Dyspepsia

Dyspepsia intestinal, dyspepsia intestinalis (from the Greek dys- prefix indicating qualitative impairment and pepsis- digestion), indigestion of food in the intestines, a disease of the intestines, long known in pediatrics but comparatively recently studied in the clinic of intestinal diseases in adults. In a number of cases, impairment of intestinal digestion is a direct consequence of organic diseases of the intestines (e.g., catarrh of the intestines, stenosis of the intestine) or the result of diseases of the stomach, liver, pancreas. Although the phenomena of intestinal D. come to the forefront in these cases, they do not exhaust the entire disease; on the other hand, very serious organic diseases of the intestines, e.g., tuberculosis, may occur without intestinal D. Frequently occurring disorders of intestinal digestion, where there is no organic disease and the entire clinical picture is the result only of impairment of the normal processes of intestinal digestion, should be classified as intestinal D., understanding it as a purely functional disease. It is necessary first of all to note that in each individual case it is not always easy to say whether the disorders of intestinal digestion are the result of purely functional, pathophysiological processes within the intestine or, along with it, there is also an organic disease of the intestinal mucosa - catarrh of it, the anatomical substrate of which in the disease does not appear possible to establish. Therefore some authors (Noordel) are inclined to completely deny intestinal D. as a separate nosological unit, believing that under it there always hides, even in mild form, intestinal catarrh. Undoubtedly between intestinal D. and catarrh of the intestines it is often difficult to draw a sharp boundary, and if catarrh of the intestines is almost always accompanied by intestinal D., then intestinal D., especially recurrent, easily and often leads to catarrh of the intestines. Despite however the theoretical disagreements of authors - Schmidt and Strasburger on the one hand, and Noorden on the other - in the question of the existence of intestinal D. as a separate disease, practically for the physician intestinal D. has exceptionally great interest, since both prevention and therapy of the most common diseases of the intestines are based on timely and correct recognition of the character and essence of functional disorders of them - intestinal D. Schmidt, founder of the doctrine of intestinal D., believed that the basis of the disease lies in constitutional weakness of the secretory apparatus of the intestines - decrease in secretion of intestinal enzymes. However later research did not confirm this theoretical premise and showed that the causes of intestinal dyspepsia are much more varied; they include: reduction of gastric digestion, quantitative and qualitative changes in pancreatic juice and bile and mainly disorders of the normal processes of fermentation and putrefaction in the intestine due to changes in intestinal flora. The normal intestine possesses considerable bactericidal ability, and in the thin intestines there is usually a very sparse flora; carriers of this bactericidal activity are bacteriostats (Bogendorfer), contained both in intestinal juice and in the epithelium of the thin intestines. In the lower part of the thin intestines, in the cecum and in the colon ascendens, fermentation processes take place under the influence of a very diverse and iodophilic flora; as a result of them cellulose is digested, the products of decomposition of which give an acid reaction. Lower along the course of the intestine putrefaction processes appear as a result of the work of proteolytic flora, causing a weakly alkaline reaction of normal feces. Impairment of the interaction of the normal work of different types of intestinal flora - fermentation microbes and putrefaction microbes - is the essence of intestinal D. (Noorden). Predisposing causes should be considered: appearance of pathogenic microbes in the intestine - infection of it, disrupting the normal balance of intestinal flora, stagnation of intestinal contents and overload of the intestine with abnormally large amounts of nutritional material. It is necessary to distinguish two main types of intestinal D.: fermentative and putrefactive; but practically mixed dyspepsias also occur, and very frequently. I. Fermentative D. was first described as a separate nosological form in 1901 by Schmidt and Strasburger and consists in impairment of digestion of carbohydrates by the intestine. Normally very little undigested carbohydrates reaches the cecum, where they are acted upon by microbial flora. In fermentative D. (the essence of which, according to A. Schmidt, consists in insufficiency of the hypothetical cellulolytic enzyme, and according to Noorden - in filling of the corresponding sections of the intestine with undissolved carbohydrates, enclosed in cells) the intestine is filled with products of fermentation of unused carbohydrates. As a result of irritation of the intestinal wall by these acid compounds, increased peristalsis and dyspeptic phenomena associated with fermentation processes occur. Fermentative D. occurs as an acute and as a chronic disease, in the latter case usually accompanied by colitis. The acute form most often occurs under the influence of dietary disturbance when switching to an unusually rich in vegetable fiber and carbohydrates food (young soldiers in barracks), often as a seasonal disease, in the autumn when fresh vegetables and fruits appear, and finally after consumption of insufficiently fermented beverages: young beer, kvass, honey. Frequent recurrences of fermentative D. due to the multiplication of fermentation microbes in the intestine they cause lead to the patient becoming sensitive to food rich in carbohydrates, and acute fermentative D. gradually passes into chronic form. Patients usually complain of diarrhea. Typical are the stools, occurring 2-4 times a day, mushy, light, yellowish in color, acidic, containing visible gas bubbles. Besides diarrhea patients complain of abdominal bloating, rumbling and significant passage of gas, usually not too foul-smelling; this abundance of gas is the result of fermentation in the intestine with the release mainly of CO₂, and then CH₄ and H. Sometimes colicky pains appear, probably due to retention of gas in the intestine. The general condition of patients in fermentative D. usually does not suffer, appetite is good, there are no phenomena of gastric D. Objectively: the tongue is clean, the abdomen is moderately distended due to meteorism, on palpation sometimes rumbling appears. The main sign of the disease - the stools. Their external appearance has already been discussed; in ground stools one can find remains of potato and formations resembling sago grains (glassy mucus clumps). Under the microscope in the preparation stained with iodine there is a large amount of potato and starch cells, appearing as dark blue spots sharply standing out over the entire field of view, and a large number of fungi, threads of Leptothrix, Clostridium and numerous rods and cocci, stained blue. The fermentation test usually gives a sharply positive result with light color of the stool and its acid reaction due to the large amount of organic acids. Fermentative D. is a relatively benign disease, however very prone to recurrence, and more often occurs not as an independent disease but as a concomitant symptom. Prophylactically one should avoid rapid transition from a mixed diet to a strictly vegetarian diet; people unaccustomed to such food should beware of consumption of large amounts of black bread, peas, beans, cabbage, cucumbers and fruits, especially not quite ripe, one should avoid consumption of insufficiently fermented beverages. This last circumstance should also be kept in mind by food inspection, especially in hot weather, when due to great demand young beer, kvass, honey etc. are released to the market. - Treatment of fermentative D. - causal. It is best to make the patient fast for 1-2 days and then, depriving him completely of carbohydrates, leave him on a diet consisting of broth (without cereals and vegetables), eggs, cottage cheese, butter, minced meat, tea with red wine without sugar; after a few days porridge from fine cereals (semolina) is allowed and later dry crackers from white bread, dry pastry from white flour. Gradually the patient can also switch to coarser carbohydrate food (later even cabbage and black bread are permissible). Of medications at first one can (a little and not for long) give opium preparations, but calcium carbonate (1.0-2.0 three to five times a day) works better, neutralizing the acidic products of fermentation. II. Putrefactive D. is the result of predominance of putrefaction processes in the intestine, mainly abnormal. Normally in the thin intestines putrefaction processes do not occur at all and even in the thick intestines they are usually expressed in a healthy person very weakly. They predominate only in the distal sections of the large intestine. Intensification of putrefaction processes in the thick intestines and their spread to more proximal sections and to the thin intestines cause putrefactive D. Its causes are very varied. A. Schmidt puts gastric digestion deficiency - achylia - in first place and believes that as a result of this significant amounts of undigested protein bodies are carried into the lower sections of the digestive tract, which serves as the cause of intensification and spread of putrefaction processes with formation of products irritating the intestinal wall, leading to a special form of diarrhea.

Since the primary cause of these diarrhea cases is pathology of gastric digestion, Schmidt called them 'gastrogenous' ('gastrogeue Diarrhoea'). Undoubtedly, in a considerable number of cases, the cause of putrefactive Dyspepsia must be recognized as insufficient gastric digestion and the passage of large amounts of undigested protein food into the intestines; the fact that this is so is proven by the daily clinical experience of brilliant recovery from such diarrhea through proper treatment of achylia of the stomach. However, it must be considered that achylia of the stomach or achylia of the pancreas by no means constitute the only cause of putrefactive intestinal Dyspepsia. Although it is not yet precisely known which microbes cause the intensification of putrefactive processes in the intestine in each individual case, it must be assumed (as Norden believes) that here too the condition of the intestinal flora is of enormous importance. These processes become pathological precisely when external causes (e.g., spoiled protein food or infection) enhance the growth of constant putrefactive agents in the intestine. This also explains intestinal Dyspepsia in cases of stagnation in the intestine. Of course, consuming an excessively large amount of protein food can intensify putrefactive processes; however, there is a very significant difference between putrefactive and fermentative Dyspepsia in that the development of putrefactive depends not only on the supply of food but also on the condition of the intestinal wall itself. For example, when the intestine is irritated by laxatives or substances acting allergically on it, abundant secretion of intestinal juice rich in protein compounds occurs, which serves as an excellent nutrient medium for putrefactive microbes. Therefore, putrefactive Dyspepsia can not only arise but also intensify even in the absence of protein food (Norden, Goif-fon). This is a serious obstacle to treating this form of Dyspepsia. Putrefactive Dyspepsia can be acute and chronic. Acute is the result of consuming spoiled or improperly prepared protein food, especially meat or fish preserves, sometimes game; this form of Dyspepsia is often observed when rapidly transitioning from a vegetable diet to an abundant protein diet (abundant festive food after fasts). Chronic putrefactive Dyspepsia arises from frequent recurrences of acute Dyspepsia or from frequent irritation of the intestine—e.g., by laxatives or as a result of eating too quickly, especially if there are defects in the chewing apparatus. The main complaint of patients with putrefactive Dyspepsia is diarrhea, which in chronic cases continues for decades. The stools are frequent, abundant, watery, dark in color, very foul-smelling, and sometimes contain macroscopically visible fragments of meat, fish, or sausage that are noticed by observant patients. These are people with so-called 'weak stomachs,' i.e., those who easily suffer from diarrhea even with relatively good food. Except during periods of exacerbation, the condition of patients is satisfactory, appetite is good, and painful gastric symptoms may be absent. The main objective sign is the characteristic stools. In addition to the above-mentioned signs, the typical appearance in crushed feces of small fragments of muscle fibers and connective tissue is noted. Microscopically, muscle fibers can be easily found in the form of truncated cylinders with unrounded edges, with transverse and longitudinal striations. Fermentative microbes and starch cells are usually absent in pure forms of putrefactive Dyspepsia. The stools in putrefactive Dyspepsia are alkaline in reaction and contain a significant amount of ammonia. The products of putrefaction in this form of Dyspepsia, by irritating the intestinal walls, cause increased secretion by the intestinal wall of large amounts of protein-rich fluid, which to a large extent supports the growth of microbial flora. Therefore, putrefactive Dyspepsia is a more persistent disease than other forms of Dyspepsia and easily complicates with inflammatory phenomena. It often presents a more severe picture of the disease with a number of general symptoms (loss of work capacity, headaches, etc.). Prevention of putrefactive Dyspepsia consists in careful treatment of functional and organic diseases of the stomach and intestines that usually occur with reduced secretory activity, in oral and pharyngeal hygiene, in restoring the chewing apparatus (dentures), and in careful supervision of food products, especially those that spoil easily, fish, meat, and others rich in protein substances, e.g., eggs, milk, etc.; one should also avoid rapid transition from a vegetable-milk diet to a meat diet. Treatment of putrefactive Dyspepsia presents a difficult task. It is best to start with 2-3 days of fasting with the patient remaining in bed; all laxatives are contraindicated to avoid irritating the intestine. When prescribing a diet, not only is protein food forbidden, but other food substances, e.g., carbohydrates, are also prescribed in a tender, minced form to spare the irritated intestine. Sweet tea, coffee, cream (but not milk!), soups with mucous broth, with oil and cream, porridge from baby flour, semolina, rice, crackers, white bread, jelly are recommended. Only after 12-14 days are eggs or an omelet allowed, and then tender meat, preferably passed through a sieve or boiled in the form of meatballs. Of medicines, if there is reduced gastric secretion, pepsin, hydrochloric acid (best in the form of Acidolpepsin lozenges), preparations of the pancreas (especially Pank-геоа at 0.4-0.5 per dose) are recommended; in cases of strong transudation into the intestine, a good effect is observed from atropine (Luria). Opiates are definitely contraindicated; astringents are of little use. With the aim of changing the intestinal flora, lactobacillin and Mutaflor have been recommended. In chronic forms, considerable relief is provided by heat procedures (hot water bottles, aromatic hot baths, mud therapy, diathermy), as well as treatment with mineral waters (Zheleznovodsk, Essentuki, Izhevsk, Staraya Russa—in small portions hot). Luria and others often saw benefit from parenteral treatment with peptone. For recognizing different forms of Dyspepsia, as indicated, a properly taken history and macro- and microscopic analysis of the stools are sufficient. A more detailed study of these functional intestinal disorders requires the use of a 'test' diet with chemical examination of the stools; a more perfect method is the determination of organic acids and ammonia in the feces. Often it is possible to establish that the patient has both forms of Dyspepsia—fermentative and putrefactive—simultaneously; this gives grounds to distinguish a third form of intestinal Dyspepsia—mixed. In treating mixed intestinal Dyspepsia, it is recommended to start by combating fermentative Dyspepsia, which is more amenable to therapy, and then, by appropriately combining the diet, direct it toward putrefactive Dyspepsia. Of course, if the intestinal Dyspepsias are only a functional expression of an organic disease of the intestine, therapy should first be oriented toward the underlying disease.

r. Lur'ya. Dyspepsia in children. The term D. is used in pediatrics to denote functional disorders of digestion with the dominant symptom of diarrhea without sharp changes in the general condition. Internationally, there is no uniform use of the term D., as there is no single, but rather many different classifications of nutritional and digestive disorders in children; therefore, for uniform designation in the USSR, congresses of pediatricians (the II All-Russian in 1925 and the IV All-Union in 1927) proposed the following working classification: A. Chronic nutritional disorders - hypotrophy, atrophy. B. Acute digestive and nutritional disorders: a) simple, toxic D. (intoxication); b) infectious colitis. This delimits the clinical concept of D. - Etiological factors of D. are divided into food, hygienic, constitutional, and infectious. In children breastfed, D. can be caused not only by overfeeding but also by underfeeding. After a period of underfeeding, especially in hydrolytic children, frequent, viscous-mucous, green stools appear. Weight falls. This phenomenon occurs more often in the first months of life and was named by Davidsonsohn as initial diarrhea. Fasting causing diarrhea can be quantitative - with hypolactation in a nursing mother, and qualitative - carbohydrate (especially in hydrolytic children) or protein. The success from adding carbohydrates in one case and proteins in another proves the correctness of accounting for the causal factor. Langstein, and before him a number of French authors, including Marfan, point out that D. can occur with a change in the composition of a mother's milk during her chronic diseases and during menstruation. Usually such a child is already in hypotrophy before seeing a doctor. An inexperienced doctor, in view of the diarrhea, restricts food, and the child may die from atrophy medico, i.e., through the fault of the doctor, as Schlossmann aptly expressed. Ribadeau-Dumas and others point out that D. can occur in infants if the nursing mother's milk has a high percentage of milk sugar. An important factor in dyspeptic diarrhea, as proven experimentally and in animals, is overheating and summer heat, with insufficient water supply and decreased need for food also playing a role. Infections play an enormous role, especially parenteral, i.e., infections in which the virus is not located directly in the intestines but rather: influenza, pneumonia, pyelitis, pyodermias, otitis, etc. The younger the child, the more they react to these infections. In such diarrhea, there is no correspondence between the height of fever and the degree of D., and vomiting is more common. These parenteral infections easily lead to a rapid transition from simple D. to a severe toxic phase (intoxication). In children with neuropathy and exudative-catarrhal diathesis, even physiological irritations for normal children can cause increased peristalsis. In newborn infants in the first weeks of life, sometimes up to 2-3 months, frequent stools are observed, 4-6 times a day, of acidic reaction, with soap-lime particles and partial green color. Weight continues to increase, general condition does not suffer. There is no excess sugar and fat in the nursing mother's milk. This D. depends on the insufficiency of the digestive and bactericidal function of the gastrointestinal tract in the newborn. Reuss calls it transitional catarrh, Medovikov and others - physiological D. Diarrhea in premature infants in the first weeks of life with 3-5 stools, with weight stagnation and loss of appetite is dangerous and can quickly transition to the toxic phase with collapse and death. In children on artificial feeding, D. occurs more often. Its causes are more diverse. Besides those mentioned (heat, overheating, constitutional anomalies and parenteral infections), many types of irrational feeding, quantitative or more often qualitative, play an etiological role. With artificial feeding, especially in hot weather, contamination of food and utensils is more likely. When feeding with cow's milk, D. from incorrect correlation of food, from deficiency of some substances, with overload by others, and from deficiency in vitamins more often occurs. With one-sided, excessively prolonged feeding with flour food, diarrhea appears with mucous brown masses, acidic reaction, positive iodine reaction, with abundant gas. Czerny distinguished this form under the name Mehlnahrschaden, i.e., nutritional disorder from flour food; with it, the general condition suffers, and hypotrophy develops, sometimes with poor prognosis hypertension. The cause is protein, fat, salt starvation and deficiency of vitamins C, as well as A and D. From the group of D., diarrhea irritative, caused either by inflammation of the intestines or hematogenous irritation of the autonomic nervous system, are also isolated as independent forms; they are persistent, violent, and close to toxicosis. The pathogenesis of D. cannot be considered clarified. Various hypotheses exist. The study of the biochemistry and flora of the gastrointestinal tract has contributed much to clarifying the genesis. Bessau and others established in the stomach delay of food, the so-called Stagnation. In the stomach of children, according to Vagralik, Demuth and Rosenbaum, there is hypochlorhydria. According to Rudnev, in infants with dyspepsia, the total acidity of gastric juice is 5.1 instead of 8.5 on average, free hydrochloric acid 0-5.25 (normally 1-9), pepsin 0-4 units (normally 1-9), labferment 8-40 units (normally 100-256) and lipase 0.25-3.9 units (normally 2-6.7). Temporary decrease in secretory enzymatic work has been confirmed by Tura and a number of foreign authors (YUpo, Marriott, Freudenberg). The biochemistry of duodenal secretion is altered. According to Rudnev, pH = 6-7 (normally 6.8-7.2), trypsin 250-1,024 units (normally 512-1,024), amylase 50-200 units (normally 500-1,000), lipase from 13.4 to 32.6, average figure 26.3 units (such figures are found in normal conditions, but the average normal figure is 38 units). Protein metabolism is usually not disturbed. Some increase in fecal nitrogen depends on increased secretion of intestinal juice. Absorption of protein and fat is reduced. In the feces, the number of undigested residues is increased; particles are found, initially resembling chopped eggs (during restorative processes in the intestines, the color of the particles is white from the transition of bilirubin to urobilinogen); they consist of lime and magnesium soaps of fatty acids and bacteria, partly casein and paracasein. In the stool, there is more neutral fat and fatty acids. More often, from enhanced oxidative processes, depending also on the oxidase enzyme brought in with leukocytes, freshly passed feces has a green color (color of spinach puree) instead of the usual one, from the transition of bilirubin to biliverdin. With enhanced fermentation, the feces foams and is expelled with gas. The smell of feces in fermentative D. is acidic, pH = 2.8-5.4 from the presence of acetic acid and a number of volatile fatty acids. In putrefactive stool from food decomposition, mainly by anaerobic Proteus or Bac. perfringens, pH = 8.2: -8.4. According to Czerny, putrefactive processes develop more easily in the first weeks of life. Combe points out that putrefactive D. causes irritation of the large intestines. In dyspepsia, the small intestines empty in 3-7/3 hours (normally 7-8 hours), and the large intestines in 2-5 hours (normally 2-14 hours), as shown by Kahn's research. In severe forms, urine ammonia increases, indicating acidothic disturbance of general metabolism. Due to the expenditure of alkalis, diverted to neutralize excessively formed acids during pathological fermentation, mineral metabolism decreases. Regarding the bacterial flora of the gastrointestinal tract, different in children on breast feeding (Bac. bifidus predominates) and artificial (Bact. coli predominates), Dobrokhotova, Escherich, Scheer, Adam, Tissier and others point out that in the stomach of a healthy child there are few microbes besides enterococcus, in the small intestines up to the ileum there are almost no microbes due to the bactericidal nature of the epithelium and alkalinity of the juice, but from the ileum their number increases. With digestive disorders - dyspepsia - the upper sections of the intestine are colonized by microbes, i.e., upward penetration occurs, or, as more often called, invasion, ascent of microbes, with the severity of the disease, according to some authors, parallel to the strength of invasion. In mild cases, microbes multiply in the food chyme, while in severe cases the intestinal wall is also infected. Dobrokhotova found Bact. coli in 82% of dyspepsia cases. According to Adam, Bact. coli found in digestive disorders is more capable of fermentation and represents a special type Dyspepsiecoli. In prolonged cases, Bact. coli is retained in the stomach and upper sections of the intestines, which causes exacerbations. However, not all authors recognize the primary role of Bact. coli. Kramer did not always find invasion of the duodenum by the bacillus coli in dyspepsia. With existing invasion, dyspepsia does not always occur. Many, including Marfan, Bernheim-Karrer, Gravinghof, consider that the presence of Bacterium coli is not pathognomonic for dyspeptic disorder and that invasion of Bact. coli is not a primary but a secondary process in diarrhea disorders without a specific virus.

The modern explanation of the pathogenesis of simple dyspepsia, according to most authors, is as follows: the basis of D. lies in a violation of the functional activity of the gastrointestinal tract, the biochemistry of digestion and emptying under the influence of a whole series of etiological factors, which have already been cited. These factors lower the activity of digestive processes. In the gastrointestinal canal, in its upper segments, conditions are created favorable for the development of intestinal flora, and an invasion of microbes occurs, which in turn distorts the processes of chemical change in the intestine with the formation of products harmful to the body. These products of non-physiological breakdown, arising partly from a decrease in enzymes, partly from unusual bacterial colonization of chyme in places where such processes are not characteristic, are mainly products of carbohydrate fermentation: acetic acid and a number of volatile fatty acids and toxins. From abnormally high acidity in areas particularly sensitive to acids as physiologically unadapted to such, a reaction of irritation-diarrhea occurs. Carbohydrates ferment easily, especially milk sugar, relatively less so polysaccharides, flour. Fats with a dyspeptic tendency in biochemistry can also break down abnormally and intensify the fermentative diarrheal disorder. French authors, and among the Germans Langstein and partly Czerny, point out that due to abnormal breakdown of proteins, putrefactive diarrhea can arise with irritation mainly of the large intestines, although such putrefactive diarrhea occurs less frequently than fermentative. In simple D., unlike the toxic phase, the function of the barrier apparatus of the intestinal epithelium and subsequent barriers of the liver, reticulo-endothelial system, adrenal glands and brain barrier with centers in the autonomic nervous system is not affected. If in D. there is an attack on these barriers to some degree, they prove to be functionally sufficient. Clinically, simple D. manifests itself with diarrhea and often vomiting. As has already been said, D. in artificially fed infants occurs more frequently than in those breastfed. The onset is either imperceptible or sudden. The child regurgitates or immediately after feeding brings up uncurdled milk or curdled through ^!hr-^l/.₂-4 hours, even after 6 hours of feeding. The degree of regurgitation varies, and can reach vomiting. The vomit contains mucus and has the smell of fatty acids. The number of bowel movements increases to 5-6-10. The stool changes to a more liquid consistency with curds, first white, then green, and takes the appearance of spinach puree, its consistency becoming watery. With abundant gas development, the stool is expelled in a stream. The general condition suffers little at first. Then the child becomes irritable, the more so the more neuropathic he is, often cries periodically in connection with incoming colic, more often wakes up at night. After defecation, passage of gas and during sucking, the child calms down. Appetite is lost. The abdomen is greatly distended with gases causing rumbling, and is painful on palpation. Pallor appears. The temperature is either normal or rises in the evening (to 38°). The cause of the rises is partly from distortion of the bacterial flora, partly from disturbed biochemistry. In parenteral D., t° depends on the primary infection. Weight stops or falls-a little in normotrophs, more in hydro-labile infants. In infants of the first weeks of life, as well as in hypotrophs, especially in atrophics, D. causes a greater loss of weight. In the blood, with unchanged amount of Hb and erythrocytes, there is an inconsistent degree of leukocytosis, sometimes monocytosis. The rate of erythrocyte sedimentation is not disturbed, but in severe cases it is somewhat accelerated. There is an increase in ammonia in the urine. The course and prognosis of D., all other things being equal, depend on the nutritional state. In normotrophs the course is short, favorable, but if D. drags on, hypotrophy may develop. In hypotrophs the course is more prolonged, and nutrition is more undermined. In atrophics D. develops very easily and more often passes into the toxic phase. The proximity of toxemia-"pretoxemia"-is recognized by a sharp drop in weight, pallor, increased restlessness and depressed general condition. Children on breast feeding or on mixed feeding, even when receiving very small amounts of breast milk, have a better prognosis. The constitutional moment (hydro-lability, exudative and neuropathic diathesis) significantly hinders recovery. A prolonged course, repeated D. and complicating infections worsen the prognosis. Treatment. First of all, eliminate the cause. In breast-fed infants-correct the dosage. In cases of fasting, increase the amount of food, give mixed feeding, Czerny mixture or buttermilk according to Kleinschmidt or whole milk with 17% sugar (Dubo of the Vienna school). In initial diarrhea-increase the amount of food so that the child receives 130-150 calories per 1 kg of weight. With sufficient amount of human milk or excess milk sugar in the milk of the nursing mother, to eliminate D. add proteins in the form of plasmon, nutrose, larosan, lactasan or, in our conditions, cottage cheese 5-10 g per day and give calcium carbonate 0.5 g 3-4 times a day. Proteins drive out alkaline juice, suppress fermentation. Calcium promotes the formation of lime soaps of fatty acids. Czerny and Raczynski give for this 100 g of whole milk per day. At the beginning of treatment of acute D. (except D. from hunger) a fasting diet is prescribed, i.e. all food is excluded as a substrate for abnormal breakdown, and only water or tea is given: in normotrophs 6-24 hours, in hypotrophs 6-12 hours, and in atrophics 4-6 hours. The amount of liquid should be administered at the rate of 150 cc per 1 kg of weight. Atrophics and in cases of persistent vomiting are advised to administer parenterally physiological or Ringer's solution and glucose in a 10% solution. It is rational to perform at first in case of delay of food in the stomach and vomiting a stomach wash with a 7% solution of soda or a 1% solution of Carlsbad salt. Through a gastric tube 100 cm³ of solution is poured in at once, it is drained off, and this is repeated several times. Some advise enemas with physiological solution, with the rubber tip being inserted to a depth of 10-15 cm. After the water diet, dietotherapy is carried out. On the first day 1/3 of the food requirement is given-35 calories, in mild cases-70 calories per 1 kg. In the following days 50-100 g of food are added per day. Human milk is prescribed, but it, as containing little protein and much sugar, can increase the frequency of stool. It acts first on the cells, improving the intermediate metabolism, and from there on the chemistry of the intestine. Therefore it is advantageous to simultaneously give the above mentioned proteins or sour buttermilk with 17% flour or protein milk with 5% sugar or concentrated protein milk with 10-20% sugar. Such combined dietotherapy is necessary in atrophics. Artificially fed infants are given as therapeutic food less fermentable carbohydrates: for 3-4 days rice 10% decoction according to Bessau, gradually adding to it each day 100 grams of milk. This decoction drives out the alkaline juice of the intestines, increases amylase, is little delayed in the stomach and little ferments. In mild cases in normotrophs one can give a mixture of milk with decoction (1:3) and with lime water with 3% sugar, then switch to milk mixture (1:2) with 5% sugar. In severe D. and in hypotrophics up to 6 months are given buttermilk with ¹/₂-1% wheat flour and 2% sugar or protein milk with 5% sugar. After 2 weeks they try to add to the buttermilk or protein milk roasted flour with oil, so-called Schwitze, or Einbrenne in the form of buttermilk according to Kleinschmidt. In atrophics treatment is more complicated. In severe cases instead of water-hunger diet 50-100 g of milk whey are given, then-scalded milk, first skimmed human milk, because the strain during sucking can cause collapse. ²/₃ of the food is given in the form of human milk, and the rest in the form of buttermilk with 1-2% wheat flour and 3% sugar. One should never give only buttermilk. In the absence of human milk protein milk is given. Protein milk is gradually brought up to 200 g per 1 kg, the percentage of sugar and flour is increased to 8-10. Protein milk can cause pallor, lethargy, decrease in immunity; it is contraindicated in infants under 2 months with weight below 3,000 g and with putrefactive stool. A favorable effect in D., including and especially in parenteral forms, is exerted in artificially fed infants by acid nutrient mixtures. In D. due to infection such strict adherence to water-hunger diet is not required. A number of Russian and foreign authors have shown that acid mixtures decrease the buffer capacity of proteins and salts, make casein flakes softer, are easily digested, increase enzyme indices, activate the work of the pancreas, increase agglutinins in the blood in relation to the coli-typhoid group of bacteria, create worse conditions for the cultivation of bacteria. From acid mixtures are given lactic acid, hydrochloric acid and citric acid milk.

To 1 liter of milk add either 8 cm³ of a 75-85% solution of lactic acid, or 50 sl³ of a 10% solution of it, or 8 drops of official 12.5% hydrochloric acid per 100 g of milk, or take 4.64 g of citric acid per 1 liter of milk, adding 5% dextrin-maltose. French pediatricians give as a starvation-water diet to avoid harm from starvation in putrefactive Dyspepsia water with 3-4% milk sugar, and in acid Dyspepsia water with 10-15% cane sugar. Then they switch to rice broth. Dried or condensed milk is willingly used in France, and in recent times buttermilk. At the beginning of Dyspepsia from overfeeding, castor oil is given in 1 teaspoon to 1 tablespoon doses. It is rational to give a 1/10 solution of hydrochloric acid with 0.25-0.5 pepsin, and in prolonged Dyspepsia-pancreatin 0.1-0.2 with 0.25 calcium lactate. If weight gain stops-try protein therapy. Prevention of Dyspepsia consists of rational feeding according to age and need, both in regard to maternal and animal milk. Full nutrition that raises immunity is necessary. Proper upbringing is of great importance. It is necessary to protect the child from infection and illness by strengthening with fresh air, light, freedom of movement, and baths. One must fight against nipples, dirt on and around the child, contamination of food, and overheating. In summer, do not wean from the breast and increase water intake. It is urgently necessary to supply the child population with 'child' quality milk from healthy animals receiving full feed. The French point out that in spring and autumn livestock are fed with waste and milk acquires harmful properties. The storage of milk and its transport must be a special concern. It is also desirable to make it possible to obtain dried maternal milk and other quality dry preparations, such as buttermilk, protein milk, etc.- Chronic Dyspepsia and stomach dilation, as the French describe, occur more often in preschoolers than in infancy. To the picture described earlier, it must be added that in these cases the child loses weight. For treatment, besides rice and buttermilk-kefir, broth, white meat, boiled and pureed vegetables and berries, macaroni, cereals, and white dried bread are given. One should pay less attention to the stool than to the general condition, and remember that prolonged undereating, frequent use of starvation diets are deeply harmful, that the child can strengthen on suitable full food according to his tolerance, and that any new infections severely disrupt the mechanism of digestion and nutrition.

M. Rudnev.