Treatment of peptic ulcer of the stomach and duodenum

Pathogenetic treatment for peptic ulcer involves the appointment of a general and dietary regimen, as well as drugs that normalize the neuroendocrine regulation of the function of the alimentary canal, providing local digestion conditions that are optimal for ulcer scarring.
The initial stage of treatment for exacerbations, it is advisable to carry out in stationary conditions in compliance with bed or semi-bed mode. This allows you to protect the child from external adverse effects. A few weeks after the start of treatment, when the condition improves, the child can be switched to a free regime, which excludes, however, significant physical and emotional stress, which adversely affects the motor function of the stomach and duodenum.
Diet therapy for peptic ulcer is based on the antacid properties of food and the influence of its ingredients on the secretory-motor function of the alimentary canal. For this purpose, food is prescribed in fractional doses, but often (6 – 7 times a day). The diet includes only mashed potatoes and liquid dishes from products that excite the secretory and motor activity of the stomach and duodenum as little as possible. The great need of a growing child’s body for complete food ingredients determines the relative frequency of application of a strict restrictive diet. The composition of this diet includes vegetarian mashed and mucous soups with milk and cream, mashed cottage cheese, yogurt, soft-boiled eggs, butter and vegetable oil, jelly, juices from carrots, cabbage, oranges, table salt – 2 g per day.
By the end of the first week, the child is transferred to a diet No. 16, which additionally contains crackers, boiled meat, passed through a meat grinder, mashed cereals. Subsequently (after 2 weeks), vegetable purees, steam cutlets, white stale bread, dry non-butter cookies are introduced (diet No. 1c). Further, as the condition of the child improves, a diet No. 1 is prescribed for 4 – 6 months, which includes, in addition to the above-mentioned dishes, low-fat boiled meat, noodles, well-soaked herring, boiled sausages and sausages, steam slightly fried cutlets, fresh bread, normal amount of salt . Further expansion of this transitional diet is carried out taking into account the patient’s condition, however, even with complete well-being for several years after peptic ulcer exacerbation, it is necessary to avoid the use of spicy foods and seasonings, pickles and beggars containing saturated fats.
In case of ulcerative bleeding, the child’s nutrition in the first days is reduced to the appointment of small portions of milk every 2 hours, mucous soup, kissel (except for cranberry ). Next, add the egg, sugar, milk and cream mixture. Subsequently, a strict antiulcer diet with a more gradual expansion is prescribed .
Given the nutritional limitations of peptic ulcer, it is necessary to additionally prescribe vitamins, especially ascorbic acid and group B, at the maximum age dosage. In recent years, give the value contained in the fresh cabbage antiulcer factor called vitamin U. Because antacid medicaments reducing pepsicheskuyu activity of gastric juice and promoting a decrease in the spasm piloroduodenalnoy zones, are most common prescription containing equal amounts of magnesium oxide, sodium carbonate (or magnesium trisilicate with a tendency to constipation), as well as bismuth nitrate. With the success also apply almagel and vikalin having, in addition, analgesic effect, gastrofarm . A distinct normalizing effect on the secretory-motor function of the stomach and intestines is exerted by peripheral anticholinergics (M- anticholinergics ) – metacin , atropine, platifillin , as well as no-shpa and quateron , which has a pronounced ganglion-blocking effect. Clinical observations indicate that treatment for peptic ulcer in children with oxyferrisorbone , which has a direct reparative , decongestant, and anti-inflammatory effect , is highly effective . The prescribed dose (half or all of the contents of the vial – 0.03 g of dry matter diluted in 3 ml of isotonic sodium chloride solution) is administered intramuscularly 1 time per day for 20 days. As stimulants, fractional hemotransfusions , metacil or pentoxyl , hormonal and non-hormonal anabolites – methandrostenolone and potassium orotate can be used . Of the physiotherapeutic procedures, iontophoresis of calcium, novocaine, bromine, hydrotherapy, shown soon after the exacerbation, is more often used. As for thermal procedures , they are permissible only in the period of stable remission. Gastrointestinal bleeding is an indication for the appointment of strict bed rest, cold on the stomach, blood or plasma transfusion and other measures used for internal bleeding. If their effectiveness is insufficient, the question of surgical intervention should be timely resolved. Sanatorium treatment for peptic ulcer in children is carried out in Zheleznovodsk, Essentuki, Truskavets and other resorts. In the complex of inpatient and outpatient treatment, mineral waters of Smirnovsky and Slavyansky sources can also be used.

Prevention of peptic ulcer of the stomach and duodenum

Among the measures to prevent peptic ulcer of the stomach and duodenum and its exacerbations, we should first name timely treatment for chronic gastritis (gastroduodenitis) and disorders of the secretory-motor function of the alimentary canal. Strict adherence to a rational general and nutritional regime is also of great importance, which is especially important for children with a family predisposition to diseases of the stomach and intestines. Observations of recent years indicate the undoubted effectiveness of the follow-up and systematic (twice a year) courses of anti-relapse treatment prescribed about a month before the expected exacerbation (a two-week cycle of administration of anticholinergic drugs or monthly vikalin , almagel ).

Gastrointestinal Primary Lymphoma

Primary gastrointestinal lymphomas are one of the most common extranodal variants of non-Hodgkin lymphomas . in the last two decades, there has been a clear tendency towards a widespread increase in the incidence of these tumors. Among all malignant tumors of the gastrointestinal tract, primary non-Hodgkin lymphomas comprise from 1 to 10%. The prognosis is favorable and depends on the primary location of the tumor: 10-year survival with lesions of the stomach is 51%, of the small intestine – 54% and with a tumor of the colon – 35%. Various sections of the digestive tube are involved in the process unequally often: the stomach – in 55-70%, the small intestine – in 20-35%, the large intestine – in 5-10%. The rarest are considered primary non-Hodgkin ‘s lymphomas of the esophagus. Primary gastrointestinal lymphomas are represented by a heterogeneous group of tumors. A variety of morphological variants of non-Hodgkin digestive tube lymphomas explains the variability of clinical manifestations and therapeutic approaches. In general, tumors do not have pathognomonic clinical signs; the symptoms of the disease are caused by the location of the main tumor node and are similar to the clinical signs of tumors of any histogenesis of this localization. Common distinguishing features of gastrointestinal lymphomas : a plurality of lesions within the digestive tube, a tendency to regional lymphogenous dissemination and a high incidence of formidable, often fatal complications (bleeding, perforation, intestinal obstruction – 20%). Determining the prevalence of the process is carried out in accordance with the classification, which takes into account all the clinical features of non-Hodgkin lymphomas of the gastrointestinal tract, approved in 1993 in Lugano. In the plan of examination of patients to the generally accepted diagnostic measures must necessarily be added: fibrolaryngoscopy and the study of all sections of the digestive tract. The most common variant of gastric lymphoma is MALT lymphoma . A characteristic feature of MALTom is their antigenic dependence on infection of the gastric mucosa Helicobacter pylori . It is known that normally there is no lymphoid tissue in the gastric mucosa. It is believed that its appearance is pathognomonic for H. pylori infection. Currently, experience is being gained using antibacterial anti-Helicobacter therapy ( omeprazole , clarithromycin , amoxicillin) for the treatment of stage I MALTOM of the stomach (low grade): the possibility of achieving complete remission has been ascertained in more than 2/3 of patients. Details of antibiotic therapy are being specified. The main goal of this effect is the eradication of H. pilori . The antitumor effect occurs gradually after the eradication of H. pilori , but the timing varies widely – from 3 to 18 months. The management of patients in this category remains a subject of scientific research. Treatment of local stages (I-II) of other morphological variants of primary non-Hodgkin lymphomas of the gastrointestinal tract begins with neoadjuvant chemotherapy: for aggressive tumors, CHOP, CHOEP, R-CHOEP regimens are used; with indolent lymphomas – chlorambucil , COP, CVP and in combination with MabThera . With an effectiveness of 2-3 courses, treatment is continued until complete remission, in the absence of effect, radical surgery is performed. Radical operations can be performed in the vast majority of patients (> 70%). In the postoperative period, adjuvant chemotherapy (3-4 cycles) is carried out in accordance with the morphological variant of the tumor. The result of this therapeutic approach is good long-term results: 10-year survival exceeds 70%, and 15-year survival is 69%. Such results could convince of the advisability of using only surgical treatment, if not for changes in the quality of life of patients after radical surgical interventions (in particular, after gastrectomy , hemicolectomy ). This is precisely what caused the current tendency to expand the use of neoadjuvant chemotherapy. The use of radiation therapy in the postoperative period, on the one hand, does not have an additional effect, on the other hand, it worsens the quality of life due to the development of radiation reactions from the abdominal organs. This explains the unpopularity of adjuvant radiation therapy. However, radiation exposure is promising as induction therapy in clinical situations when, for one reason or another, the drug or surgical method cannot be used. The total focal dose to the lesion is 32-36 Gy. A special clinical variant of non-Hodgkin lymphoma of the small intestine is IPSID. Previously , the terms “heavy alpha chain disease” or “Mediterranean lymphoma ” were used to refer to this lymphoma . The leading clinical symptom of the disease is malabsorption in the small intestine, which leads to sharp persistent weight loss, a significant deterioration in general condition and low tolerance to standard chemotherapy. The disease occurs mainly in the countries of the Middle East, northern Africa, Central America, affecting more often men aged 20-30 years. Tumor infiltration spreads throughout the small intestine with maximum damage to the duodenum and ileum. The pathogenesis remains unknown; it is assumed that the basis is the hyperproliferation of heavy chains of immunoglobulin A. The prognosis is poor, 5-year survival does not exceed 20%. Radiation therapy is ineffective. Surgical treatment is also not successful due to the extent of intestinal lesions. The use of chemotherapy (regimens used for both indolent and aggressive non-Hodgkin lymphomas ) is not very effective . The use of antibacterial drugs of the tetracycline group seems promising; however, the rarity of the pathology and little international experience do not allow us to recommend the developed treatment regimen. Primary non – Hodgkin lymphoma of the rectum is found with the least frequency . Tumors are usually represented by aggressive B-cell lymphomas . Combined treatment: intensive chemotherapy in combination with local radiation therapy (30-40 Gy per tumor site in a daily dose of 1.5-2.0 Gy). Surgical treatment does not improve results. Generalization of the process is the main type of progression (> 75%), develops mainly in the first 2-3 years after local methods of exposure and requires treatment in accordance with the principles of treatment of common non-Hodgkin’s lymphomas .

Diseases of the operated stomach

This term refers to syndromes that sometimes occur after resection of the stomach. Some of them appear in a few weeks, while others only a few months after the operation. Conventionally, local ( recurrence of peptic ulcer , chronic gastritis of the stump of the stomach , “adherent loop” syndrome ) and general ( dumping syndrome and malabsorption syndrome ) disorders are conventionally distinguished .

Peptic ulcer anastomosis

Often develops directly in the area of ​​the anastomosis or in the jejunum, less often the stomach stump. The main factor leading to the development of this complication is considered to be the remaining secretion due to incomplete removal of the antrum and preservation of cells secreting gastrin . When an ulcer forms, intense pain characteristic of peptic ulcer develops, it is often complicated by gastrointestinal bleeding.
With a peptic ulcer of the anastomosis that developed after an insufficiently radical operation, in which part of the antrum is preserved , a higher resection or proximal vagotomy is performed . In rare cases, the peptic ulcer of the anastomosis can penetrate into the colon adjacent to the anastomosis, forming a gastrointestinal fistula. In this case, after eating, rumbling in the abdomen, loose stools with the remains of undigested food are observed. In patients, absorption is significantly impaired, severe general dystrophy may develop. An X-ray examination does not always reveal the presence of an anastomosis between the stomach (or jejunum) and the colon. The presence of a fistula can be confirmed by the administration of a staining solution (for example, methylene blue) in the enema, simultaneously with gastric probing, in which rapid staining of the gastric contents is observed. Timely repeated surgical intervention can save the life of such a patient.

Chronic gastritis of the stump of the stomach

Chronic atrophic gastritis, which occurs after resection of the pylorus, is to some extent inevitable, since after this operation there are no G-cells and thus the second most important phase of gastric digestion falls out. The fundus glands remaining in the stomach cult , deprived of physiological stimulation by gastrin , cannot fully function and gradually atrophy. Thus, during resection of the stomach, preservation of part of the pyloric stomach leads to the appearance of a peptic ulcer of the anastomosis, and its complete removal is one of the reasons for the subsequent development of chronic gastritis. In addition to the lack of stimulation of gastric secretion, regurgitation of duodenal contents into the stomach is also important in the development of gastritis of the gastric stump .
Impaired iron absorption may also be of some importance.
Chronic gastritis of the gastric stump, depending on its severity, can cause various symptoms – from a slight feeling of discomfort that occurs after eating, to severe gastric dyspepsia with belching, nausea, and vomiting, while there is often an admixture of bile in the vomit. Patients with chronic gastritis of the stump of the stomach are shown a strict diet, fractional nutrition. With a decrease in secretion, gastric juice may be prescribed.
Cancer can also develop in a stomach cult, usually many years later (up to 10 years or more) after resection of the stomach. For the diagnosis of chronic gastritis of the stump of the stomach and the determination of its severity, as well as the exclusion of cancer, gastroduodenoscopy and clinical follow-up are necessary .

Loopback Syndrome

It usually occurs after Billroth-2 surgery, in which a more distal section of the intestine is sutured to the stomach and a small section of the proximal part of the intestine remains stitched , i.e., a blind section of the intestine forms. In these cases, food and gastric contents can be thrown into the blind section of the intestine, causing a feeling of heaviness in the epigastric region, dull pain, vomiting, sometimes with an admixture of bile. Two variants of the afferent loop syndrome are described. At the first, dyspeptic phenomena are mainly observed due to stagnation of food in the blind segment of the intestine. Unpleasant sensations appear 30-60 minutes after eating. Often, an increase in the secretion of bile and pancreatic juice, stimulated, apparently, from the blind section of the intestine, as well as an increase in the level of blood amylase, is often determined. The second option is due to the development of the infectious process in the blind segment of the intestine against the background of stasis, which subsequently leads to the development of chronic enteritis with malabsorption syndrome . In both variants of the lead loop syndrome, reconstructive surgery is indicated, including the elimination of the lead loop. In the second option, antimicrobial therapy is preliminarily performed.

Dumping syndrome

It develops as a result of the rapid entry of food through the anastomosis into the small intestine. Rapid emptying of the stomach stump causes stretching of the loops of the jejunum and an increase in pressure in its lumen. The osmolarity of food not sufficiently diluted with bile and pancreatic juice is usually higher than under normal conditions. The ingestion of such food into the small intestine leads to the appearance of fluid flow from tissue and blood into the intestinal lumen. As a result, after 20-30 minutes after eating (early, or true, dumping syndrome), the patient has a feeling of heat in the body, dizziness, palpitations, cold sweat, as well as nausea, vomiting, pain, sometimes diarrhea, the more pronounced the higher the osmolarity of food. Such an attack lasts 30-60 minutes and passes on its own. In the development of an attack, they also attach importance to an increase in the release of biologically active substances (histamine, serotonin, adrenaline), both due to an increase in the tone of the sympathetic nervous system during intestinal distension and the rapid advancement of food, as well as osmotic disorders. The release of biologically active substances causes the appearance of unpleasant sensations 11 / g-3 hours after a meal. The development of late dumping syndrome depends on the nature of the food taken, the presence of easily digestible carbohydrates in it. In the origin of late dumping syndrome, hypoglycemia, resulting from an inadequately high release of insulin, is of great importance, due to a dysregulation due to a violation of the integrity of the stomach and an unusual route of food passage. As a rule, a dumping -indrom does not lead to any grave consequences; basically, only more or less pronounced unpleasant subjective sensations arise. In mild expressed syndrome shows diet correction: the exception of sugar and sweet dishes are too hot or cold food, postprandial recommended to take a horizontal position. In more severe cases, during an exacerbation, it is generally necessary to recommend a meal in a horizontal position. Only in relatively rare cases, they resort to surgical treatment.

Malabsorption syndrome

As a result of resection of the stomach, the absorption of food may be impaired. The severity of malabsorption syndrome depends on the degree of digestion compensation in the lower parts of the gastrointestinal tract. Patients may experience weight loss, sometimes osteoporosis and osteomalacia, iron deficiency and B ^ -deficient or folic-deficiency anemia. Severe malabsorption syndrome develops in rare cases when the patient had latent small bowel disease or chronic pancreatitis before surgery.

Chronic gastritis

Chronic gastritis is a disease accompanied by an indigestion in the stomach; morphological changes are reduced to non-specific inflammation of the gastric mucosa with the gradual development of atrophy. The anatomical and physiological features and close functional connections of the stomach with various body systems explain the frequent involvement in the pathological process in gastritis of other parts of the digestive system, as well as the nervous and endocrine. This equally determines the possibility of developing chronic gastritis in diseases of the intestines, liver, biliary tract, neuro-endocrine disorders, etc. The relationship between chronic gastritis and clinically similar functional secretory-motor disorders of the stomach, not accompanied by typical morphological changes in its mucous membrane, is one of the unresolved issues of gastroenterology. Given that the diagnosis of chronic gastritis in pediatrics is based primarily on the materials of clinical and functional observations, and the intravital histological study of the gastric mucosa in childhood is often significant difficulty, a strict distinction between the aforementioned functional disorders and chronic gastritis must be recognized as largely artificial ( M. B. Kossyura ). In each individual case, an attempt at such differentiation may be justified, but it should be remembered that the commonality of the etiology, clinic, and patterns of development allows us to talk about the pathogenetic unity of both pathological processes, one of which is, in fact, only a functional pre-stage of the possible development of chronic gastritis, with characteristic structural-morphological changes that have already arisen (O. L. Gordon). It is the difference in views on the essence of chronic gastritis and functional secretory-motor disorders of the stomach, as well as the lack of a unified classification and nomenclature that explains, first of all, the significant variety of information about the frequency of the disease in childhood. The most reliable are the data of A. V. Mazurin, obtained by endoscopy performed in 507 children with complaints of abdominal pain. Phenomena of chronic gastritis and gastroduodenitis (more often) were detected in 333 children (68.2%). The older the children, the more often they experience chronic gastritis. According to N. M. Smirnov, the ratio between the frequency of the disease in children of preschool, primary and high school age is approximately.

Chronic gastritis

In the development of chronic gastritis, the influence of various exogenous and endogenous factors plays a role. In childhood, violation of the regime and diet is of particular importance: improper feeding rhythm with long breaks between meals; dry eating, fast and insufficient chewing of food; the use of excessively spicy, rough food; systematic overeating.
They also attach great importance to neuro-reflex and toxic effects associated with various diseases of the food canal, the presence in the child’s body of foci of chronic infection, neurosis, endocrine disorders.
M.S. Maslov, D.A. Bertova point to the role of acute gastritis as one of the reasons for the subsequent development of a chronic inflammatory process of the gastric mucosa. Attention is also drawn to experimental and clinical observations, indicating the likelihood in some cases of an allergic origin of chronic gastritis.
A certain role in the occurrence of chronic gastritis can be played by a congenital predisposition, which indicates the need for a thorough clarification of the family history.
Based on a histological examination of sections of the gastric mucosa obtained by aspiration biopsy, C. G. Masevich distinguishes superficial gastritis, gastritis with lesions of the glands without atrophy, as well as atrophic gastritis.
Pathogenesis. The variety of essentially etiological factors of chronic gastritis determines the complexity of its pathogenesis, unequal in various forms of the disease. At the same time, they attach great importance to the breakthrough of the so-called protective mucous barrier formed by a viscous secretion and a layer of mucus-forming epithelium located above the main and parietal cells of the gastric mucosa. Violation of the protective barrier and normal continuous regeneration of the cells of the mucous membrane can result from the ingestion of caustic and toxic substances, roughage into the stomach. Finally, functional, and then structurally-organic changes can be caused by prolonged neuro-reflex, humoral disorders, and eating disorders.
Currently, there is no single universally recognized classification of chronic gastritis that develops in childhood. Below is one of the working classifications, built taking into account the etiology and clinical and functional characteristics of the disease. Working classification of chronic gastritis 1. According to the etiological criterion, alimentary, neurogenic, infectious-toxic, irritative, metabolic-endocrine, allergic, unclear etiology. 2. On a functional basis. a) gastritis with preserved (or increased) secretory function; b) gastritis with secretory insufficiency. 3. According to the clinical course: a) mild, moderate or severe; b) often or rarely exacerbated; c) phase of exacerbation, decaying exacerbation, remission. An approximate sample of diagnosis according to this classification: chronic nutritional gastritis with secretory insufficiency; light form; rarely exacerbating, in the phase of decaying exacerbation.

Clinic of chronic gastritis

Chronic gastritis is characterized by a distinct cyclical course. Its exacerbations can occur at any time of the year, but more often in spring and autumn. Until puberty, girls are more likely to get sick. The onset of the disease in more than half of the children coincides with the time of entry to school, which can be attributed to a sharp change in the general and nutritional regime, increased emotional and physical stress.
A distinctive feature of the clinic of chronic gastritis is, as a rule, a rich subjective symptomatology of the disease, characterized by an abundance of bright, distinct sensations and symptoms with a comparative scarcity of data from an objective study. Therefore, a thorough and directed history is of particular importance for the correct and timely diagnosis of the disease. It should be borne in mind that some patients, especially those of preschool age, unable to understand their feelings, find it difficult to describe them and prefer to remain silent about them.
Observations indicate certain differences in the clinical manifestations of chronic gastritis in children, occurring with reduced or increased secretion of gastric juice.
A constant symptom of the disease is abdominal pain, often localized in the epigastric and right hypochondrium. With reduced secretion of gastric juice, it is dull, spilled, usually appears soon after eating and does not depend on the nature of the food. Chronic gastritis with preserved and increased secretion is characterized by acute paroxysmal pain, most often occurring 1 to 2 hours after eating and often provoked by the consumption of spicy, rough food.
The most pronounced pain syndrome is expressed in a combination of inflammatory lesions of the gastric mucosa and duodenum – gastroduodenitis. In these cases, pain often appears 2 to 3 hours after eating and subsides soon after it, often night pain occurs. Gastroduodenitis in children is almost always accompanied by a constant increase in gastric secretion, its level on an empty stomach. The state of the secretory function of the stomach in chronic gastritis significantly affects the features of dyspeptic syndrome. So, with gastritis with secretory insufficiency, there is a decrease in appetite, an aversion to cereals and dairy dishes, often nausea and vomiting, which occurs 2 to 3 hours after eating. With hypersecretion and increased acidity, most children have good appetite, nausea and vomiting are much less common, at the same time, belching is acidic, heartburn comes to the fore, half of patients have a tendency to constipation. Children with chronic gastritis usually do not lag behind their peers in physical development. Many of them are irritable, emotionally unstable. An objective study often reveals a significant overlay of the tongue, sensitivity is constantly determined during striking or deep palpation in the epigastric region. Radiologically in chronic gastritis, a change in the relief of the gastric mucosa, as well as motor and secretory disorders, are often noted. However, this does not play a significant role in the diagnosis of the disease due to the significant variability of the x-ray picture of the relief of the mucous membrane and motility of the stomach of healthy children in the conditions of administration of a contrast medium.

Differential diagnosis of chronic gastritis

In contrast to chronic gastritis, with functional secretory-motor disorders of the stomach, pain and dyspeptic symptoms are less associated with food intake, are less stable and quickly disappear after correction of the diet and successful treatment of the underlying disease (rheumatism, tuberculosis intoxication, etc.).

Treatment and prevention of chronic gastritis

The variety of etiology and pathogenetic features of various forms of chronic gastritis determines the diversity of measures to prevent the disease and its exacerbations. The main one is to ensure the diet and diet according to the age of the child. In this case, it is necessary to monitor the thorough chewing of food, its moderate temperature, limit or exclude the use of hot seasonings and canned food. It is also necessary to ensure timely detection and treatment of somatic diseases, neuro-endocrine disorders, focal infectious processes, ascariasis, which contribute to the development of chronic gastritis after functional secretory-motor disorders of the stomach. In this light, clinical examination of children with the risk of developing chronic gastritis or undergoing its exacerbation is of great importance. It is necessary to remember the role of a hereditary predisposition to diseases of the stomach, in particular to chronic gastritis.
The basis of the complex of therapeutic measures for chronic gastritis is diet therapy, built taking into account the clinical, functional (primarily secretory) features and phase of the disease. Regardless of the form of gastritis, the diet includes 5 – 6 feedings per day in reduced portions. With hyposecretion, this is explained by the desire to reduce the residence time of food masses in the stomach, as well as maximize the use of the reduced digesting ability of gastric juice.
With hypersecretion and increased acidity, an increase in food intake helps to some extent prevent the adverse effects of gastric juice on the wall of an empty stomach in conditions of an impaired mucous protective barrier.
In the initial period of exacerbation, mashed non-meaty soups, jelly, white crackers, butter, tea are prescribed . Being chemically and mechanically gentle, this diet almost does not irritate the mucous membrane of the patient’s stomach. A few days later, boiled ground lean meat, fish, eggs, vegetable and fruit purees are introduced into the diet. Such nutrition can be immediately prescribed to patients who are poorly tolerated by food restriction, malnourished children.
As the condition of patients improves, the diet is expanded. For gastritis with secretory insufficiency, diet number 2 is prescribed for several months, including products that stimulate secretion quite strongly – meat and fish decoctions, soaked chopped herring, caviar, etc. In the future, cutlets, fried meat, low-fat sausages are introduced into the diet casseroles. The diet should be full in composition and energy value, fortified, which contributes to reparative processes in the gastric mucosa. Fatty meats and fish, fresh bread, foods containing a large amount of crude fiber, spicy and canned foods, and cold drinks are still not recommended. With increased acidity, a fairly complete, but sparing and less sokogonny diet No. 1 with a subsequent expansion of the diet is prescribed for the same period .
Clinical experience convinces of the advisability of starting treatment of chronic gastritis in a hospital. This allows you to immediately change the usual stereotype in the conditions of which the disease arose, it is better to examine the child and establish the optimal therapeutic and dietary regimen. A prerequisite for successful treatment in the hospital and at home is a calm benevolent environment, a rational regime with the correct alternation of classes and rest, a long stay in the air, enough time for night and day sleep.
In gastritis with secretory insufficiency, a 2% solution of diluted hydrochloric acid should be prescribed in a dessert or tablespoon 4 times a day, natural gastric juice or tablets of beta-acid or acidin- pepsin in an age-related dosage. A plantaglucid has a good therapeutic effect , a freshly prepared solution of which (1/2 – 1 teaspoon of granules in 1/4 cup of warm water) the child takes 3 times a day 20 minutes before meals for 3 to 4 weeks. In gastritis with high acidity and the corresponding symptoms, alkali (drinking soda, magnesium oxide), vicalin , which, like other antacids, should be taken 30 to 40 minutes after a meal, washed down with 1/3 cup of warm water. Almagel is also effective – 1 teaspoon 20 minutes before meals 3 times a day, gastropharma . Favorably affect the tone and motility of the stomach, contribute to the removal of pain quateron , no-spa, platifillin , drugs of the belladonna group. Ascorbic acid, nicotinic acid, pyridoxine and cyanocobalamin are also shown . Patients with reduced appetite and significant emaciation should undergo a course of treatment with non-hormonal and hormonal anabolic drugs – potassium orotate , nerobol . Treatment for gastritis that occurs as a complication of a disease should be carried out in combination with intensive care of the underlying disease. Sanatorium treatment of chronic gastritis in children is carried out in Essentuki, Zheleznovodsk, Truskavets and other resorts.

Rotavirus gastroenteritis

In highly developed countries, more than 60% of acute gastroenteritis is caused by viruses from the Reoviridae family . Among them, rotaviruses dominate . The genus Rotavirus includes human rotaviruses and viruses that cause diarrhea in animals. The latter are non-pathogenic for humans. Human rotaviruses cause mainly gastroenteritis in children under three years of age and the elderly. The causative agent is transmitted by the fecal-oral route through household contacts. The high resistance of viruses in the environment contributes to the development of outbreaks of gastroenteritis, especially in winter (up to 90%). For protein antigens, rotaviruses are divided into 4 serovariants .

Material for laboratory diagnostics

The material for laboratory diagnosis is stool and blood. Fecal samples are taken in the first hours and days of illness in sterile penicillin vials and sent to the virology laboratory in ice containers. A 10-20% suspension in Hanks solution is prepared , centrifuged for 30 minutes at 3000 rpm. The centrifugate is transferred into a sterile vial, add Freon 113 or 1000 IU / ml of penicillin and 500 IU / ml of streptomycin, placed in the refrigerator for 10-12 hours. Blood for serological reactions is taken in the first 2-3 days of illness and after 12-14 days. Laboratory diagnosis of viral diarrhea is based on the rapid detection of viruses in the feces using electron and immune electron microscopy, an indirect hemagglutination reaction with antibody erythrocyte viral diagnostics . The enzyme-linked immunosorbent assay in the solid-phase variant is also used for the coaglutination reaction , the method of cloned RNA probes and the polymerase chain reaction. In the early days of the disease, the content of rotaviruses in copromaterials reaches 106-108 per 1 g, therefore, their detection by direct electron microscopy is possible without additional concentration. A drop of the test material is applied to special films of nitrocellulose and microscopic at a magnification of 50,000. The method is sensitive and reliable, allows you to quickly detect the virus and examine its morphology. If 5-6 virions are found in almost every field of view, the diagnosis of rotavirus gastroenteritis can be reliably confirmed . The method of immunoelectronic microscopy is of even greater diagnostic value . Its principle is that the immune antiviral serum is added to the fecal suspension illuminated by low-speed centrifugation, kept for 60 minutes at room temperature and another 12 hours at 4 ° C, then centrifuged at 15,000 rpm to precipitate viral particles and immune complexes. The precipitate is resuspended in 2-3 drops of distilled water, contrasted in phosphoric tungsten acid and examined under an electron microscope. Characteristic accumulations of rotaviruses are found in the preparations . The high efficiency of the method is practically independent of the initial concentration of viruses in the studied samples.

Virological studies

Virological studies to isolate rotaviruses in cell cultures or laboratory animals in routine virological laboratories are not carried out . The enzyme immunoassay is most commonly used in the diagnosis of viral gastroenteritis. Its principle is; that the wells of the polystyrene plate are first sensitized with antibodies against rotaviruses , and then an illuminated feces suspension is added to them, incubated for 1 hour in an incubator. An antigen-antibody complex is formed in the wells after washing three times with phosphate buffer and manifested by the addition of antiglobulin serum conjugated to the enzyme. After incubation, chromogenic substrates are added in a thermostat until a colored reaction product appears. Analysis is carried out using an enzyme-linked immunosorbent analyzer. In small laboratories, a reverse indirect hemagglutination reaction is often performed using an antibody rotavirus erythrocyte diagnosticum . It is easy by the method of formulation, although it is less sensitive than the reaction enzimmichenih antitel.V practice laboratory diagnosis of viral infections are also administered test koaglyutinatsii for indicating rotavirus antigen in the stool of patients. A drop of a suspension of staphylococci ( Cowan strain 1) sensitized with rotavirus serum is applied to a glass slide and a drop of centrifuged copromaterial is added . In the presence of rotaviruses , agglutination of staphylococci loaded with antibodies occurs after 30-60 s. A very sensitive way to quickly diagnose viral gastroenteritis is a method for detecting virus-specific RNAs using molecular hybridization. It is based on the hybridization of labeled RNA probes fixed on nitrocellulose filters. Labeling is carried out with biotin or an enzyme, which greatly simplifies and cheapens the method compared to radioisotope labels.

Rotavirus RNA Assay

The analysis of rotavirus RNA, despite its high cost, is increasingly being introduced into practice, especially after the development of the polymerase chain reaction method. The latter is a sensitive and specific diagnostic method, which, of course, is a new generation diagnostic test, the so-called “gold standard”. However, the formulation of this reaction still requires highly qualified researchers, expensive reagents and sophisticated equipment.

Serological diagnosis

Serological diagnosis is aimed at identifying specific antibodies in paired sera taken at a two-week interval. For this purpose, various neutralization or precipitation tests and an indirect immunofluorescence reaction are used . But enzyme-linked immunosorbent assay has been widely used recently. Previously, for the serodiagnostics, CSCs were widely used using pre-selected feces of patients with gastroenteritis or calf rotaviruses as antigen . But in its sensitivity and specificity, it is significantly inferior to the method of enzyme immunoassay. To detect specific antibodies to rotaviruses, they also put inhibition of indirect hemagglutination with paired sera. Gastroenteritis in children can also cause caliciviruses , astroviruses and Norwalk viruses . All of them are excreted with feces in the first 2-3 days of the disease, do not reproduce in cell cultures or are poorly reproduced without cytopathic effect. For laboratory diagnosis of gastroenteritis caused by these viruses, mainly using the method of immune electron microscopy. There are no other diagnostic methods available for virology laboratories.

Therapeutic nutrition for gastritis

Therapeutic nutrition for acute gastritis should include in the first hours and days of the disease the most complete mechanical, chemical and thermal sparing of the gastric mucosa. Careful monitoring of the water-electrolyte balance is required. On the 1st day of the disease, it is necessary to refrain from eating, drinking up to 2 liters per day is allowed (broth of wild rose, sweet tea with lemon). On the 2nd day, liquid beggar is prescribed : slimy sun , kissel, jelly, meat soufflé. On the 3rd day, white crackers, steam cutlets, meatballs, dumplings, low-fat broth, potato or carrot puree, mashed compote are allowed. From the 4th-5th day – milk soups, boiled chicken without skin, porridge and shore in a thicker form, fruit juices. When the process attenuates, gradually (after 1-2 weeks ) the patient is transferred to diet No. 15.
If acute gastritis has developed due to any infectious disease, a nutritious diet rich in protein containing all the necessary amino acids in optimal proportions (meat, fish, cottage cheese) is prescribed , eggs). Diet mechanically and chemically sparing, not irritating to the stomach. In the presence of diarrhea, milk is excluded from the diet. The diet contains a sufficient amount of fats, carbohydrates, mineral salts and vitamins.

Therapeutic nutrition for chronic gastritis with secretory insufficiency

Diet therapy is leading in the comprehensive treatment of chronic gastritis. It is built depending on the stage of the disease. The most strict diet is prescribed during the period of exacerbation. As the patient’s well-being improves, the diet gradually expands, and during the period of clinical and endoscopic remission, the food is held as healthy with the exception of indigestible (smoked meats, fatty meats and fish) and irritating the gastric mucosa (spicy, salty, seasoned dishes) types of food.
When building a diet, the state of the secretory, acid and enzyme-forming functions of the stomach should be taken into account .
With all forms of chronic gastritis, nutrition should ensure the intake of a sufficient amount of protein, fat and vitamins. In the period of exacerbation of the disease, it is advisable to take food at least 4-5 times a day.

Therapeutic nutrition for chronic gastritis with preserved and increased secretion

Diet therapy is built on the same principles as for gastric ulcer and duodenal ulcer (diet No. 1).
Chronic gastritis with secretory insufficiency. The main requirements for therapeutic nutrition for gastritis with secretory insufficiency:
full- day nutrition, which contributes to the development of compensatory-adaptive reactions of the digestive system and slows down the rate of progression of chronic gastritis;
fractional diet, in which the processes of digestion and absorption of food substances improve . Diet therapy for patients with chronic gastritis with secretory insufficiency (diet No. 2) is based on mechanical sparing of the gastric mucosa and chemical stimulation of its glandular apparatus with food irritants. This diet is most justified in cases where there is an inflammatory process in the mucous membrane of the stomach, leading to inhibition of secretion.
Particular attention is paid to vitamin therapy (nicotinic, ascorbic acid, vitamins B6 and B12). Niacin and pyridoxine increase the acidity of gastric juice.

General characteristic of diet No. 2

The diet is physiologically full-chain , rich in extractive substances. It has a stimulating effect on the secretory apparatus of the stomach, promotes compensatory and adaptive reactions of the body, and prevents the development of the disease.
Culinary processing. Allowed dishes with varying degrees of grinding and a variety of heat treatment (boiling, baking, frying without breading). The chemical composition and calorie content. Proteins 90-100 g, fats 90-100 g, carbohydrates 400-450 g. Calories 3000-3200 kcal. Free liquid 1.5 l, table salt up to 15 g. The total weight of the daily diet is 3 kg. Fractional diet (4-5 times a day). Food temperature: hot dishes from 57 to 62 ° C, cold – not lower than 15 ° C. The diet can be prescribed for a long time both in the hospital and on an outpatient basis. List of recommended products and dishes Bread and bakery products. Wheat bread white and gray yesterday’s baking, unprofitable varieties of bakery products and cookies. Soups On fat-free meat and fish broth, on vegetable broths with mashed vegetables and cereals. Meat and fish dishes. Cutlets of low-fat beef, veal, poultry, chopped fish products (before frying, do not roll in breadcrumbs so that a rough crust does not form). Partial fish, chicken – in boiled form. Dishes and side dishes from vegetables . Mashed potatoes from various vegetables, puddings, vegetable patties, baked and fried so that a crust forms (not seasoned in flour or breadcrumbs), boiled cauliflower with butter, zucchini and stewed pumpkin, tomato salad. The finely chopped early greens can be added to various dishes. Dishes and side dishes from cereals and pasta. Baked cereals, puddings, cereals cutlets, fried so that a rough crust does not form; finely chopped pasta, boiled vermicelli. Fruits, berries, sweet dishes. Mashed compotes, mashed potatoes, jelly, jelly, mousses from sweet varieties of fruits and berries. Sugar, honey. Milk and dairy products. Milk with tea and other drinks and as part of various dishes, cottage cheese, yogurt, kefir, acidophilus milk. Dishes from eggs. Soft-boiled eggs, scrambled eggs. Nanitki . Tea with milk, cocoa and coffee on the water and with milk. A broth of wild rose and wheat bran, fruit and berry juices (diluted). Snacks Uncooked cheese (grated), soaked herring, doctor’s sausage, low-fat ham. Fats. Butter, sunflower, olive. Sauces: meat, fish, sour cream. Forbidden: pastry, fried meat and fish, boneless in breadcrumbs; canned meat, mushrooms and other snack foods; raw vegetables and fruits; legumes, in-kind milk, brown bread, carbonated drinks, lard, goose, duck, pickles, smoked products, marinades, very hot and cold dishes. A sample menu for patients with chronic gastritis with secretory insufficiency is given in table. Chronic atrophic gastritis develops gradually and is not diagnosed for a long time due to the compensatory activity of the pancreas and intestines. If chronic atrophic gastritis is asymptomatic, it is necessary to stimulate the compensatory capabilities of the digestive tract to prevent the pathological process in other digestive organs and to ensure the physiological nutritional needs of the body. Physiologically complete diet No. 15 meets these requirements without mechanical and chemical dandruff . The content of proteins, fats, carbohydrates and calories correspond to the diet of a healthy person who is not engaged in physical labor, and vitamins are prescribed in an increased amount. Exclude fatty meat, beef, lamb and lard, pastry; spices – in moderation. Culinary processing is conventional rational with the preservation of vitamins. Eating 4-5 times per depot . Treatment of both acute and chronic gastritis of various etiologies should be comprehensive, individualized. In the complex treatment of chronic gastritis, spa treatment is widely used (Essentuki, Pyatigorsk, Zheleznovodsk), local gastrointestinal sanatoriums with salt-alkaline sources. Acceptance of alkaline and salt-alkaline mineral waters 15-20 minutes before a meal stimulates gastric secretion, intake of the same waters 1.5-2 hours before a meal has an inhibitory effect on gastric secretion. Under the influence of mineral waters acting on the interoreceptors of the stomach, evacuation and motor function of the stomach improves.

Dumping syndrome

Dumping syndrome is a condition characterized by the occurrence of severe weakness, dizziness, palpitations, a feeling of heat 10-15 minutes after a meal and is regarded as a reaction of the body’s adaptation to altered digestion processes.

Etiology, pathogenesis of dumping syndrome

The trigger mechanism of dumping syndrome is the accelerated intake of insufficiently processed, concentrated food, mainly easily digestible carbohydrates, from the stomach into the jejunum . Dumping syndrome occurs, as a rule, in patients after surgery on the stomach. Moreover, its severity depends on the nature of the operation. When the duodenum is switched off from the passage, the manifestations of dumping syndrome are more pronounced, but they can also be detected in unoperated patients. Neuromuscular mechanisms are involved in the occurrence and development of dumping syndrome, accompanied by redistribution of blood with an increase in its flow to the digestive canal organs and a violation of the central hemodynamics. In addition, to normalize the processes of absorption and create an isotonic environment, a significant amount of fluid enters the small intestine, which leads to hypovolemia. In dumping syndrome, there are a number of disorders of the digestive function of the stomach, small intestine, liver, and pancreas, due to their functional state and transferred surgical intervention.

Clinic of dumping syndrome

The clinic of dumping syndrome is very characteristic and manifests itself 10-15 minutes after eating. Clinical manifestations begin with a feeling of fullness in the epigastric region and are accompanied by an unpleasant feeling of heat in the upper half of the body or throughout the body. The perspiration sharply amplifies. Then come weakness, drowsiness, dizziness. In some cases, these phenomena reach such strength that the patient is forced to lie down. Attacks are accompanied by tachycardia, sometimes shortness of breath, headache, paresthesia in the upper and lower extremities, vasomotor rhinitis, polyuria. Dyspeptic phenomena during an attack are diverse: salivation, dry mouth, heartburn, belching. Very often there is rumbling in the abdomen, diarrhea at the end of the attack or some time after it. The intensity of the attacks can vary.
In a horizontal position, the general condition of the patient improves, which causes severe manifestations of dumping syndrome to take food in bed and lie for some time after eating. Dumping syndrome is most often triggered by dairy and carbohydrate foods.
Depending on the severity of clinical manifestations, there are 3 degrees of severity of the disease: I ( mild ) degree is characterized by periodically occurring short (15-20 minutes) seizures after ingestion of milk and carbohydrate foods. During an attack, the heart rate increases by 10-15 in 1 min, blood pressure can increase or decrease by 10-15 mm Hg . (1.3-2 kPa). The deficit of body weight does not exceed 5 kg. Performance saved. Drug treatment and the exclusion of foods that cause dumping syndrome from the diet gives a good effect. II ( moderate severity ) degree is characterized by attacks of weakness that constantly occur after eating, dizziness, pain in the heart, sweating, and diarrhea. The duration of attacks is 20-40 minutes with any nature of the food. During an attack, the pulse increases by 20-30 in 1 min, blood pressure rises by 15-20 mm Hg . (2-2.7 kPa). The deficit of body weight is 5-10 kg. Performance reduced. Conservative therapy “gives short-term effect. III of ( severe ) degree – persistent, pronounced attacks with kollaptoid – nym . Condition, diarrhea, do not depend on the nature and quantity of food intake, lasting about 1 hour during the attack on the pulse quickens 20-30 1 min, blood pressure decreases by 20-30 mm Hg (2.7-4 kPa). Weight deficit exceeds 10 kg. Patients are not able to work. Treatment is ineffective.

Forecast and workability of dumping syndrome

With a mild degree of severity of the dumping syndrome, the working capacity is not impaired, with an average – reduced, and with a severe one – patients are not able to work.

Acute gastric expansion

Expansion of the stomach is acute – a sudden abrupt increase in the stomach due to the accumulation of fluid and gas in it.

Etiology and pathogenesis of acute expansion of the stomach

The basis of this rare disease is paralysis of the neuromuscular apparatus of the stomach, manifested by atony of the wall of the stomach while maintaining its secretory activity. In the pathogenesis of the disease, a significant role is given to disturbances in the water-electrolyte balance and CBS. The pathology is rare, it can occur in diseases such as myocardial infarction, peritonitis, pneumonia, gastric vascular thrombosis, prolonged pyloric stenosis

Clinic for acute expansion of the stomach

Acute enlargement of the stomach is manifested by signs of obstruction of the stomach. The leading clinical symptoms are abdominal heaviness, nausea, vomiting, heartburn. In some cases, spilled abdominal pain is disturbing.
When examining a patient, a significant, rapidly increasing protrusion in the epigastric region, a wide zone of tympanitis extending beyond the center line to the left, tachycardia, and a drop in cardiac activity are determined. Symptoms quickly increase, there are fears of complications (violation of the blood supply to the stomach wall, rupture of it) due to compression of the heart.

Diagnosis of acute gastric expansion

Along with the clinical manifestations of the disease is extremely important yavdlyaetsya X-ray examination in which reveal the high standing of the left dome of the diaphragm, a sharp increase in volume, with a lot of liquid and gas bubble stomach. When examining a patient in an upright position in the stomach, two horizontal fluid levels can be detected due to an excess of the stomach on the ligamentous apparatus. The radiological symptoms of the absence of peristalsis of the gastric wall with a long delay in the evacuation of barium suspension from the stomach are important.