulting from a special sensitivity of the body to this or that food substance, which is essentially harmless but represents an allergen for a given organism even in minimal quantities; this includes acute G. after insignificant amounts of caviar, crayfish, strawberries, etc. These diseases, having an anaphylactic character, have more than once given rise to incorrect interpretation and completely incorrect therapy. Of course, when acute G. appears, the physician should also consider the possibility of intoxication, especially by arsenic preparations. Prevention and treatment of acute G. can be considered together with therapy of its chronic forms. Chronic G. represents a less sharply defined and determined clinical form than acute gastroenteritis. If only in individual and mildest cases of acute G. it is difficult to differentiate the inflammatory process of the mucous membrane of the stomach and intestines from purely functional digestive disorders - gastro-intestinal dyspepsia, then in chronic G. the matter is much more complicated. Since the boundaries between purely functional digestive disorders and organic intestinal diseases are very unclear, some authors (von Noorden) do not even see grounds for recognizing the existence of purely functional intestinal dyspepsias and believe that in these cases it is always a matter of catarrh of the intestines, with the only difference that poorly expressed patho-anatomical changes are rarely established even by microscopic examination of the mucous membrane. The intimate connection existing between gastric and intestinal digestion, and a number of compensatory processes appearing from the side of the intestine in defects of gastric digestion, make understandable the frequent appearance of enteritis as a result of chronic gastritis, both irritative and toxicemic. Often in such cases it is possible to establish that the symptoms of the stomach disease appear much earlier, but careful research soon reveals in the patient functional disorders from the intestines; in long-standing chronic gastritis, it is precisely these intestinal disorders that often come to the forefront in the picture of chronic G. Chronic gastroenteritis can be the result of frequently repeated acute catarrhs of the stomach and small intestines, if they are not thoroughly cured or if the patient does not take appropriate preventive measures against relapses of G. However, infections, which play such a large role in acute G., recede far to the background here, and for the origin of chronic G., the causes that cause chronic disease of the gastric mucous membrane are of primary importance (see Gastritis). Research of recent decades (Hauser, K. Faber, Bloch, Konjetzny, Lubarsch, etc.) with the application of new techniques force us, regarding the frequency of gastritis, to return to the views of physicians of the early 19th century (Broussais) and to recognize that gastritis is one of the most common diseases of the stomach. This determines the necessity to consider chronic G. as a significantly more common disease than physicians thought in the second half of the 19th century and at the beginning of the 20th century. The main etiological factor of chronic G. should be considered chronic dietary errors, and if in acute G. the quality of food in the sense of its inferiority, decomposition of food products or contamination is of decisive importance, then here the matter is rather about quantitative dietary errors, overeating, as a result of which, especially with defects in gastric (sub-, anaciditas, achylia gastrica) or pancreatic (achylia pancreatica) digestion, excesses of undigested food enter the small intestines and the lower sections of the intestine and cause a change in the bacterial flora of the intestines (v. Noorden). As a result of these dietary errors, there appears now fermentative, now putrefactive, now mixed intestinal dyspepsia (see) with the formation of a number of abnormal products of fermentation and putrefaction (organic acids, aromatic compounds), causing irritation of the intestinal wall and as a result of it catarrh of the intestines. That is why both etiologically and pathogenetically chronic gastritis and enteritis are so closely connected and why the isolation of chronic G. as a separate nosological unit is fully justified. Besides dietary errors, which include, among other things, excesses not only in food but also in drink, especially young beer and kvass, in the origin of chronic G., endogenous causes also have significance. This includes a number of diseases of other organs and systems. Besides stagnant catarrhs on the basis of decompensation of cardiac activity, great importance is attached to stagnations in the area of portal circulation and not only in chronic cirrhotic processes of the liver, but more often due to so-called plethora of the abdomen, for example, in persons who lead a sedentary lifestyle for a long time. Catarrhs of the intestines of endogenous origin also include those in patients with metabolic disorders, especially in gouty patients suffering from obesity, and in patients with insufficient kidney function. Heredity and constitutional factors play no small role in the origin of chronic G.; clinical experience teaches us that chronic G. is undoubtedly more common in certain families, although it is difficult to say in each individual case whether the cause is hereditary inadequacy of the digestive apparatus or a certain way of life, with dietary errors transmitted from generation to generation. Finally, all the above-mentioned reasons, especially when considering the etiology of acute G., for its origin, especially colds, explain why G. is often also a professional disease arising from working conditions related to a given production. Thus, G. is noted in workers of hot shops of various productions, for example, in glass production or where (as for example in tinsmiths) the lower part of the body is subjected to cooling (Schtitte). G. often develops also in cases where the production is associated with swallowing alkaline vapors and fatty acids that change the chemistry of the stomach, for example, in the margarine, candle, or soap industries. It should be noted, however, that G. as a professional disease has been little studied, all the more so because working conditions are often so closely connected with living conditions (improper nutrition) that it is difficult to determine which of the etiological factors predominates in the origin of G. Patho-anatomical changes in chronic G.: the mucous membrane has a grayish, sometimes cyanotic (in stagnant G.) tint, is usually thinned, smooth, devoid of velvetiness and folds; these atrophic phenomena, often clearly expressed in the stomach in chronic gastritis, are rarely found in the intestine; sometimes polypoid formations (gastritis, enteritis polyposa) are observed, sometimes the gastric mucous membrane takes on a continuous shagreen-like appearance (so-called etat mamelonne) due to the formation of a mass of papillary outgrowths as a result of stretching of the glands of the mucous membrane. Microscopically it is very difficult to distinguish postmortem changes of the intestinal mucous membrane from catarrhal antemortem processes. There is observed induration and sometimes wrinkling of the connective tissue of the stomach (see Gastricerosis); in the submucous layer as well as in the mucous membrane, a nest-like small-cell infiltration is often noticeable. The clinical picture of chronic G. does not have that definiteness as in acute G. Essential symptoms are functional digestive disorders, often appearing only at times and separated from each other by clear intervals of the patient's good health.

From the stomach side, there are dyspeptic phenomena: variable appetite, belching (most often of food eaten), a feeling of fullness or heaviness in the epigastric region, heartburn, sometimes nausea and very rarely, only after dietary indiscretions, vomiting. The disturbance of intestinal digestion is significantly more important. The characteristic feature of chronic G. must be considered the tendency of the patient to diarrhea. Depending on the state of gastric digestion and defects in the fermentative (amylolytic and proteolytic) processes in the stomach, as well as in the upper sections of the intestine where the digestive action of pancreatic juice takes place, diarrhea takes on one or another typical form. Obviously, the tendency of the patient to either fermentative or putrefactive dyspepsy is of enormous importance. In the first case, the stools are pasty, light yellow, bubbly, of acidic reaction; in the second case, they are very liquid, dark, alkaline, and sharply foul-smelling. In both cases in G., there is little or no mucus in the stools. It is especially important to determine the utilization of various components of food, and microscopically it is easy, for example, to detect the presence in the feces of muscle fibers with transverse and longitudinal striation, connective tissue, and in fermentative dyspepsy - a significant amount of undigested starch (blue coloring with Lugol's solution). For catarrh of the small intestine, the presence of a significant amount of bilirubin in the stools, instead of the normal urobilinogen (sublimate test), is characteristic. Subjectively, patients complain of frequent diarrhea, usually from trivial causes or even without any visible cause; diarrhea appears either early in the morning, depriving the patient of sleep, or the urges to defecate become disorderly, sometimes appearing immediately after a meal and forcing the patient to leave the table. During exacerbation of chronic G., the subjective sensations and objective data coincide with the phenomena described above in the picture of acute G. From the stomach side, objective examination most often reveals a decrease in its secretory activity (from subaciditas to anacidity) and a significant increase in motor function, as a result of which food masses leave the stomach very early; this is especially clearly detected by gastroscopy. With proper diet, patients with chronic G. feel well, but even a small dietary indiscretion (overeating, cold food or drink) very easily causes exacerbation of the disease. This necessity to lead a very moderate lifestyle and frequent recurrences have a harmful effect on the psyche of patients and sometimes make them neuropaths (hypochondria intestinalis of old doctors), fixing the patient's attention on sensations from the stomach and intestines. The general condition of patients with chronic G. fluctuates sharply; they lose weight rapidly during exacerbation of the process, sometimes arousing suspicion of malignancy of the intestinal disease (tuberculosis of the intestines). Sometimes in persons suffering from chronic G., the appearance of pernicious anemia is observed, and a number of authors see in anaemia perniciosa the result of chronic toxemia due to disturbance of proper intestinal digestion; however, this view is not shared by all, and the causal relationship between achylia gastrica, chronic G. and pernicious anemia cannot be considered established. The course of chronic G. is extremely long, and usually these patients consult a doctor after 2-3 years of digestive disturbance, most often as sufferers from chronic diarrhea. The disease lasts for many years, often 2-3 decades, without sharply affecting the general condition of the patient, except during periods of exacerbation. Giving in general a favorable prognosis for life, exacerbation of chronic G. can, however, have a heavy, and sometimes decisive, influence on the course of other diseases, for example, influenza, and even become the cause of death in the elderly, causing phenomena of cardiac weakness, up to and including collapse. It is very difficult to establish what mortality chronic G. gives. The statistical data appearing in official reports are not very convincing, since even at autopsy it is difficult, on the basis of the macroscopic picture, to speak of chronic G. as the direct cause of death; this can be said rather in acute cases, where G., complicating, for example, influenza or appearing in the elderly, can be the cause of death. Thus, in Moscow, out of 33,568 autopsies for the period 1923-1927, G. was established 160 times, not counting alimentary disorders that were the cause of death in infants. With proper treatment, especially with proper dietary prophylaxis, exacerbations of chronic G. become less and less frequent, and the patient can recover. The diagnosis of chronic G. is not always easy. Practically, the question is about the differential diagnosis between various forms of chronic diarrhea. First of all, diarrhea due to other organic diseases of the intestine (tuberculous, syphilitic ulcers, stenoses with fecal stasis, chronic appendicitis, etc.), diarrhea of endocrine origin (dysthyroidoses, Addison's disease), psychoneurotic diarrhea, and finally, still little studied but undoubtedly having certain practical significance, anaphylactic and allergic diarrhea (Luria, Funk, Storm van Leeuwen, Kammerer) should be excluded. If the question is decided in favor of an inflammatory process of the intestinal mucosa, it is necessary to establish the topical diagnosis of the disease and distinguish G. from colitis. The more persistent the diarrhea, the less frequently it alternates with constipation, the less digested the muscle fibers, starch and connective tissue, the less visible mucus and the more bilirubin there is in the stools, the more probable the diagnosis of enteritis becomes. However, even under these conditions, it is difficult in each individual case to determine whether there is only a functional disturbance of the intestine, one or another form of intestinal dyspepsy, or a purely organic disease of it - catarrh of the intestines. The presence simultaneously of enteritis and gastritis, i.e., the presence of G., is determined by the presence of the above-mentioned gastric phenomena. Prevention and treatment. Prevention of acute forms of G. reduces to public and personal measures for preventing the disease. The first includes systematic sanitary supervision over the food products themselves, especially in summer (sausage, meat, confectionery goods), as well as over the preparation and storage of food; these preventive measures are especially important in collective forms of nutrition (factory kitchens, institutions of People's Commissariat of Food, sanatorium, school canteens, etc.). Personal preventive measures should include the prohibition of overeating, especially when quickly changing from one diet, for example, vegetable, to another, for example, with abundance of animal and fatty food, and vice versa; one should also avoid taking cold food and drink, especially after preliminary heating (physical exercises, on a march, after a bath, in hot summer weather). Treatment. The main methods of treatment of acute gastroenteritis are considered to be the removal from the stomach and intestine of the content irritating their mucous membrane and providing as long a rest as possible to the diseased organs. Despite the diarrhea, a laxative is always prescribed to the patient (one to two tablespoons of castor oil, calomel 0.3, repeat the dose after 2-3 hours if there are no greenish stools); if there is nausea without vomiting, especially when suspicion of intoxication from spoiled food, it is useful to prescribe an emetic (Apomorphin. hydrochlor. cryst. 0.005-0.01) subcutaneously. The second indication - to spare the stomach and intestine - is carried out by a starvation diet. For 1-2 days the patient remains without food, to quench thirst only liquid tea is given, preferably without sugar, with a small amount of red wine; if this starvation diet continues for more than two days, the use of warm salt enemas is recommended. On the second-third day, mucilaginous soup (oatmeal, strained barley soup), sweet tea, rice porridge with butter are allowed; then a very cautious and gradual transition to ordinary food. Of medications, after thorough emptying of the intestine, 5-10 drops of T-rae Opii 2-3 times to reduce pain and diarrhea. In sharply expressed infectious G. with signs of intoxication, Carbo animalis medicinalis Merck one tablespoonful 3 times a day in 150 cubic cm of warm water is recommended. Other drugs, for example, disinfecting the intestine (salol, benzonaftol, etc.), are unnecessary. Of physiotherapeutic procedures, heat in the form of hot-water bottles on the abdomen or warming compresses of vodka on the entire abdomen is of great benefit. Constipations, which usually appear after acute G., do not require intervention, especially laxatives are contraindicated in them; when switching to ordinary diet, constipations disappear by themselves. The treatment of chronic G. is prophylactically reduced to the thorough cure of acute G. and to observance of the corresponding diet after the appearance of exacerbation of the disease; on the other hand, long-term prophylactic treatment, mainly dietary, is necessary.

This circumstance, considering the widespread prevalence of chronic G. in the population and the impossibility of maintaining the necessary diet under the conditions of ordinary working life, makes it imperative to demand the organization of a special dietary table for patients with gastrointestinal diseases in institutions of collective nutrition, and constitutes a very serious task of social prevention of digestive disorders. Individual prevention comes down primarily to limiting the amount of food taken; in any case, the patient should avoid overeating any food and especially limit that food which, as examination of the excreta shows, is insufficiently digested by his stomach and intestines (e.g., carbohydrates and plant food in fermentative, and proteins in putrefactive dyspepsia), or to receive this food in a correspondingly already processed form, facilitating its digestion by the intestines. Considerable importance is attached to putting in order the oral cavity, nasopharynx, and especially the chewing apparatus (filling cavities, prosthetic teeth). The treatment of chronic G. should begin with an assessment of the functional activity of the stomach and be based on the results of examination of the excreta, preferably after a trial diet containing all types of food substances. It is best to begin treatment, especially after an exacerbation of G., with one or two fasting days and to build the diet depending on the type of intestinal dyspepsia accompanying gastroenteritis (see Dyspepsia). In any case, a number of food substances are excluded from the diet of G. patients for a long time. These patients tolerate poorly milk, animal fats (lard), rich pastry (pies), certain varieties of meat (pork, goose, duck), fatty varieties of fish, smoked fish and meat, canned goods, mushrooms, sour varieties of fruits, cabbage, and among beverages-young beer, kvass, young koumiss, carbonated cold waters. However, general rules for the diet of G. patients cannot be established; more than anywhere else, it is necessary to assess the individual peculiarities of the patient's digestion and to carefully build the diet based on them. It is only necessary to protect the patient from the prescription of a stereotyped, so-called "strict diet" (broth, crackers, chicken, minced meat), which is usually unjustified, sharply undermining the patient's general nutrition and causing a number of psychogenic digestive disorders (fear of food, psychogenic diarrhea). Drug treatment should also take into account primarily the state of gastric digestion. With reduced secretion of the stomach, the prescription of large doses of hydrochloric acid with pepsin, Acidolpepsin, natural gastric juice is very useful. Pancreatin (0.5 each) or Pancreon (0.5 each) two or three times a day is of great benefit. In the presence of significant intestinal secretion and very watery excreta, the prescription of calcium preparations (Calcium carbonicum, Calcium phosphoricum 1.0 each, two or three times a day) or bismuth preparations [Bismut. salicylicum, Bismut. sub-gallicum (Dermatol), Bismut. tribromphenilicum (Xeroform), Bismon, Bismutosa, etc.] is especially indicated. Often, great benefit is derived from treatment with atropine internally or subcutaneously (1/x - 1 mg), significantly reducing intestinal spasms and secretion of pathological intestinal juice. Sometimes, persistent results from the treatment of G. by stomach lavage have been observed, especially when accompanied by atonic catarrh. Good results were observed in the treatment of certain forms of G. by parenteral administration of Witte-peptone [2-3 cubic cm of 5% sterile solution every two to three days, one injection each (Luria, Dikhovsky, Justmann)].- Resort treatment is of enormous importance for chronic G. Among the resorts of the USSR, depending on the state of the secretory activity of the stomach, one should keep in mind Essentuki, Zheleznovodsk, Borjomi, and among European resorts-Karlovy Vary, Homburg, Neuenahr, Bad Kissingen, Vichy. Drinking mineral waters outside the resort is of incomparably less benefit. However, with an appropriate diet, the prescription of Essentuki water No. 17 in hot form (up to 40-45°) in sips and in small doses (from half to one glass), 2-3 times a day is indicated: on an empty stomach, one hour before lunch and before dinner.- Along with dietary, balneological, and drug treatment, good results can also be expected from physiotherapeutic methods of treatment, especially from hot (32-35°) aromatic sitz baths, mud cakes, and diathermy. Undoubtedly, all these physiotherapeutic procedures, in addition to their local effect on the diseased organs, change the condition of the entire organism in a favorable direction, contributing to the very difficult task of treating chronic gastroenteritis, a task requiring great patience and endurance from both the patient and the physician.

Luria. Gastroenteritis in children. In children, gastroenteritis occurs in both acute and chronic forms. Acute G. belongs to the most frequent diseases in children and is observed all the more frequently, the younger the children. The resistance of the digestive organs, which is extremely weak in infants, however, is so great after the age of 2 years that G. in them rarely takes the severe form which is so often observed in the earliest age. (On gastrointestinal diseases in early childhood - see Dyspepsia and Intoxication.) Most often, weak children who have had rickets and have suffered from gastrointestinal disorders already in the first years of life become ill. In some children, there is undoubtedly a certain pre-existing weakness of the gastrointestinal tract as a predisposing factor for G. The frequency of G. is strongly influenced by the time of year. In hot summer weather, G. develops especially easily both due to the rapid spoilage of food at high ambient temperature and on the basis of excessive consumption of unripe berries and fruits. The overheating of the body also has unquestionable importance as a factor lowering immunity. The immediate cause of G. is the introduction of food in excessive amounts, especially fatty foods, sweets and fruits, and spoiled food (meat, fish, milk, sausage). But even greater importance in the origin of G. are infectious causes, explaining the sometimes epidemic spread of this disease. The intermediary for transmission of infection is most often food and water contaminated with pathogenic bacteria. Infection gets into food not only during its unclean preparation; a large role in food contamination also belongs to flies, which often carry infection on their legs and with their excrements directly from the excreta of the sick to food. Of the bacterial species known to us, special importance is attributed to the Bact. coli group, but it is undoubtedly that G. is also caused by many other microorganisms. The symptoms of G. often accompany infectious diseases that have no direct relation to the gastrointestinal canal, especially often influenza, measles, scarlet fever, and septic diseases. The symptoms of acute G., sometimes very severe, also accompany poisoning by certain poisons, for example, sublimate, arsenic, phosphorus. The onset of G. is usually sudden, but sometimes indefinite precursors are observed in the form of general malaise, elevated temperature, nausea, headache, and abdominal pain. Then vomiting usually appears, most often of food, sometimes very profuse, and the vomit often consists of food taken many hours before the onset of the disease. Soon diarrhea joins the vomiting. In other cases, gastric symptoms are not sharply expressed, and the disease begins directly with abdominal pain and diarrhea. The first stools still have more or less a normal appearance, the following ones are already liquid and foul-smelling; they are quite abundant, do not contain large masses of mucus, are not very frequent (up to 10 times a day), and are accompanied by colicky pains in the abdomen, rumbling, and gas discharge. Objectively, a coated tongue, bloating, and tenderness of the abdomen are noted. In milder cases, this is all that the picture of the disease includes, and after emptying the gastrointestinal canal, children quickly recover. In more severe cases, however, vomiting and diarrhea are more persistent, and to them, especially in small children, severe general symptoms join: extreme weakness, weakness of cardiac activity, and much less often - severe symptoms from the nervous system: clouding of consciousness, rarely convulsions. In most cases, however, especially with proper treatment measures, these symptoms quickly subside and only rarely take a life-threatening character. The diagnosis of G. as such presents no difficulties. Doubts arise only regarding the etiology of the disease, when it is necessary to decide whether we are dealing with a functional disease that appeared on the basis of overeating (acute gastrointestinal dyspepsia), with an intestinal infection, with a general infection, or with poisoning. Acute colitis and dysentery, which mainly affect the large intestine, are distinguished by frequent stools consisting of mucus (and blood), with a sunken and retracted abdomen. The prognosis for acute G. in children over 2 years is generally favorable, and only exceptionally severe infections, poisonings, and the presence of already marked exhaustion in the child before the onset of the disease can lead to a fatal outcome. The treatment of acute G. consists in emptying the gastrointestinal canal and prescribing an appropriate diet. Of the laxatives, castor oil is best, but it is often vomited up. In such cases, enemas can be used. For 12-24 hours, only liquid tea and water are given, then mucilaginous soups (rice, barley). The transition to regular food should be gradual: crackers, broth, tea with milk, semolina porridge, jelly, etc. In very small children with persistent diarrhea, the use of protein milk and corresponding preparations and mixtures is often recommended. Of medications, salol, bismuth nitrate, and, for severe abdominal pain, in addition to a heating compress, opium (with great caution) can be used. Chronic G. in most cases develops from an acute gastrointestinal catarrh if it is not properly treated, especially when the function of the digestive apparatus is weakened by disorders already suffered in the earliest age. In some children, on the contrary, the disease develops gradually as a consequence of improper nutrition, but it is not always possible to determine the onset of the disease and the cause that caused it. Probably, the weakness of the digestive organs, sometimes observed as a familial peculiarity, plays a large role here. In the picture of chronic G., sometimes dyspeptic symptoms from the stomach and signs of a decrease in its motor function (stomach dilation) come to the forefront. The diarrhea observed in this condition is closely connected with the disease of the stomach and develops as a result of the transition into the intestine of insufficiently digested and often already decomposed food. In other cases, there are no noticeable gastric symptoms, and diarrhea is the main symptom of the disease. The stools are not particularly frequent, sometimes only 2-3 times a day. They are liquid or semi-liquid, with a sour or putrefactive smell, contain more or less mucus, and under the microscope - many undigested food residues. In chronic G., in most cases, the general condition of the child also suffers to one degree or another, emaciation, anemia, and a decline in strength develop. In an extremely severe degree, these symptoms are observed in that still insufficiently clarified pathological condition which is known under the name 'intestinal infantilism'. The diagnosis of chronic G. is based on the symptoms mentioned above. With great exhaustion of the child and gradual progression of the disease, it is necessary to consider the possibility of tuberculosis of the mesenteric glands, peritoneum, and the intestine itself. The prognosis, generally favorable for life, as regards cure depends on the strict implementation of rational therapeutic measures. In the treatment of chronic G., it is necessary to prescribe a certain diet, which at first is very strict. Mucilaginous soups (rice, barley), stomach coffee with a small admixture of milk, crackers are given. While gradually reducing the time of such a strict diet, stale bread, broth, noodles, semolina porridge, rice porridge, jelly, potato puree, chicken are added. Especially with diarrhea with a putrefactive smell of the stools, the use of soured milk or kefir is very appropriate. Often, especially when indicating fermentative processes in the intestine, perfectly prepared and fresh cottage cheese is very useful. Great hopes should not be placed on medications. The use of mineral waters can be beneficial, especially with more pronounced symptoms from the stomach. In resort treatment, however, children do not need it, but a stay in the village is very beneficial. Of medications, those used in acute G. can be recommended. Preventive measures against chronic G. consist in eliminating those harmful factors which can be the cause of acute G. In this sense, strict supervision over the quality of food products and the dissemination of information on the proper nutrition of children are of great importance. Particular importance is attached to the care for the development of an active appetite in children, e.g., through systematic feeding, the establishment of a daily routine, walks, air and sun baths, etc.