Gastrointestinal tract disorder UCD 10. Intestinal colic: causes, symptoms, diagnosis and treatment. Functional stomach disorder

In patient medical histories, functional stomach disorder according to ICD 10 is encrypted as a separate nosological unit. There is a single official document for medical institutions, in which all existing diseases are included and classified.

This document is called the International Statistical Classification of Diseases, 10th revision, developed in 2007 by the World Health Organization.

This document is the basis for conducting statistics of morbidity and mortality among the population. Each medical history is coded according to the final diagnosis.

The FDF code according to ICD 10 belongs to class XI - “Diseases of the digestive organs” (K00-K93). This is a fairly extensive section in which each disease is considered separately. ICD 10 code for functional bowel disorder: K31 – “ Other diseases of the stomach and duodenum».

What is FRF

Functional indigestion is the occurrence of pain, digestive disorders, motility, and secretion of gastric juice in the absence of any anatomical changes. This is a kind of exclusion diagnosis. When all research methods do not reveal any organic disorders, and the patient has complaints, this diagnosis is determined. Functional disorders include:

• Functional dyspepsia, which can manifest itself in different ways - heaviness in the stomach, rapid satiety, discomfort, a feeling of fullness, bloating. Nausea, vomiting, aversion to certain types of food, and belching may also occur. In this case, no changes in the gastrointestinal tract are detected.
• Swallowing air(aerophagia), which is then either regurgitated or absorbed into the intestinal tract.
• Functional pylorospasm– the stomach is spasmed, food does not pass into the duodenum and vomiting of the eaten food develops.

For these complaints, an X-ray examination, ultrasound and FEGDS are required - however, no changes or disturbances are observed.

Functional gastrointestinal disorders are treated symptomatically, since the exact cause of the disease is not known. Prescribed diet, enzyme preparations, antispasmodics, adsorbents, gastroprotectors, drugs that reduce stomach acidity and normalize motility. Sedatives are often used.

FUNCTIONAL DYSPEPSIA

ICD-10 codes

K30. Dyspepsia.

K31. Other diseases of the stomach and duodenum, including functional stomach disorders.

Functional dyspepsia is a symptom complex in children over the age of one year, in which there is pain, discomfort or a feeling of fullness in the epigastric region, associated or not associated with food intake or physical activity, as well as early satiety, bloating, nausea, regurgitation, intolerance to fatty foods. food, etc.

Functional dyspepsia in childhood is very common, the true prevalence is not specified.

Etiology and pathogenesis

There are three levels of somatic symptom formation (determined by complaints): organ, nervous, mental (Fig. 3-1). The symptom generator can be located at any level, but the formation of an emotionally charged complaint occurs only at the mental level. Pain that appears outside of organ damage is no different from that resulting from true damage. The causes of functional disorders are associated with a violation of the nervous or humoral regulation of gastrointestinal motility, in which there are no structural changes in the gastrointestinal tract.

Rice. 3-1. Levels of formation of clinical manifestations of functional gastrointestinal disorders

Motility disorders of the digestive organs of any origin inevitably cause secondary changes, the main of which are disturbances in the processes of digestion, absorption and intestinal microbiocenosis.

The listed changes aggravate motor disorders, closing a pathogenetic vicious circle.

Clinical picture

Symptoms of functional disorders are varied, but complaints should be observed over a long period of time - at least once a week for the last 2 months or more. It is also important that symptoms are not related to bowel movements or changes in the frequency and nature of stool.

In children it is difficult to differentiate the variants of functional dyspepsia, so they are not distinguished.

Diagnostics

Due to the fact that the diagnosis of functional dyspepsia is a diagnosis of exclusion with chronic gastrointestinal diseases, a comprehensive examination is required, including a general clinical minimum, exclusion of helminthic-protozoal infestation, biochemical studies, endoscopic examination, functional tests (gastric intubation or pH-metry), etc. .

Differential diagnosis

Differential diagnosis is carried out with organic pathology of the gastroduodenal zone: chronic gastritis, gastroduodenitis, ulcer, as well as with diseases of the biliary system, pancreas, and liver. With these pathologies, characteristic changes in laboratory and instrumental studies are revealed, while with functional dyspepsia there are no changes.

Treatment

Mandatory components of the treatment of functional dyspepsia are the normalization of the vegetative status and psycho-emotional state, and, if necessary, consultation with a neuropsychiatrist or psychologist.

Diagnosis and treatment of functional dyspepsia can be rationally divided into two stages.

At the first stage, the doctor, based on clinical data (including excluding symptoms of anxiety) and a screening study (complete blood count, scatology, fecal occult blood test, ultrasound), with a high degree of probability assumes the functional nature of the disease and prescribes treatment for a period of 2 -4 weeks The lack of effect from the therapy is considered as a

This is an important signal and serves as an indication for examination in a consultation center or gastroenterology department of a hospital (second stage).

Prokinetics are prescribed for dyskinetic disorders. The drug of choice is domperidone, prescribed at a dose of 2.5 mg per 10 kg of body weight 3 times a day for 1-2 months.

Antacids, antisecretory drugs, as well as myotropic antispasmodics are indicated for pain and spastic conditions. Papaverine is prescribed orally (regardless of food intake), 2-3 times a day: children 1-2 years old - 0.5 tablets; 3-4 years - 0.5-1 tablet; 5-6 years - 1 tablet, 7-9 years - 1.5 tablets, over 10 years old and adults - 1-2 tablets, drotaverine (no-spa*, spasmol*) 0.01-0.02 g 1-2 times a day; children over 6 years old - mebeverine (duspatalin*) at a dose of 2.5 mg/kg in 2 doses 20 minutes before meals, children 6-12 years old - 0.02 g 1-2 times a day; for school-age children - pinaveria bromide (dicetel*), a selective blocker of calcium channels in intestinal cells, 50-100 mg 3 times a day.

Forecast

The prognosis for functional disorders is ambiguous. Although the Rome criteria indicate a stable and favorable nature of their course, in practice their evolution into organic pathology is often possible. Functional dyspepsia can transform into chronic gastritis, gastroduodenitis, and ulcers.

CHRONIC GASTRITIS AND GASTRODUODENITIS

ICD-10 code

K29. Gastritis and duodenitis.

Chronic gastritis and gastroduodenitis are polyetiological, steadily progressing chronic inflammatory-dystrophic diseases of the stomach and/or duodenum.

According to official data, their incidence is 100-150 per 1000 children (58-65% in the structure of gastroenterological pathology).

If we take the morphological diagnostic method as a basis, the prevalence of diseases will be 2-5%. HP infection, which occurs in 20-90% of the population (Fig. 3-2), may be associated with chronic gastroduodenitis (CGD). Only a clinical approach to the problem of CGD, without examination, leads to overdiagnosis of HP disease. In Russia, compared to Western European countries, there are 3-6 times more infected children, which corresponds to the level of infection in underdeveloped countries.

Rice. 3-2. Prevalence H. pylori in the world

Etiology and pathogenesis

According to the Sydney classification (1996), gastritis is divided into types and their corresponding formation mechanisms (Fig. 3-3). Burdened heredity is realized when the body is exposed to unfavorable exogenous and endogenous factors.

Rice. 3-3. Variants of chronic gastritis and their features

Exogenous factors risk of developing CGD:

Nutritional: dry food, abuse of spicy and fried foods, deficiency of protein and vitamins in the diet, violation of diet, etc.;

Psycho-emotional: stress, depression;

Environmental: the state of the atmosphere, the presence of nitrates in food, poor quality of drinking water;

Taking certain medications: nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, antibiotics, etc.;

Food allergies;

Unsatisfactory condition of the dental system;

Bad habits;

Hormonal dysfunctions. Endogenous factors risk of developing CGD:

HP infection;

Reflux of bile into the stomach;

Endocrine disorders.

Infection HP occurs in childhood; if left untreated, the bacteria persist in the body indefinitely, causing gastrointestinal diseases.

Source of infection: infected person, animal (cats, dogs, rabbits). Routes of spread: alimentary (with contaminated food), water (HP can be in cold water for several days) and contact (dirty hands, medical instruments, kiss). Mechanisms of infection: fecal-oral and oral-oral (for example, through a kiss). HP sown from feces, water, dental plaque.

The pathogenesis of HP infection is presented in the section “Peptic ulcer”.

Classification

The classification of chronic gastritis and duodenitis is presented in table. 3-1.

Table 3-1. Classification of chronic gastritis and gastroduodenitis (Baranov A.A., Shilyaeva R.R., Koganov B.S., 2005)

Clinical picture

Clinical manifestations of CGD are varied and depend on the nature of the violations of the secretory and evacuation functions of the stomach, the age and characterological characteristics of the child. Clinical features of chronic gastritis in the period of exacerbation are associated with the state of hydrochloric acid secretion.

Syndromes characteristic of increased (or normal) secretion of hydrochloric acid (more often with type B gastritis)

Pain syndrome: intense and prolonged, associated with food intake. Early pain is characteristic of fundal gastritis, late pain is characteristic of antral gastritis, pain at night is characteristic of duodenitis. There is no clear connection with the time of year or dietary disorders. In older children, palpation shows moderate pain in the epigastrium and pyloroduodenal area.

Dyspeptic syndrome: sour belching, air belching, heartburn, tendency to constipation.

Syndromes of nonspecific intoxication And asthenia variable: autonomic instability, irritability, rapid exhaustion during mental and physical stress, sometimes low-grade fever.

Syndromes with reduced secretion of hydrochloric acid (more often with gastritis type A)

Pain syndrome mild, characterized by dull diffuse pain in the epigastrium. After eating, there is a feeling of heaviness and fullness in the upper abdomen; pain occurs and intensifies depending on the quality and volume of food. Palpation reveals slight diffuse pain in the epigastrium.

Dyspeptic syndrome prevails over pain: belching food, nausea, a feeling of bitterness in the mouth, decreased appetite, flatulence, unstable stool. There may be a decrease in appetite, an aversion to certain foods (porridge, dairy products, etc.).

Nonspecific intoxication syndrome expressed, asthenia predominates. Patients are pale, their body weight is reduced due to a violation of the gastric stage of food digestion and secondary disorders of the pancreas; in severe cases, manifestations of hypopolyvitaminosis and anemia are noted.

With reflux gastritis (usually with type C gastritis) due to the constant reflux of gastric and duodenal contents (gastroesophageal and duodenogastric reflux), the symptoms of upper (gastric) dyspepsia are mainly characteristic: heartburn, sour belching, belching with air, a feeling of bitterness in the mouth, loss of appetite.

Features of clinical manifestations of DR infection:

There is no seasonal nature of exacerbations;

There is no periodicity in the course of the disease (symptoms of gastritis are observed almost constantly);

Often nausea, vomiting and other manifestations of dyspeptic syndrome;

There may be signs of infection: low-grade fever, mild intoxication, moderate leukocytosis in the blood, increased ESR;

Bad breath (halitosis).

Diagnostics

Signs of gastritis or gastroduodenitis during esophagoduodenoscopy:

Hypersecretion of gastric contents;

Mucus, often an admixture of bile;

Mainly hyperemia and swelling of the mucous membrane of the stomach and/or duodenum;

Swelling and thickening of folds, follicular hyperplasia (Fig. 3-4, a), sometimes erosion (Fig. 3-4, b);

Pale, dull, thinned mucous membrane of the stomach and/or duodenum, unevenly smoothed folds, sometimes mosaic of the mucous membrane (Fig. 3-4, c).

Rice. 3-4. Endoscopic picture: a - exudative gastritis with follicular hyperplasia of the mucous membrane; b - erosive gastritis; c - exudative duodenitis

Endoscopic signs are more common HP-associated gastritis:

Multiple ulcers and erosions in the duodenal bulb;

Cloudy gastric secretion;

Lymphoid hyperplasia, hyperplasia of epithelial cells, the mucous membrane has the appearance of a cobblestone pavement (see Fig. 3-4, a).

Intragastric pH-metry allows you to assess the pH in the body and antrum of the stomach. The normal pH of the body of the stomach on an empty stomach in children over 5 years of age is 1.7-2.5, after administration of a stimulant (histamine) - 1.5-2.5. The antrum of the stomach, which neutralizes acid, normally has a pH of more than 5, i.e. The difference between the pH of the body and the antrum is normally above 2 units. A decrease in this difference indicates a decrease in neutral

tralizing ability of the antrum and possible acidification of the duodenum.

Gastric intubation allows you to evaluate secretory, evacuation, and acid-producing functions. In children, increased or preserved acid-producing function is more often detected. At HP-infections in children do not have hypochlorhydria, acid production is always increased. In adolescents, with subatrophy of the mucous membrane, acidity often decreases. The presence or absence of subatrophy and atrophy, the degree of atrophy can only be assessed histologically.

Diagnostics HP-infection is mandatory to clarify the type of gastroduodenitis and subsequent treatment (see Chapter 1).

Pathomorphology

The most complete picture of gastric damage is provided by a comprehensive study of biopsy specimens of the antrum, fundus (body) sections and the angle of the stomach (Fig. 3-5).

Before getting acquainted with the histomorphological changes in the gastric mucosa, let us recall the features of its cellular structure (Fig. 3-5, a). The main glands have 5 types of cells: integumentary epithelium, main, lining (parietal), mucous (goblet). The chief cells produce pepsin, the parietal cells produce hydrochloric acid ingredients, and the goblet and integumentary cells produce mucoid secretions. In the antrum, the pyloric glands produce an alkaline secretion. The antrum plays a role in the humoral and neuro-reflex regulation of gastric secretion. At the bottom of the crypts of the duodenum and small intestine there are Paneth cells, which provide antibacterial protection to the gastrointestinal tract. The main protective molecules produced by Paneth cells are α-defensins, lysozyme, phospholipase A2, and cationic peptides.

Histologically they are characterized by: active diffuse gastritis, superficial gastritis with damage to the glands without atrophy, with subatrophy or atrophy, in which a gradual change in cellular composition is observed (see Fig. 3-5, a). For HP-infection is characterized by restructuring of the epithelium (metaplasia) of the pyloric or intestinal type, which is more often detected in atrophic gastritis.

Rice. 3-5. Changes in chronic gastritis: a - norm and changes in chronic gastritis: diagram of the cellular and histological structure of the gastric mucosa (staining with hematoxylineosin. χ 50; b - sections and parts of the stomach

Differential diagnosis

The disease is differentiated from functional dyspepsia, ulcers, diseases of the biliary system, pancreas, and liver.

Treatment

Drug therapy is carried out in accordance with the type of gastritis.

Considering that the predominant number of cases of type B gastritis is caused by HP, the basis of treatment, especially of erosive gastritis and/or duodenitis, is eradication HP(anti-Helicobacter therapy is presented in the section “Peptic ulcer”). It is carried out only if it is detected HP one invasive or two non-invasive research methods. It is advisable to treat all family members.

For increased gastric secretion, antacids are prescribed: algeldrat + magnesium hydroxide (Maalox*, Almagel*), aluminum phosphate (phosphalugel*), Gastal*, gastrofarm* in suspension, tablets.

Maalox* is prescribed orally for children from 4 to 12 months, 7.5 ml (1/2 tsp), over one year old - 5 ml (1 tsp) 3 times a day, for adolescents - 5-10 ml (suspension, gel) or 2-3 tablets 0.5-1 hour before meals and at night. After achieving a therapeutic effect, maintenance therapy is carried out with 5 ml or 1 tablet 3 times a day for 2-3 months. The suspension or gel must be homogenized before use by shaking the bottle or thoroughly kneading the bag with your fingers.

Almagel* in suspension is used for children under 10 years old at a dose of 1/3, 10-15 years old - 1/2, over 15 years old - 1 measuring spoon 3-4 times a day 1 hour before meals and at night.

Phosphalugel* is prescribed orally; it can be diluted in 1/2 glass of water before use. Children under 6 months - 4 g (1/4 sachet), or 1 tsp, after each of 6 feedings; over 6 months - 8 g (1/2 sachet), or 2 tsp. - after each of 4 feedings. In older children, the recommended dose is 1-2 sachets of gel 2-3 times a day.

In case of severe hyperacidity, an antisecretory agent is used, M 1 -anticholinergic pirenzepine (gastrocepin*) in 25 mg tablets, children from 4 to 7 years old - 1/2 tablet, 8-15 years old - in the first 2-3 days, 50 mg 2 -3 times a day 30 minutes before meals, then 50 mg 2 times a day. The course of treatment is 4-6 weeks. The maximum daily dose is 200 mg. Histamine H2 receptor blockers (famotidine, ranitidine) can be prescribed to children over 10 years of age for a period of 2 weeks at a dose of 0.02-0.04 g per night.

For erosive gastritis caused by NSAIDs, gastroprotectors are used.

Film-forming drugs are also used, for example sucralfate (Venter *), in the form of an oral gel and 1 g tablets, which, without chewing, are washed down with a small amount of water. Children - 0.5 g 4 times a day, adolescents - 0.5-1 g 4 times a day or 1-2 g in the morning and evening 30-60 minutes before meals. The maximum daily dose is 8-12 g; course of treatment - 4-6 weeks, if necessary - up to 12 weeks.

Prostaglandins - misoprostol (Cytotec *) are used for adolescents (preferably over 18 years of age) orally, during meals, 400-800 mcg/day in 2-4 divided doses.

A sedative herbal preparation of hawthorn fruits + extract of black elderberry flowers + valerian rhizomes with roots (Novo-Passit*) is indicated for children from 12 years of age. Valerian medicinal rhizomes with roots are prescribed orally as an infusion 30 minutes after meals: for children from 1 to 3 years old - 1/2 tsp. 2 times a day, 3-6 years - 1 tsp. 2-3 times a day, 7-12 years old - 1 dessert spoon 2-3 times a day, over 12 years old - 1 tbsp. l. 2-3 times a day. It is recommended to shake the infusion before use. Valerian extract * in tablets for children over 3 years old is prescribed 1-2 tablets orally 3 times a day.

Anticholinergics and antacids are not prescribed for type A gastritis.

In the presence of pain and dyspeptic syndromes, a good effect is achieved with oral administration or intramuscular injections of metoclopramide, sulpiride, no-shpa*, butylscopolamine bromide (buscopan*), drotaverine. Enveloping and astringent herbal remedies are widely recommended: infusion of plantain leaves, yarrow, chamomile, mint, St. John's wort before meals for 2-4 weeks.

In order to stimulate the secretory function of the stomach, you can use a medicinal herbal preparation - extract of plantain leaves (plantaglucide*). Planta glucid * in granules for the preparation of a suspension for oral administration is prescribed to children under 6 years old - 0.25 g (1/4 tsp), 6-12 years old - 0.5 g (1/2 tsp. ), over 12 years old - 1 g (1 tsp) 2-3 times a day 20-30 minutes before meals. The duration of treatment is 3-4 weeks. To prevent relapses, the drug is used in the above doses 1-2 times a day for 1-2 months.

Pepsin, betaine + pepsin (acidin-pepsin tablets*) and other drugs are used for replacement purposes. Acidin-pepsin tablets* are prescribed orally, 0.25 g, during or after meals, pre-dissolved in 50-100 ml of water, 3-4 times a day. The course of treatment is 2-4 weeks.

To improve the trophism of the gastric mucosa, agents are used that enhance microcirculation, protein synthesis and reparative processes: nicotinic acid preparations, vitamins B and C orally and by injection, dioxomethyltetrahydropyrimidine (methyluracil *), solcoseryl *. Methyluracil* in 500 mg tablets is prescribed:

children from 3 to 8 years old - 250 mg, over 8 years old - 250-500 mg 3 times a day during or after meals. The course of treatment is 10-14 days.

In the treatment of type C gastritis (reflux gastritis), which occurs with motility disorders, the prokinetic drug domperidone (Motilium*, Motilak*, Motinorm*, Domet*) is used orally 15-20 minutes before meals, for children under 5 years of age - in suspension for administration orally 2.5 mg/10 kg body weight 3 times a day and, if necessary, additionally before bedtime.

For severe nausea and vomiting - 5 mg/10 kg body weight 3-4 times a day and before bedtime; if necessary, the dose can be doubled. For children over 5 years of age and adolescents, domperidone is prescribed in tablets of 10 mg 3-4 times a day and additionally before bedtime, with severe nausea and vomiting - 20 mg 3-4 times a day and before bedtime.

Prokinetics (coordinax *, peristil *) are prescribed to older children at 0.5 mg/kg in 3 divided doses 30 minutes before meals, the course of treatment is 3-4 weeks.

Physiotherapeutic treatment in the acute period: electrophoresis of platiphylline - on the epigastric region, bromine - on the collar area, in the subremission phase - ultrasound, laser therapy.

Prevention

Dispensary observation is carried out according to accounting group III, the frequency of examinations by a pediatrician is at least 2 times a year, by a gastroenterologist - 1 time a year. Esophagogastroduodenoscopy is performed once a year for pain syndrome.

the appointment of massage, acupuncture, physical therapy. Sanatorium-resort treatment is desirable.

A child with CGD is subject to removal from the dispensary register subject to 5 years of clinical and endoscopic remission.

Forecast

The prognosis is favorable, but CGD occurring after infection HP, accompanied by increased acid production, which can lead to erosive

gastritis and duodenal ulcer. Over time, in the absence of treatment, atrophy of the mucous membrane and a decrease in acid production occur, leading to metaplasia and dysplasia, i.e. precancerous conditions.

ULCER DISEASE

ICD-10 codes

K25. Stomach ulcer.

K26. Duodenal ulcer.

A chronic relapsing disease occurring with alternating periods of exacerbation and remission, the main symptom of which is the formation of an ulcer in the wall of the stomach and/or duodenum.

Prevalence

The incidence of ulcer is 1.6±0.1 per 1000 children, 7-10% among the adult population. In schoolchildren, PU occurs 7 times more often than in preschoolers, in children living in the city - 2 times more often than in rural areas. In 81% of cases, the location of the ulcerative defect is the duodenum, in 13% - the stomach, in 6% there is a combined localization. In girls, ulcer is observed more often (53%) than in boys, but the combination of gastric and duodenal ulcer is 1.4 times more common in boys. Complications of ulcers were observed in children of all age groups with the same frequency.

Etiology and pathogenesis

PU is a polyetiological disease. The following are involved in its formation and chronicization:

Microorganisms (infection with HP);

Neuropsychic factors (stress in children is the leading factor in PU: emotional stress, negative emotions, conflict situations, etc.);

Hereditary-constitutional (increased mass of parietal cells, increased release of gastrin in response to food intake, deficiency of trypsin inhibitor, blood group I, etc. - about 30% of patients);

Medicinal and toxic effects;

Endocrine disorders;

Violations of the regime, eating habits, etc.

The pathogenesis of ulcer is based on imbalances between the factors of aggression and defense (Fig. 3-6).

Rice. 3-6.“Scales” Neck with peptic ulcer (according to Saluper V.P., 1976)

In PU, the ratio of antral G- and D-cells changes towards an increase in G-cells, which is reliably associated with hypergastrinemia, and hypergastrinemia with hyperacidity. Hyperplasia of gastrin cells may be an initial feature of the endocrine apparatus of the gastrointestinal tract, often genetically determined.

Microorganisms - urease-producing HP, discovered in 1983 by Australian scientists - play a role in enhancing the aggressive properties of gastric contents and weakening the protective properties of the mucous membrane of the stomach and duodenum. V. Marshall And /. Warren(Fig. 3-7). They are detected in approximately 90% of patients with duodenal ulcer and in 70% with gastric ulcer. But HP is not an obligatory pathogenetic factor of duodenal ulcer in children, especially under the age of 10 years.

Rice. 3-7. Factors influencing virulence HPTable 3-2. Classification of BU (Mazurin A.V., 1984)

Clinical picture

PU is diverse, the typical picture is not always observed, which greatly complicates diagnosis.

Features of the course of ulcer in children at present:

Leveling the seasonality of exacerbations;

Asymptomatic in 50% of patients;

Obliterated clinical manifestations in some patients with rapid development of complications of duodenal ulcer in the form of bleeding or perforation.

The leading complaint is pain. It is localized in the epigastric, peri-umbilical areas, sometimes spread throughout the abdomen. In a typical case, the pain becomes constant, intense, takes on a nocturnal and “hungry” character, and decreases with food intake. A Moynihan rhythm of pain appears (hunger - pain - food intake - light interval - hunger - pain, etc.). Dyspeptic disorders: heartburn, belching, vomiting, nausea - with increased

as the duration of the disease increases. Appetite is reduced in 1/5 of patients, and physical development may be delayed. There is a tendency to constipation or unstable stool. Asthenic syndrome is manifested by emotional lability, sleep disturbance due to pain, and increased fatigue. Hyperhidrosis of the palms and feet, arterial hypotension, red dermographism, and sometimes bradycardia may be observed.

During a physical examination, a coated tongue is determined, upon palpation - pain in the pyloroduodenal zone, epigastrium, sometimes in the right hypochondrium, a positive Mendelian sign (pain when percussed with bent fingers of the right hand in the area of ​​the greater and lesser curvature of the stomach).

The main thing in diagnosing the disease is endoscopic examination due to the asymptomatic onset and often manifestation with complications (Fig. 3-8, a).

Among the complications recorded:

Bleeding (vomiting with blood, melena (black stool), weakness, dizziness, tachycardia, hypotension) (Fig. 3-8, b);

Perforation (rupture of an ulcer into the abdominal cavity), which occurs acutely and is accompanied by sharp pain in the epigastric region, tension in the anterior abdominal wall and symptoms of peritoneal irritation;

Penetration (penetration of an ulcer into other organs) - persistent pain syndrome, sharp pain radiating to the back, vomiting that does not bring relief;

Pyloric stenosis, resulting from the formation of scars at the site of “kissing” ulcers on the anterior and posterior walls of the duodenum (Fig. 3-8, c);

Perivisceritis (adhesive process), developing with ulcer between the stomach or duodenum and neighboring organs (pancreas, liver, gallbladder)

Rice. 3-8. Diagnosis of duodenal ulcer: a - esophagogastroduodenoscopy technique; b - gastric bleeding from a peptic ulcer; c - stenosis of the duodenal bulb

rem). Characterized by intense pain, intensifying after a heavy meal, during physical exertion and shaking the body. Among the complicated forms of ulcer, bleeding predominates (80%), stenosis (10%), perforation (8%) and ulcer penetration (1.5%) are observed less frequently; perivisceritis (0.5%) and malignancy are extremely rare.

Diagnostics

The most optimal diagnostic method is esophagogastroduodenoscopy (Table 3-3), which is used to perform a targeted biopsy of the mucous membrane of the stomach and duodenum to clarify the nature and severity of pathomorphological changes.

Table 3-3. Results of esophagogastroduodenoscopy for ulcerative disease

Endoscopic examination reveals 4 stages of the ulcerative process (see Table 3-2). During therapy, the transition from stage I to stage II is observed after 10-14 days, from stage II to III - after 2-3 weeks, from stage III to IV - after 30 days. Complete regression of concomitant inflammatory changes in the mucous membrane of the gastroduodenal zone occurs after 2-3 months.

X-ray of the stomach and duodenum with barium is justified only if congenital malformations of the gastrointestinal tract are suspected or it is technically impossible to perform esophagogastroduodenoscopy (Fig. 3-9, a).

Diagnosis of HP infection is performed using invasive and non-invasive methods, with the gold standard being detection HP in a biopsy of the mucous membrane of the stomach and/or duodenum (see Chapter 1).

The state of the secretory function of the stomach is assessed by pH-metry or gastric intubation.

Pathomorphology

Macroscopically, 1-3 ulcerative defects with fibrinous plaque and roller-shaped edges are detected (Fig. 3-9, b). Around the defects, the mucous membrane is hyperemic, with pinpoint hemorrhages. Microscopically, necrosis with fibrinous deposits is visible at the bottom of the ulcerative defect, around which there is an accumulation of leukocytes and congestion of the vessels. A deep ulcerative defect of the mucous membrane (almost to the muscular plate) with purulent-necrotic changes in the walls and bottom is shown in Fig. 3-9, c.

Rice. 3-9. a - radiography: a symptom of a niche with an ulcerative defect in the stomach; b - macroscopic specimen of the mucous membrane of the duodenum (arrows indicate defects); c - microscopic picture of an ulcerative defect in the duodenal wall (staining with hematoxylineosin, χ 100)

Differential diagnosis

Differential diagnosis is carried out with acute ulcers developing against the background of acute stress, burns (Curling's ulcer), trauma (Cushing's ulcer), infections (cytomegalovirus, herpes, etc.) or taking medications (NSAIDs, etc.).

Treatment

Treatment is carried out according to a staged principle. Treatment goals:

Relief of inflammation, healing of ulcers, achieving stable remission;

Eradication of HP infection;

Prevention of relapse, prevention of exacerbations and complications.

In case of exacerbation, hospitalization in the gastroenterology department is required. (first stage of treatment). Bed rest is prescribed for 2-3 weeks.

Among medications, antacids are prescribed for young children. Algeldrat + magnesium hydroxide (maalox*) is used orally, for children from 4 to 12 months - 7.5 ml (1/2 tsp), over 1 year - 15 ml (1 tsp) 3 times a day day, for adolescents - 5-10 ml (suspension, gel), or 2-3 tablets 30 minutes before meals and at night, if necessary, the RD is increased to 15 ml, or 3-4 tablets.

IPN. Omeprazole (Losec*, Omez*) is prescribed from 12 years of age, 1 capsule (20 mg) once a day on an empty stomach. The course of treatment for duodenal ulcer is 2-3 weeks, if necessary, maintenance treatment is carried out for another 2-3 weeks; for gastric ulcer - 4-8 weeks. Lansoprazole (Helicol*, Lanzap*) - 30 mg/day in one dose in the morning for 2-4 weeks, if necessary - up to 60 mg/day. Pantoprazole (Panum*, Peptazole*) is prescribed orally, without chewing, with liquid, 40-80 mg/day, the course of treatment for scarring of duodenal ulcer is 2 weeks, gastric ulcer and reflux esophagitis is 4-8 weeks. Rabeprazole (Pariet*) is prescribed from 12 years of age, 20 mg orally once a day in the morning. The course of treatment is 4-6 weeks, if necessary - up to 12 weeks. The capsules are swallowed whole without chewing.

H2-histamine receptor blockers. Famotidine (gastrosidine*, quamatel*, famosan*) is prescribed orally at 0.5 mg/kg per day before bedtime or 0.025 mg 2 times a day. For children weighing less than 10 kg orally, 1-2 mg/kg per day, divided into 3 doses; for children weighing more than 10 kg - orally at a dose of 1-2 mg/kg per day, divided into 2 doses.

The film-forming gastroprotector sucralfate (Venter*) is prescribed in the form of an oral gel and tablets 1 hour before meals and before bedtime. Children are prescribed 0.5 g 4 times a day, adolescents - 0.5-1 g 4 times a day, or 1 g in the morning and evening, or 2 g 2 times a day (after waking up in the morning and before bedtime). empty stomach); maximum DM - 8-12 g. Course of treatment - 4-6 weeks, if necessary - up to 12 weeks.

When HP infection is confirmed, HP eradication is carried out with bismuth or omese-containing 1st and 2nd line regimens in combination with one or two antibacterial drugs. Success is achieved in 70-90% of patients, however, complications, side effects (Table 3-4) and resistance (resistance) to PPIs, antibiotics (in particular, metronidazole) and other drugs affect the success of therapy.

Table 3-4. Side effects of eradication therapy

First line treatment options (triple)

Based on bismuth preparations:

Bismuth subcitrate (de-nol*) 8 mg/kg (up to 480 mg/day) + amoxicillin (flemoxin*, hiconcil*) 25 mg/kg (up to 1 g/day) or clarithromycin (fromilid*, clacid*) 7.5 mg/kg (up to 500 mg/day) + nifuratel (Macmiror*) 15 mg/kg or furazolidone 20 mg/kg;

Bismuth subcitrate + clarithromycin + amoxicillin.

Based on IPN:

PPI + clarithromycin or (in children over 8 years old) tetracycline 1 g/day + nifuratel or furazolidone;

PPI + clarithromycin or (in children over 8 years old) tetracycline + amoxicillin.

The combination of amoxicillin (flemoxin solutab*) + bismuth preparation (bismuth subcitrate) + PPI has a local bactericidal effect in combination with enveloping, cytoprotective, antibacterial and antisecretory effects, which makes it possible to avoid the use of a second antibacterial agent in the eradication therapy regimen for children with ulcerative disease.

Second line therapy(quad therapy) is recommended for eradication of strains HP, resistant to antibiotics, with unsuccessful previous treatment. More often, bismuth subcitrate + amoxicillin or clarithromycin is prescribed; in children over 8 years old - tetracycline + nifuratel or furazolidone + PPI.

The inclusion of probiotics containing lactobacilli, which are HP antagonists, in the treatment regimen can reduce the incidence of side effects and improve the tolerability of anti-Helicobacter therapy.

Drug therapy includes vitamins (C, U, group B), sedatives, antispastic drugs (papaverine, no-spa*), cholinergic receptor blockers. General methods of physiotherapy are indicated during all periods of the disease; local procedures are used starting from stage II of the ulcer, thermal procedures (paraffin, ozokerite) - only during the healing period of the ulcer. In the treatment of the acute stage of ulcer while taking medications, physical methods play a purely auxiliary role, but during the period of clinical and endoscopic remission they become leading.

Along with psychopharmacotherapy (tranquilizers, antidepressants, herbal remedies), in most cases psychotherapy (family and individual) is indicated, the tasks of which include relieving affective tension and eliminating stress.

The clinical and economic effectiveness of new approaches to the diagnosis and treatment of ulcers and CGD (Fig. 3-10) in general can lead to the following results:

Reducing the number of relapses of the disease from 2-3 times a year to 0;

Reducing the number of complications of ulcerative disease by 10 times;

Refusal of surgical treatment of ulcer;

Treatment of more than 80% of patients is carried out on an outpatient basis.

Rice. 3-10. Evolution of therapy for chronic diseases of the upper digestive system

Treatment for complications of ulcer carried out inpatiently, in surgical departments. Absolute indications for surgical intervention are perforation (perforation - a breakthrough of an ulcer into the free abdominal cavity with the contents of the stomach or duodenum entering it), penetration of an ulcer (germination of a stomach or duodenal ulcer into surrounding organs or tissues), profuse bleeding, decompensated scar-ulcerative pyloric stenosis , malignancy of ulcer.

At gastrointestinal bleeding the strictest observance of three principles is necessary: ​​cold, hunger and rest. The child must be transported only on a stretcher. A rubber balloon with ice is placed on the stomach area, local hemostatic therapy is carried out, for which the stomach is washed with ice solutions. Emergency esophagogastroduodenoscopy is indicated to determine the location of the source of bleeding and perform endoscopic hemostasis.

Infusion-transfusion replacement therapy (transfusion of blood products and blood substitutes) is necessary. Along with the above measures, during the first 2-3 days, omeprazole 20-40 mg is administered intravenously every 8 hours or ranitidine 25-50 mg or famotidine 10-20 mg is administered every 6 hours. In the presence of hemorrhagic erosions, sucralfate is additionally used at a dose of 1-2 g orally every 4 hours. After successful resuscitation and hemostatic courses, a standard eradication course is prescribed and the use of a Na+, K+-ATPase blocker or a H2-histamine receptor blocker is always prolonged for at least 6 months Only if there is no effect, surgical treatment is indicated.

Relative indications Recurrent bleeding, subcompensated pyloric stenosis, and ineffectiveness of conservative treatment indicate surgical intervention. In case of perforation or penetration of a stomach and/or duodenal ulcer with symptoms of peritonitis, profuse bleeding, surgical intervention is performed according to emergency indications, in other cases it is carried out as planned.

Prevention

Primary prevention includes organizing proper nutrition and regimen, creating a favorable environment in the family, refusing to take ulcerogenic medications, and fighting bad habits. Overloading with audiovisual information is unacceptable. It is necessary to actively identify individuals who have an increased risk of developing ulcers (hereditary predisposition,

functional hypersecretion of hydrochloric acid, CGD with increased acid formation), and the appointment of esophagogastroduodenoscopy.

Secondary prevention PUD - continuation of rehabilitation therapy.

Second stage of rehabilitation- sanatorium-resort, carried out no earlier than 3 months after discharge from the hospital if it is not possible in an outpatient setting. If the urease test result is positive for HP infection, second-line eradication therapy is indicated.

Third stage of rehabilitation- dispensary observation in a clinic with a gastroenterologist for a period of 5 years or more. Its goal is to prevent exacerbation of the disease. Anti-relapse treatment is carried out 2-3 times a year during school holidays. A protective regime is prescribed, dietary table No. 1 for 3-5 days, then table No. 5, vitamin and antacid preparations, and, if necessary, physiotherapeutic treatment: galvanization and medicinal electrophoresis of various microelements with a transverse arrangement of electrodes - copper sulfate, zinc sulfate, aloe solution , bromine electrophoresis on the collar area. To resolve scar changes in the stomach and duodenum, electrophoresis of solutions of lidase or terrilitin is used. The therapeutic use of hyperbaric oxygenation (8-10 sessions) to improve local microcirculation and oxygenation of damaged tissues is pathogenetically justified. To correct concomitant psychosomatic and autonomic disorders, low-frequency currents are used using the electrosleep technique.

In some cases, sinusoidal modulated currents, an ultra-high frequency electromagnetic field in the decimeter range, and ultrasound are prescribed to the upper abdomen and paravertebral area. Mildly influencing factors include an alternating magnetic field.

Esophagogastroduodenoscopy is performed at least once a year; it is recommended for complaints, positive results of a fecal occult blood reaction or a urease breath test.

If necessary, patients are limited to school workload - 1-2 days a week (schooling at home), exempted

exempt from exams, assigned a special health group (restrictions on physical education).

Forecast

The prognosis is serious, especially if the child has multiple ulcerative defects of the mucous membrane or the ulcer(s) is located behind the duodenal bulb. In such cases, the disease is more severe and complications are often observed. Children who have undergone surgery are given a disability status. Clinical observation of the patient by a pediatric gastroenterologist, compliance with the rules of seasonal and maintenance prevention of exacerbations significantly improves the prognosis of the disease.

PYLOROSPASM AND PYLOROSTENOSIS

In early childhood, a functional disorder of the motor function of the stomach with a spastic increase in the tone of its outlet part, as well as a congenital organic narrowing of the pyloric part of the stomach are problems that require special attention of a pediatrician in terms of differential diagnosis and the choice of a conservative or surgical method of treatment.

Pylorospasm

ICD-10 code

K22.4. Esophageal dyskinesia: spasm of the esophagus.

Pylorospasm is a disorder of the motor function of the stomach, accompanied by a spastic increase in the tone of its outlet part, observed mainly in infants.

Etiology and pathogenesis

The pyloric section of the stomach is the narrowest part of this organ, which corresponds to the border between the stomach and duodenum. The name comes from the word pylorus- "gatekeeper". In the pyloric region of the stomach there is a massive muscle layer (contractor muscle), which is relatively well developed at birth. If its tone is disturbed as a result of functional disorders of the neuromuscular system, the evacuation of food from the stomach into the duodenum becomes difficult, it is retained in the stomach, and vomiting occurs. Violation of the regulatory function of the central nervous system and its autonomic department is more often observed in children with birth trauma and after intrauterine hypoxia, therefore the disease is regarded as a reflection of dysfunction of the autonomic nervous system.

Clinical picture

From the first days of life, with pylorospasm, regurgitation is observed; as the volume of food increases, delayed vomiting of curdled acidic contents without bile appears, not exceeding the volume of food eaten. The child, despite vomiting, gains body weight, although not enough, and if treatment is not started in a timely manner, malnutrition may develop.

Classification

There are atonic and spastic forms of pylorospasm. In the atonic form, the contents of the stomach slowly and gradually flow out of the mouth. With spasticity, it is released intermittently, in sharp jerks in the form of vomiting.

Diagnostics

Radiologically, the pathology is not determined, but after 2 hours there is a delay in the evacuation of the contrast mass. At

An endoscopic examination reveals a closed pylorus in the form of a slit, through which one can always pass with an endoscope, which allows one to exclude organic causes of pyloroduodenal obstruction.

Differential diagnosis

The disease is observed very often, it must be differentiated from a fairly common malformation - pyloric stenosis (Table 3-5).

Table 3-5. Differential diagnosis of pyloric stenosis and pylorospasm

Treatment

It is necessary to maintain a sleep-wake schedule, as well as hold the child 5-10 minutes after feeding in an upright position for several minutes, after which he is placed on his side to prevent vomit or milk from entering the trachea in case regurgitation occurs.

Among medications, 0.5-1.0 ml of a 2% solution of papaverine hydrochloride or a 2% solution of no-shpa*, diluted in 10-15 ml of boiled water, is used orally. From 3 months - promethazine 2.5% solution, 1-2 drops 15 minutes before feeding. In severe cases, children, depending on age, can use drugs that reduce the gag reflex: 0.1% atropine sulfate solution - 0.25-1.0 mg subcutaneously, intramuscularly or intravenously 1-2 times a day . The maximum RD is 1 mg, the daily dose is 3 mg. You can recommend vitamin B 1, suppositories with papaverine.

Physiotherapy: electrophoresis of papaverine hydrochloride, drotaverine on the epigastric area No. 5-10; paraffin applications on the abdominal area No. 5-6 every other day.

Forecast

The prognosis is favorable; by 3-4 months of life, pylorospasm symptoms usually disappear.

Pyloric stenosis

ICD-10 codes

Q40.0. Pediatric pyloric stenosis.

K31.8. Other specified diseases of the stomach and duodenum: narrowing of the stomach in the form of an hourglass.

Pyloric stenosis is a congenital malformation of the pyloric part of the stomach (Fig. 3-11, a), degeneration of the muscular layer of the pylorus, its thickening associated with impaired innervation, as a result of which the pylorus takes on the appearance of a white tumor-like formation resembling cartilage. In adolescents and adults, pyloric stenosis is considered as a complication of gastric ulcer or tumor of this section.

The incidence is 1 in 300 infants aged 4 days to 4 months. In boys, compared to girls, the defect occurs 4 times more often.

Etiology and pathogenesis

The main etiopathogenetic factors in children come down to the following reasons:

Disturbance of innervation, underdevelopment of the pyloric ganglion;

Intrauterine delay in the opening of the pyloric canal;

Hypertrophy and swelling of the muscles of the pyloric part of the stomach (see Fig. 3-11, a).

The severity and time of onset of symptoms of pyloric stenosis depend on the degree of narrowing and length of the pylorus, the compensatory capabilities of the child’s stomach.

In adults, pyloric stenosis is often a consequence of gross scarring due to ulcerative disease or malignant neoplasm.

Classification

There are acute and protracted forms of congenital pyloric stenosis, stages of compensation, subcompensation and decompensation.

Clinical picture

Usually there is a gradual increase in symptoms. Signs of the defect appear in the first days after birth, but more often in the 2-4th week of life. The skin becomes dry, facial features become sharper, a hungry expression appears, and the child looks older than his age.

The first and main symptom of pyloric stenosis is fountain vomiting, which occurs between feedings, is rare at first, then becomes more frequent. The volume of vomit, consisting of curdled milk with a sour odor, without admixture of bile, exceeds the dose of a single feeding. The child becomes restless, malnutrition and dehydration develop, urination becomes rare, and a tendency to constipation appears.

When examining the abdomen in the epigastric region, swelling and increased segmentation visible to the eye are determined.

current gastric peristalsis is a symptom of an hourglass (Fig. 3-11, b). In 50-85% of cases, under the edge of the liver, at the outer edge of the rectus muscle, it is possible to palpate the pylorus, which has the appearance of a dense, plum-shaped tumor, moving from top to bottom.

In later stages, dehydration and impaired water-salt metabolism develop. Due to the loss of chlorine and potassium through vomiting, their level in the blood decreases, metabolic alkalosis and other severe water-electrolyte and metabolic disorders develop. Possible aspiration syndrome. Late manifestations include deficiency anemia and increased hematocrit as a result of blood thickening.

Diagnostics

To confirm the diagnosis of pyloric stenosis, ultrasound is used, which reveals a long pylorus with thickened walls. Diagnostic errors can be 5-10%.

An X-ray contrast study of the stomach reveals an increase in its size and the presence of a fluid level when examined on an empty stomach, a delay in the evacuation of barium suspension (Fig. 3-11, c), narrowing and lengthening of the pyloric canal (beak symptom).

One of the most informative methods for diagnosing pyloric stenosis is esophagogastroduodenoscopy. With pyloric stenosis, endoscopy reveals pinpoint

Rice. 3-11. Pyloric stenosis: a - schematic representation of the place of transition of the stomach into the duodenum; b - visible enlargement of the pylorus and peristalsis in the form of an hourglass; c - X-ray examination: retention of contrast agent in the stomach

an opening in the pylorus, convergence of the folds of the mucous membrane of the antrum of the stomach towards the narrowed pylorus. During insufflation with air, the pylorus does not open, and it is impossible to pass the endoscope into the duodenum. During the atropine test, the pylorus remains closed (unlike pylorospasm). In many cases, antrum gastritis and reflux esophagitis are detected.

Differential diagnosis

Pyloric stenosis should be distinguished from various vegetosomatic disorders accompanied by pylorospasm (see Tables 3-5) and pseudopyloric stenosis (Debre-Fibiger syndrome - a complex endocrine disorder of the mineralocorticoid and androgenic functions of the adrenal cortex).

Treatment

Treatment of pyloric stenosis is only surgical. Surgical intervention should be preceded by preoperative preparation aimed at restoring water-electrolyte and acid-base balance, and the use of antispasmodics. The technique of open (preferably laparoscopic) surgery is pyloromyotomy. Feeding after surgery is dosed; by the 8-9th day after surgery, its volume is gradually increased to the age norm. Fluid deficiency is replenished parenterally and with nutritional enemas.

Forecast

As a rule, surgery promotes complete recovery.

Functional indigestion is a dysfunction of an organ without organic damage to its parts. The disease is characterized by a wide variety of symptoms, but instrumental examination does not reveal pathological changes in the mucosa.

We talk about the causes of the disease, its diagnosis and treatment.

The development of functional gastric disorder (FSD) is based on two main reasons:

1. Hereditary predisposition. Very often, disorders of the gastrointestinal tract of functional origin can be traced in several generations of the same family. This is associated with genetically determined characteristics of neurohumoral regulation, the type of nervous activity and inherited characteristics of the autonomic nervous system.
2. Excessive mental and physical stress. Acute and chronic stress play an important role.

For the development of FGD, even in conditions of hereditary burden, the body must be exposed to a whole complex of unfavorable factors. Let's look at the main ones.

1.Primary causes. Associated with the influence of exogenous factors, these include:

2.Secondary causes. Associated with the adverse effects on the digestive tract of diseases of other organs and systems:

• chronic diseases of the pancreas, gall bladder and liver;
• duodenitis, duodenal ulcer;
• chronic colitis, diverticulosis of the large intestine;
• vegetative-vascular dystonia (VSD);
• chronic heart failure;
• kidney disease;
• unsanitized foci of infection in the body - carious teeth, indolent otitis media, sinusitis, sinusitis.

How does functional indigestion develop?

Irregular food intake leads to disruption of the rhythm of production of hormones that regulate the secretory and motor function of the digestive tract. As a rule, their hypersecretion develops, which stimulates the formation of gastric juice. Excessively spicy and fatty foods, as well as nicotine and caffeine, have a similar effect.

In secondary disorders, the main role in the development of pathology is played by excessive activation of the parasympathetic nervous system and, as a consequence, the effect of impulses from the vagus nerve on the stomach. This leads to disruption of the motor function of the organ and the appearance of pain.

Why does my stomach hurt due to nervousness?

Violation of the nervous regulation of the gastrointestinal tract leads to the following:

Usually one of the dysregulations predominates in the patient, so there are several forms of FRD:

1. Ulcer-like. Develops with hyperproduction of hydrochloric acid. It manifests itself predominantly as pain in the epigastric region.
2. Dyskinetic. Caused by impaired motility of the stomach and duodenum, as well as changes in the sensitivity of internal (visceral) receptors.

Identification of the leading link in the development of the disease plays an important role in prescribing treatment.

Symptoms of functional gastric dyspepsia

The peculiarity of FDD symptoms is their inconstancy and inconsistency. The complaints of patients are quite vague and of an emotional nature, one of the most common is that their stomach hurts after stress. Most patients have an asthenic physique and signs of vegotovascular dystonia.

One of the main manifestations of the disease is pain that occurs after stress or errors in diet. Typical localization is in the epigastric region or around the navel. The pain is usually aching, of moderate intensity, in some cases it is sharp and paroxysmal.

Typically, patients complain of the following symptoms:

• nausea,
• vomiting
• rotten burps,
• feeling of heaviness in the stomach,
• heartburn,
• intestinal dyspepsia (flatulence, abdominal pain),
• unstable stool (alternating diarrhea and constipation).

FDD occurs not only in adults, but also in children. The child makes the same complaints. The main cause of the disorder in children is the effect of stress factors.

Diagnosis of the disease

Functional stomach disorder – ICD code K31.0. To make a diagnosis, you need to contact a therapist or gastroenterologist. For differential diagnosis with organic lesions of the gastrointestinal tract, such as gastritis, peptic ulcer disease, reflux esophagitis, esophagogastroduodenoscopy (EGD), gastric pH-metry, and fluoroscopy of the stomach are performed.

Gastroscopy allows you to examine the walls of the stomach from the inside and identify violations of the contraction of the stomach walls. In case of functional disorders, damage and inflammatory processes in the mucous membrane are not detected.

pH-metry makes it possible to determine the profile of hydrochloric acid secretion, both basal and stimulated. Fluoroscopy is used to assess organ motility disorders, size, and sphincter function. These parameters are determined by the rate of evacuation of barium sulfate.

Useful video

What is important to know about the disease can be heard from this video.

Treatment

The basis of FRD therapy is the prescription of drugs that relieve symptoms of the disease, diet, and correction of the state of the nervous system. To eliminate organ motility disorders, antispasmodics are prescribed ( No-shpa, Papaverine), anticholinergics ( Buscopan), prokinetics ( Cerucal, Motilium).

For ulcer-like forms of the disease, antacids are effective ( Malaox, Gaviscon, Almagel), proton pump inhibitors ( Pariet, Omez, Beret). In some cases, the use of homeopathy methods is effective.

An important role in the treatment of FDD is played by normalizing the tone of the autonomic system, as well as reducing the patient’s general nervousness. For this purpose, physiotherapy is used:

• electrosleep;
• electrophoresis with calcium and bromine;
• massage;
• circular shower.

In severe cases, psychotherapy and the use of drug sedation methods are indicated - the prescription of tranquilizers, antidepressants).

Treatment at home

To relieve increased nervousness, you can use herbal teas with a calming effect. Infusions of mint, valerian, and motherwort show high effectiveness with long-term and regular use. For prophylactic purposes, gastric and antiulcer preparations are used.

Diet

One of the first recommendations that a doctor gives to both adult patients and children is to change the type and mode of nutrition. It is advisable to eat food 3-4 times a day. You should eat a hot meal at least once a day. Fast food, spicy and fatty foods that irritate the stomach are excluded.

Stomach pain due to nervousness, what to do

When a person regularly develops symptoms of indigestion, it is important to understand the cause. If FRF is associated with excessive nervous stress, it is necessary to take measures to cope with stress, especially with a labile psyche. Taking sedatives, normalizing your lifestyle, and following a work and rest schedule can help.

1. If you are very nervous, try to calm down. Try to breathe deeply and calmly - this reduces the tone of the autonomic nervous system.
2. If necessary, take valerian or motherwort tablets in a single dose. The herbal preparation Persen relieves nervous tension well.
3. Often, under stress, people violate their usual diet (overeat, abuse junk food). Try not to let this happen.
4. If symptoms of stomach upset increase, consult your doctor for a thorough examination.

The human intestine performs one of the important functions in the body. Through it, nutrients and water enter the blood. Problems associated with disruption of its functions in the initial stages of diseases, as a rule, do not attract our attention. Gradually, the disease becomes chronic and makes itself felt with manifestations that are difficult to miss. What could be the reasons that caused a functional disorder of the intestine, and how these diseases are diagnosed and treated, we will consider further.

What does pathology mean?

Functional bowel disorder includes several types of intestinal disorders. All of them are united by the main symptom: impaired motor function of the intestines. The disorders usually appear in the middle or lower parts of the digestive tract. They are not the result of neoplasms or biochemical disorders.

Let us list what pathologies this includes:

• Syndrome
• The same pathology with constipation.
• Irritable bowel syndrome with diarrhea.
• Chronic functional pain.
• Fecal incontinence.

The class of “diseases of the digestive organs” includes a functional disorder of the intestine; in ICD-10 the pathology is assigned code K59. Let's look at the most common types of functional disorders.

This disease refers to a functional disorder of the intestine (in ICD-10 code K58). In this syndrome, there are no inflammatory processes and the following symptoms are observed:

• Colon motility disorder.
• Rumbling in the intestines.
• Flatulence.
• The stool changes - sometimes diarrhea, sometimes constipation.
• On examination, pain in the area of ​​the cecum is characteristic.
• Chest pain.
• Headache.
• Cardiopalmus.

There may be several types of pain:

• Bursting.
• Pressing.
• Dumb.
• Cramping.
• Intestinal colic.
• Migration pain.

It is worth noting that pain can intensify as a result of positive or negative emotions, in case of stress, as well as during physical activity. Sometimes after eating. Passing gas and stool can relieve pain. As a rule, the pain goes away when you fall asleep at night, but may return in the morning.

In this case, the following course of the disease is observed:

• After defecation there is relief.
• Gases accumulate and a feeling of bloating appears.
• The stool changes its consistency.
• The frequency and process of defecation is disrupted.
• There may be mucus discharge.

If several symptoms persist for some time, the doctor will diagnose irritable bowel syndrome. A functional disorder of the intestine (ICD-10 identifies such a pathology) also includes constipation. Let us consider further the features of the course of this disorder.

Constipation - bowel dysfunction

According to the ICD-10 code, such a functional disorder of the intestine is numbered K59.0. With constipation, transit slows down and dehydration of feces increases, and coprostasis is formed. Constipation has the following symptoms:

• Bowel movements less than 3 times a week.
• Lack of feeling of complete bowel movement.
• The act of defecation is difficult.
• The stool is hard, dry, and fragmented.
• Cramps in the intestines.

Constipation with spasms, as a rule, does not have organic changes in the intestines.

Constipation can be divided according to severity:

• Easy. Stool once every 7 days.
• Average. Stool once every 10 days.
• Heavy. Stool less than once every 10 days.

When treating constipation, the following directions are used:

• Integral therapy.
• Rehabilitation measures.
• Preventive actions.

The disease is caused by insufficient mobility during the day, poor diet, and disturbances in the functioning of the nervous system.

Diarrhea

ICD-10 classifies this disease as a functional disorder of the large intestine according to the duration and degree of damage to the intestinal mucosa. An infectious disease belongs to A00-A09, a non-infectious disease - to K52.9.

This functional disorder is characterized by watery, liquefied, unformed stools. Defecation occurs more often than 3 times a day. There is no feeling of bowel movement. This disease is also associated with impaired intestinal motility. It can be divided according to severity:

• Easy. Stool 5-6 times a day.
• Average. Stool 6-8 times a day.
• Heavy. Stool more often than 8 times a day.

It can become chronic, but is absent at night. Lasts for 2-4 weeks. The disease may recur. Diarrhea is often associated with the psycho-emotional state of the patient. In severe cases, the body loses a large amount of water, electrolytes, protein, and valuable substances. This can lead to death. It should also be taken into account that diarrhea may be a symptom of a disease not related to the gastrointestinal tract.

Common Causes of Functional Disorders

The main reasons can be divided into:

• External. Psycho-emotional problems.
• Internal. Problems are associated with poor intestinal motor function.

There are several common causes of functional disorders of the intestines in adults:

• Long-term use of antibiotics.
• Dysbacteriosis.
• Chronic fatigue.
• Stress.
• Poisoning.
• Infectious diseases.
• Problems of the genitourinary organs in women.
• Hormonal imbalances.
• Menstruation, pregnancy.
• Insufficient water intake.

Causes and symptoms of functional disorders in children

Due to the underdevelopment of the intestinal flora, functional intestinal disorders in children are common. The reasons may be the following:

• Lack of adaptation of the intestines to external conditions.
• Infectious diseases.
• Infection of the body with various bacteria.
• Psycho-emotional state disorder.
• Heavy food.
• Allergic reaction.
• Insufficient blood supply to certain areas of the intestine.
• Intestinal obstruction.

It is worth noting that in older children the causes of functional impairment are similar to those in adults. Small children and infants are much more susceptible to intestinal diseases. In this case, you cannot manage with diet alone; drug treatment and consultation with a doctor are necessary. Severe diarrhea can lead to the death of a child.

The following symptoms may be noted:

• The child becomes lethargic.
• Complains of abdominal pain.
• Irritability appears.
• Attention decreases.
• Flatulence.
• Increased frequency of bowel movements or absence of bowel movements.
• There is mucus or blood in the stool.
• The child complains of pain during bowel movements.
• Possible rise in temperature.

In children, functional intestinal disorders can be infectious or non-infectious. Only a pediatrician can determine. If you notice any of the above symptoms, you should take your child to the doctor as soon as possible.

According to ICD-10, a functional disorder of the large intestine in a teenager is most often associated with a violation of the diet, stress, taking medications, and intolerance to a number of foods. Such disorders are more common than organic intestinal lesions.

General symptoms

If a person has a functional bowel disorder, symptoms may include the following. They are characteristic of many of the above diseases:

• Pain in the abdominal area.
• Bloating. Involuntary passage of gas.
• Lack of stool for several days.
• Diarrhea.
• Frequent belching.
• False urge to defecate.
• The consistency of the stool is liquid or hard and contains mucus or blood.

The following symptoms are also possible, which confirm intoxication of the body:

• Headache.
• Weakness.
• Cramps in the abdominal area.
• Nausea.
• Heavy sweating.

What needs to be done and which doctor should I contact for help?

What diagnostics are needed?

First of all, you need to go for an examination to a therapist, who will determine which specialist you should see. It can be:

• Gastroenterologist.
• Nutritionist.
• Proctologist.
• Psychotherapist.
• Neurologist.

To make a diagnosis, the following tests may be prescribed:

• General analysis of blood, urine, feces.
• Blood chemistry.
• Examination of stool for the presence of occult blood.
• Coprogram.
• Sigmoidoscopy.
• Colonofibroscopy.
• Irrigoscopy.
• X-ray examination.
• Biopsy of intestinal tissue.
• Ultrasonography.

Only after a complete examination does the doctor prescribe treatment.

Making a diagnosis

I would like to note that in case of an unspecified functional disorder of the intestine, the diagnosis is made on the basis that the patient continues to have the following symptoms for 3 months:

• Abdominal pain or discomfort.
• Defecation is either too frequent or difficult.
• The consistency of the stool is either watery or compacted.
• The process of defecation is disrupted.
• There is no feeling of complete bowel movement.
• There is mucus or blood in the stool.
• Flatulence.

Palpation is important during examination; it should be superficial and deep sliding. You should pay attention to the condition of the skin and the increased sensitivity of certain areas. If you look at a blood test, as a rule, it does not have any pathological abnormalities. An X-ray examination will show signs of dyskinesia of the large intestine and possible changes in the small intestine. Irrigoscopy will show painful and uneven filling of the large intestine. An endoscopic examination will confirm swelling of the mucous membrane and an increase in the secretory activity of the glands. It is also necessary to exclude gastric and duodenal ulcers. The coprogram will show the presence of mucus and excessive fragmentation of stool. Ultrasound reveals pathology of the gallbladder, pancreas, pelvic organs, osteochondrosis of the lumbar spine and atherosclerotic lesions of the abdominal aorta. After examining the stool using bacteriological analysis, an infectious disease is excluded.

If there are postoperative sutures, it is necessary to consider adhesive disease and functional bowel pathology.

What treatment methods are there?

In order for treatment to be as effective as possible, if a diagnosis of “functional bowel disorder” is made, it is necessary to perform a set of measures:

1. Establish a work and rest schedule.
2. Use psychotherapy methods.
3. Follow the recommendations of a nutritionist.
4. Take medications.
5. Apply physiotherapeutic procedures.

Now a little more about each of them.

A few rules for the treatment of intestinal diseases:

• Walk outdoors regularly.
• Do exercises. Especially if the job is sedentary.
• Avoid stressful situations.
• Learn to relax and meditate.
• Take a warm bath regularly.
• Avoid snacking on junk food.
• Consume probiotic foods and those containing lactic acid bacteria.
• If you have diarrhea, limit your intake of fresh fruits and vegetables.
• Perform abdominal massage.

Psychotherapy methods help cure functional intestinal disorders that are associated with stressful conditions. Thus, the following types of psychotherapy can be used in treatment:

• Hypnosis.
• Methods of behavioral psychotherapy.
• Abdominal autogenic training.

It should be remembered that when constipation occurs, first of all it is necessary to relax the psyche, and not the intestines.

• Food should be varied.
• Drinking should be plentiful, at least 1.5-2 liters per day.
• Do not eat foods that are poorly tolerated.
• Do not eat cold or very hot food.
• You should not eat vegetables and fruits raw or in large quantities.
• Do not overuse products with essential oils, whole milk products and those containing refractory fats.

Treatment of functional intestinal disorders includes the use of the following drugs:

• Antispasmodics: “Buscopan”, “Spasmomen”, “Dicetep”, “No-shpa”.
• Serotonergic drugs: Ondansetron, Buspirone.
• Carminatives: Simethicone, Espumisan.
• Sorbents: “Mukofalk”, “Activated carbon”.
• Antidiarrheal drugs: Linex, Smecta, Loperamide.
• Prebiotics: Lactobacterin, Bifidumbacterin.
• Antidepressants: Tazepam, Relanium, Phenazepam.
• Neuroleptics: Eglonil.
• Antibiotics: Cefix, Rifaximin.
• Laxatives for constipation: Bisacodyl, Senalex, Lactulose.

The attending physician should prescribe medications, taking into account the characteristics of the body and the course of the disease.

Physiotherapeutic procedures

Each patient is prescribed physiotherapy individually, depending on the functional disorders of the intestines. These may include:

• Baths with carbon dioxide bischofite.
• Treatment with interference currents.
• Application of diadynamic currents.
• Reflexology and acupuncture.
• Medical and physical training complex.
• Electrophoresis with magnesium sulfate.
• Intestinal massage.
• Cryomassage.
• Ozone therapy.
• Swimming.
• Yoga.
• Laser therapy.
• Autogenic exercises.
• Warming compresses.

Good results have been observed when using mineral waters in the treatment of the gastrointestinal tract. It is worth noting that after undergoing physiotherapeutic procedures, drug treatment is sometimes not required. Bowel function is improving. But all procedures are possible only after a full examination and under the supervision of a doctor.

Prevention of functional intestinal disorders

It is easier to prevent any disease than to treat it. There are rules for the prevention of intestinal diseases that everyone should know. Let's list them:

1. Food should be varied.
2. It is better to eat fractionally, in small portions 5-6 times a day.
3. The menu should include whole grain bread, cereals, bananas, onions, bran, containing a large amount of fiber.
4. Eliminate gas-forming foods from your diet if you are prone to flatulence.
5. Use natural laxative products: plums, lactic acid products, bran.
6. To live an active lifestyle.
7. Controlling your food leads to diseases of the digestive system.
8. To refuse from bad habits.

By following these simple rules, you can avoid diseases such as functional intestinal disorders.