FUNCTIONAL DYSPEPSIA
ICD-10 codes
K30. Dyspepsia.
K31. Other diseases of the stomach and duodenum, including functional disorders of the stomach.
Functional dyspepsia is a symptom complex in children over the age of one year, in which there are pain, discomfort or a feeling of fullness in the epigastric region, associated or not associated with eating or physical activity, as well as early satiety, bloating, nausea, regurgitation, intolerance to fatty food, etc.
Functional dyspepsia in childhood is very common, the true prevalence is not specified.
Etiology and pathogenesis
There are three levels of formation of a somatic symptom (determined by complaints): organ, nervous, mental (Fig. 3-1). The symptom generator can be located at any level, but the formation of an emotionally colored complaint occurs only at the mental level. The pain that appeared outside the lesion of the organ is no different from that that arose as a result of true damage. The causes of functional disorders are associated with a violation of the nervous or humoral regulation of the motility of the gastrointestinal tract, in which there are no structural changes in the organs of the gastrointestinal tract.
Rice. 3-1. Levels of formation of clinical manifestations of functional disorders of the gastrointestinal tract
Motility disorders of the digestive organs of any origin inevitably cause secondary changes, the main of which are violations of the processes of digestion, absorption and intestinal microbiocenosis.
These changes exacerbate motor disorders, closing the pathogenetic vicious circle.
Clinical picture
Symptoms in functional disorders are diverse, 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 the symptoms are not associated with defecation or changes in the frequency and nature of the stool.
In children, it is difficult to differentiate variants of functional dyspepsia, so they are not isolated.
Diagnostics
Due to the fact that the diagnosis of functional dyspepsia is a diagnosis of exclusion with chronic diseases of the gastrointestinal tract, a comprehensive examination is required, including a general clinical minimum, exclusion of helminthic-protozoal invasion, 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, PU, as well as diseases of the biliary system, pancreas, liver. With these pathologies, characteristic changes in laboratory and instrumental studies are revealed, while there are no changes in functional dyspepsia.
Treatment
Mandatory components of the treatment of functional dyspepsia are the normalization of the vegetative status and psycho-emotional state, if necessary, consultation with a psychoneurologist, 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 anxiety symptoms) and a screening study (general blood count, coprology, 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 requirement.
an important signal and serves as an indication for examination in a consultation center or gastroenterological department of a hospital (second stage).
Prokinetics are prescribed for dyskinetic disorders. The drug of choice is domperidone, administered 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, spastic conditions. Papaverine is prescribed orally (regardless of food intake), 2-3 times a day: for children 1-2 years old - 0.5 tablets; 3-4 years - 0.5-1 tablet; 5-6 years old - 1 tablet each, 7-9 years old - 1.5 tablets each, over 10 years old and adults - 1-2 tablets each, drotaverine (no-shpa*, spasmol*) 0.01-0.02 each g 1-2 times a day; children from 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; school-age children - pinaverium bromide (dicetel *), a selective blocker of calcium channels of 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, ulcer.
CHRONIC GASTRITIS AND GASTRODUODENITIS
ICD-10 code
K29. Gastritis and duodenitis.
Chronic gastritis and gastroduodenitis are polyetiological, steadily progressive 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 method of diagnosis 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 CHD, without examination, leads to overdiagnosis of HP disease. In Russia, compared with 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 types and their corresponding formation mechanisms are distinguished (Fig. 3-3). Burdened heredity is realized when the body is exposed to adverse exogenous and endogenous factors.
Rice. 3-3. Variants of chronic gastritis and their features
Exogenous factors risk of HCG:
Alimentary: 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, the poor quality of drinking water;
Taking certain drugs: non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, antibiotics, etc .;
food allergy;
Unsatisfactory condition of the dental system;
Bad habits;
Hormonal dysfunctions. Endogenous factors risk of developing CHD:
HP infection;
Reflux of bile into the stomach;
endocrine disorders.
infection HP occurs in childhood, if untreated, the bacteria persist in the body indefinitely, causing diseases of the gastrointestinal tract.
Source of infection: infected person, animal (cats, dogs, rabbits). Ways of distribution: 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 faeces, water, 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 diverse and depend on the nature of the violations of the secretory, 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 secretion of hydrochloric acid.
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 fundic 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, dietary disorders. In older children, palpation shows moderate pain in the epigastrium and pyloroduodenal zone.
Dyspeptic syndrome: sour belching, belching of air, heartburn, tendency to constipation.
Syndromes of nonspecific intoxication And asthenia variable: vegetative instability, irritability, rapid exhaustion during mental and physical stress, sometimes subfebrile temperature.
Syndromes with reduced secretion of hydrochloric acid (more often with type A gastritis)
Pain syndrome weakly expressed, characterized by dull diffuse pain in the epigastrium. After eating, there is a feeling of heaviness and fullness in the upper abdomen; pains arise and amplify depending on quality and volume of food. Palpation reveals a slight diffuse soreness in the epigastrium.
Dyspeptic syndrome prevails over pain: belching food, nausea, feeling of bitterness in the mouth, loss of appetite, flatulence, unstable stool. There may be a decrease in appetite, an aversion to certain foods (cereals, dairy products, etc.).
Syndrome of nonspecific intoxication pronounced, asthenia predominates. Patients are pale, their body weight is reduced due to a violation of the gastric stage of digestion of food and secondary disorders of the pancreas, in severe cases, manifestations of hypopolyvitaminosis, anemia are noted.
With reflux gastritis (more often with type C gastritis) due to the constant reflux of gastric and duodenal contents (gastroesophageal and duodenogastric reflux), symptoms of upper (gastric) dyspepsia are mainly characteristic: heartburn, sour belching, belching with air, a feeling of bitterness in the mouth, decreased 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, unexpressed intoxication, moderately pronounced leukocytosis in the blood, increased ESR;
Bad breath (halitosis).
Diagnostics
Signs of gastritis or gastroduodenitis with esophagoduodenoscopy:
Hypersecretion of gastric contents;
Mucus, often - an admixture of bile;
Predominantly hyperemia and swelling of the mucous membrane of the stomach and / or duodenum;
Edema and thickening of the 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;
Turbid stomach secret;
Lymphoid hyperplasia, hyperplasia of epithelial cells, the mucous membrane looks like a cobblestone pavement (see Fig. 3-4, a).
Intragastric pH-metry allows you to evaluate 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 older than 5 years is 1.7-2.5, after the introduction of a stimulant (histamine) - 1.5-2.5. The antrum of the stomach, which neutralizes the 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 it.
trawling ability of the antrum and possible acidification of the duodenum.
Gastric sounding allows you to evaluate the secretory, evacuation, acid-producing functions. In children, an increased or preserved acid-producing function is more often detected. At HP-infection in children does not occur 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 the lesion of the stomach gives 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, parietal (parietal), mucous (goblet). The chief cells produce pepsin, the parietal cells produce the ingredients of hydrochloric acid, the goblet and integumentary cells produce the mucoid secret. 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 are Paneth cells that provide antibacterial protection to the gastrointestinal tract. The main protective molecules produced by Paneth cells are α-defensins, lysozyme, phospholipase A2, cationic peptides.
Histologically characterized: active diffuse gastritis, superficial gastritis with glandular lesions without atrophy, with subatrophy or atrophy, in which there is a gradual change in the cellular composition (see Fig. 3-5, a). For HP-infection is characterized by restructuring of the epithelium (metaplasia) according to the pyloric or intestinal type, which is more often detected with atrophic gastritis.
Rice. 3-5. Changes in chronic gastritis: a - normal and changes in chronic gastritis: scheme 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, ulcer, diseases of the biliary system, pancreas, liver.
Treatment
Drug therapy is carried out in accordance with the type of gastritis.
Given that the predominant number of cases of type B gastritis is caused by HP, the basis of treatment, especially erosive gastritis and / or duodenitis, is eradication HP(anti-helicobacter therapy is presented in the section "Peptic ulcer"). It is carried out only if HP one invasive or two non-invasive research methods. Treatment of all family members is desirable.
With increased gastric secretion, antacids are prescribed: algeldrate + magnesium hydroxide (maalox *, almagel *), aluminum phosphate (phosphalugel *), gastal *, gastrofarm * in suspension, tablets.
Maalox * is administered orally to children from 4 to 12 months, 7.5 ml (1/2 tsp), older than a year - 5 ml (1 tsp) 3 times a day, 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 in 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 carefully kneading the sachet 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 scoop 3-4 times a day 1 hour before meals and at night.
Phosphalugel * is prescribed orally, it can be pure or diluted in 1/2 glass of water before taking. Children under 6 months - 4 g (1/4 sachet), or 1 tsp, after each of 6 feedings; older than 6 months - 8 g (1/2 sachet), or 2 tsp. - after each of 4 feedings. In older children, the RD is 1-2 sachets of gel 2-3 times a day.
With severe hyperacidity, an antisecretory agent is used, M 1 - anticholinergic pirenzepine (gastrocepin *) in tablets of 25 mg, 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 older than 10 years for a period of 2 weeks at a dose of 0.02-0.04 g at night.
With erosive gastritis caused by NSAIDs, gastroprotectors are used.
Film-forming preparations are also used, such as sucralfate (venter *), in the form of a gel for oral administration and tablets of 1 g, which are not chewed, 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 by adolescents (preferably from 18 years of age) inside, during meals, 400-800 mcg / day in 2-4 doses.
A sedative herbal preparation of hawthorn fruit + black elder flower extract + 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 eating: 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 from 3 years of age is prescribed 1-2 tablets 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-shpy*, butylscopolamine bromide (buscopan*), drotaverine. Enveloping and astringent herbal remedies are widely recommended: an 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 - an extract of the leaves of the plantain large (plantaglucid *). Planta glucid * in granules for the preparation of a suspension for oral administration is prescribed for 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 the course of treatment is 3-4 weeks. For the prevention of 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 substitution purposes. Acidin-pepsin tablets * are administered orally at a dose of 0.25 g, during or after a meal, previously 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 of groups B and C orally and in injections, dioxomethyltetrahydropyrimidine (methyluracil *), solcoseryl *. Methyluracil * in tablets of 500 mg is prescribed:
children from 3 to 8 years - 250 mg, over 8 years - 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) occurring with motor disorders, the prokinetic domperidone (motilium*, motilak*, motinorm*, domet*) is used orally 15-20 minutes before meals, for children under 5 years old - in suspension for administration inside 2.5 mg/10 kg of body weight 3 times a day and, if necessary, additionally at bedtime.
With severe nausea and vomiting - 5 mg / 10 kg of body weight 3-4 times a day and at bedtime, if necessary, the dose can be doubled. For children over 5 years old and adolescents, domperidone is prescribed in tablets of 10 mg 3-4 times a day and additionally at bedtime, with severe nausea and vomiting - 20 mg 3-4 times a day and at 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: platyfillin electrophoresis - on the epigastric region, bromine - on the collar region, in the subremission phase - ultrasound, laser therapy.
Prevention
Dispensary observation is carried out according to the III group of accounting, the frequency of examinations by a pediatrician is at least 2 times a year, by a gastroenterologist - 1 time per year. Esophagogastroduodenoscopy is performed once a year for pain syndrome.
appointment of massage, acupuncture, physiotherapy exercises. Preferably spa treatment.
A child with CHD is subject to removal from the dispensary, subject to a 5-year clinical and endoscopic remission.
Forecast
The prognosis is good, but post-infection CGD HP, accompanied by increased acid production, which can lead to erosive
leg 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.
Peptic ulcer
ICD-10 codes
K25. Gastric ulcer.
K26. Duodenal ulcer.
A chronic relapsing disease that occurs 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 PU is 1.6±0.1 per 1000 children, 7-10% among the adult population. In schoolchildren, PU occurs 7 times more often than in preschool children, in children living in the city - 2 times more often than in rural areas. In 81% of cases, the place of localization of the ulcer defect is the duodenum, in 13% - the stomach, in 6% there is a combined localization. In girls, PU is observed more often (53%) than in boys, but the combination of PU of the stomach and duodenum is 1.4 times more common in boys. Complications of PU 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 chronization:
Microorganisms (HP infection);
Neuropsychic factors (stress in children is the leading factor in PU: emotional overstrain, negative emotions, conflict situations, etc.);
Hereditary-constitutional (an increase in the mass of parietal cells, an increase in the release of gastrin in response to food intake, a deficiency of a trypsin inhibitor, blood group I, etc. - about 30% of patients);
Medicinal and toxic effects;
endocrine disorders;
Violations of the regime, the nature of nutrition, etc.
The pathogenesis of PU is based on imbalance 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 significantly associated with hypergastrinemia, and hypergastrinemia with hyperacidity. Hyperplasia of gastrin cells may be the initial feature of the endocrine apparatus of the gastrointestinal tract, often hereditarily conditioned.
In strengthening the aggressive properties of gastric contents and weakening the protective properties of the mucous membrane of the stomach and duodenum, microorganisms play urease-producing HP, discovered in 1983 by Australian scientists W. Marshall And /. Warren(Fig. 3-7). They are detected in approximately 90% of patients with duodenal ulcer and in 70% of gastric ulcers. But HP is not an obligatory pathogenetic factor of duodenal ulcer in children, especially those under the age of 10 years.
Rice. 3-7. Factors affecting virulence HPTable 3-2. Classification of PU (Mazurin A.V., 1984)
Clinical picture
PU is diverse, a typical picture is not always observed, which greatly complicates the diagnosis.
Features of the course of BU in children at the present time:
Leveling the seasonality of exacerbations;
Asymptomatic course in 50% of patients;
Erased clinical manifestations in some patients with the rapid formation of complications of duodenal ulcer in the form of bleeding or perforation.
Pain is the leading complaint. It is localized in the actual epigastric, paraumbilical regions, sometimes spilled over the entire abdomen. In a typical case, the pain becomes constant, intense, takes on a nocturnal and "hungry" character, and decreases with food intake. The Moinigan rhythm of pain appears (hunger - pain - food intake - light interval - hunger - pain, etc.). Dyspeptic disorders: heartburn, belching, vomiting, nausea - with increasing
increase in the duration of the disease. Appetite is reduced in 1/5 of patients, there may be a delay in physical development. There is a tendency to constipation or unstable stools. Asthenic syndrome is manifested by emotional lability, sleep disturbance due to pain, increased fatigue. There may be hyperhidrosis of the palms and feet, arterial hypotension, red dermographism, and sometimes bradycardia.
On physical examination, the lining of the tongue is determined, on palpation - soreness in the pyloroduodenal zone, epigastrium, sometimes in the right hypochondrium, a positive Mendel symptom (pain on percussion with half-bent fingers of the right hand in the region of the greater and lesser curvature of the stomach).
The main thing in the diagnosis of 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 (breakthrough of an ulcer into the abdominal cavity), which occurs acutely and is accompanied by sharp pain in the epigastric region, tension of the anterior abdominal wall and symptoms of peritoneal irritation;
Penetration (penetration of an ulcer into other organs) - persistent pain syndrome, sharp pains 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 wall of the duodenum (Fig. 3-8, c);
Perivisceritis (adhesive process) that develops in PU 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, aggravated after a heavy meal, with physical exertion and shaking the body. Among the complicated forms of PU, bleeding prevails (80%), stenosis (10%), perforation (8%) and ulcer penetration (1.5%) are less common, perivisceritis (0.5%) and malignancy are extremely rare.
Diagnostics
The most optimal diagnostic method is esophagogastroduodenoscopy (Table 3-3), with the help of which a targeted biopsy of the mucous membrane of the stomach and duodenum is performed to clarify the nature and severity of pathomorphological changes.
Table 3-3. The results of esophagogastroduodenoscopy in PU
Endoscopic examination reveals 4 stages of the ulcerative process (see Table 3-2). Against the background of therapy, the transition from I to II stage is observed after 10-14 days, from II to III - after 2-3 weeks, from 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).
HP infection is diagnosed using invasive and non-invasive methods, with detection being the gold standard. HP in a biopsy of the mucous membrane of the stomach and / or duodenum (see Chapter 1).
Assessment of the state of the secretory function of the stomach is carried out by the method of pH-metry or gastric sounding.
Pathomorphology
Macroscopically, 1-3 ulcerative defects with fibrinous plaque and ridge-like edges are found (Fig. 3-9, b). Around the defects, the mucous membrane is hyperemic, with punctate hemorrhages. Microscopically, in the bottom of the ulcer defect, necrosis with fibrinous deposits is visible, around which accumulation of leukocytes and vascular plethora are observed. 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 - X-ray: a symptom of a niche with an ulcerative defect in the stomach; b - macropreparation of the duodenal mucosa (arrows indicate defects); c - microscopic picture of an ulcerative defect of the duodenal wall (staining with hematoxylineosin, χ 100)
Differential Diagnosis
Differential diagnosis is carried out with acute ulcers that develop against the background of acute stress, burns (Curling's ulcer), trauma (Cushing's ulcer), infections (cytomegalovirus, herpes, etc.) or medication (NSAIDs, etc.).
Treatment
Treatment is carried out in stages. Treatment goals:
Relief of inflammation, healing of ulcers, achievement of stable remission;
Eradication of HP infection;
Prevention of relapse, prevention of exacerbations and complications.
In case of exacerbation, hospitalization in the gastroenterological department is mandatory (first stage of treatment). Assign bed rest for 2-3 weeks.
Of the drugs, antacids are prescribed to young children. Algeldrate + 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 a day, 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 (losek*, omez*) is prescribed from 12 years old, 1 capsule (20 mg) once a day on an empty stomach. The course of treatment for duodenal ulcer is 2-3 weeks, if necessary, supportive treatment is carried out for another 2-3 weeks; with gastric ulcer - 4-8 weeks. Lansoprazole (helicol *, lanzap *) - 30 mg / day in a single dose in the morning for 2-4 weeks, if necessary - up to 60 mg / day. Pantoprazole (panum *, peptazol *) is prescribed orally, without chewing, with liquid, 40-80 mg / day, the course of treatment for scarring duodenal ulcer - 2 weeks, gastric ulcer and reflux esophagitis - 4-8 weeks. Rabeprazole (pariet *) is prescribed from the age of 12, 20 mg orally 1 time per day in the morning. The course of treatment - 4-6 weeks, if necessary - up to 12 weeks. The capsules are swallowed whole, without chewing.
Blockers of H 2 -histamine receptors. Famotidine (gastrosidin *, quamatel *, famosan *) is administered orally at 0.5 mg / kg per day at 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 as a gel for oral administration and tablets 1 hour before meals and at 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 going to bed for empty stomach) maximum DM - 8-12 g. The course of treatment - 4-6 weeks, if necessary - up to 12 weeks.
Upon confirmation of HP infection, HP eradication is carried out with bismuth or omez-containing schemes of the 1st and 2nd lines in combination with one or two antibacterial drugs. Success is achieved in 70-90% of patients, however, complications, side effects (Tables 3-4) and resistance (resistance) to PPIs, antibiotics (particularly metronidazole) and other drugs affect the success of therapy.
Table 3-4. Side effects of eradication therapy
First line therapy options (triple)
Based on bismuth preparations:
Bismuth subcitrate (de-nol*) 8 mg/kg (up to 480 mg/day) + amoxicillin (flemoxin*, chiconcil*) 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 PPI:
PPI + clarithromycin or (in children older than 8 years) tetracycline 1 g/day + nifuratel or furazolidone;
PPI + clarithromycin or (in children older than 8 years) 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 refuse the use of the second antibacterial agent in the eradication therapy of children with PU.
second line therapy(quadrotherapy) is recommended for the eradication of strains HP, resistant to antibiotics, with unsuccessful previous treatment. More often prescribed bismuth subcitrate + amoxicillin or clarithromycin; in children older than 8 years - tetracycline + nifuratel or furazolidone + PPI.
To reduce the frequency of side effects, improve the tolerability of anti-Helicobacter therapy allows the inclusion in the treatment regimen of probiotics containing lactobacilli, which are HP antagonists.
Medical therapy includes vitamins (C, U, group B), sedatives, antispastic drugs (papaverine, no-shpa *), cholinergic receptor blockers. General methods of physiotherapy are indicated in all periods of the disease; local procedures are used starting from stage II of the ulcer, thermal procedures (paraffin, ozokerite) - only during the healing of the ulcer. In the treatment of the acute stage of PU 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 the removal of affective tension and the elimination of stress.
The clinical and economic efficiency of new approaches to the diagnosis and treatment of PU 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 PU by 10 times;
Refusal of surgical treatment of PU;
Treatment of more than 80% of patients on an outpatient basis.
Rice. 3-10. The evolution of therapy for chronic diseases of the upper digestive system
Treatment for complications of PU carried out permanently, in surgical departments. Absolute indications for surgical intervention are perforation (perforation - a breakthrough of an ulcer into the free abdominal cavity with the entry of the contents of the stomach or duodenum into it), ulcer penetration (germination of a stomach or duodenal ulcer into surrounding organs or tissues), profuse bleeding, decompensated cicatricial-ulcerative pyloric stenosis , ulcer malignancy.
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. Shown emergency esophagogastroduodenoscopy to establish the localization of the source of bleeding and 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 (iv) every 8 hours or ranitidine 25-50 mg or famotidine 10-20 mg every 6 hours. In the presence of hemorrhagic erosions, sucralfate is additionally used at 1-2 g orally every 4 hours. After successful resuscitation and hemostatic courses, a standard eradication course is prescribed and the intake of Na +, K + -ATPase blocker or H 2 -histamine receptor blocker is always prolonged for at least 6 months Only if there is no effect, surgical treatment is indicated.
Relative readings to surgical intervention are recurrent bleeding, subcompensated pyloric stenosis, ineffectiveness of conservative treatment. In case of perforation or penetration of a stomach ulcer and / or duodenal ulcer with symptoms of peritonitis, profuse bleeding, surgery is performed according to emergency indications, in other cases, it is carried out in a planned manner.
Prevention
Primary prevention includes the organization of proper nutrition, regimen, the creation of a favorable environment in the family, the refusal to take ulcerogenic drugs, the fight against bad habits. Overloading with audiovisual information is unacceptable. It is necessary to actively identify individuals with an increased risk of PU (hereditary predisposition,
functional hypersecretion of hydrochloric acid, CGD with increased acid formation), and the appointment of esophagogastroduodenoscopy.
Secondary prevention PU - continuation of rehabilitation therapy.
The second stage of rehabilitation- sanatorium-resort, carried out no earlier than 3 months after discharge from the hospital if it is impossible in an outpatient setting. With a positive result of the urease test for HP infection, second-line eradication therapy is indicated.
The third stage of rehabilitation- dispensary observation in a polyclinic with a gastroenterologist for a period of 5 years or more. Its goal is to prevent an exacerbation of the disease. Anti-relapse treatment is carried out 2-3 times a year during school holidays. Assign a protective regimen, diet table No. 1 for 3-5 days, then table No. 5, vitamin and antacid preparations, if necessary, physiotherapy treatment: galvanization and drug electrophoresis of various microelements with a transverse arrangement of electrodes - copper sulphate, zinc sulfate, aloe solution , electrophoresis of bromine on the collar zone. For resorption of cicatricial changes in the stomach and duodenum, electrophoresis of solutions of lidase or terrilitin is used. The therapeutic use of hyperbaric oxygen therapy (8-10 sessions) is pathogenetically justified to improve local microcirculation and oxygenation of damaged tissues. To correct accompanying psychosomatic and vegetative disorders, low-frequency currents are used according to the electrosleep method.
In some cases, sinusoidal modulated currents, an electromagnetic field of an ultra-high frequency of the decimeter range, ultrasound are prescribed for the upper half of the abdomen and paravertebral. The soft influencing factors include an alternating magnetic field.
Esophagogastroduodenoscopy is carried out at least 1 time per year, recommended for complaints, positive results of fecal occult blood reaction or urease breath test.
If necessary, patients are limited to school workload - 1-2 days a week (homeschooling),
yut from exams, assign a special health group (restrictions in 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 bulb of the duodenum. In such cases, the disease is more severe and complications are often observed. Children who have undergone surgery are given disability. Dispensary observation of the patient by a pediatric gastroenterologist, compliance with the rules of seasonal and maintenance prevention of exacerbations significantly improve 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 output 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 output part, observed mainly in infants.
Etiology and pathogenesis
The pyloric part of the stomach is the narrowest part of this organ, which corresponds to the border between the stomach and the duodenum. The name comes from the word pylori- "gatekeeper". In the pyloric part of the stomach there is a massive muscular layer (compressor muscle), which is relatively well developed at birth. If its tone is disturbed as a result of functional disorders of the neuromuscular apparatus, the evacuation of food from the stomach to the duodenum becomes difficult, it lingers in the stomach, and vomiting occurs. Violation of the regulatory function of the CNS and its autonomic department is more often observed in children with birth trauma and after intrauterine hypoxia, so 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 noted, as the volume of nutrition increases, delayed vomiting of curdled acidic contents without bile appears, not exceeding the amount of food eaten. The child, despite vomiting, gains in body weight, although not enough, and with untimely treatment, 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 spastic - it is released intermittently, with sharp shocks in the form of vomiting.
Diagnostics
Radiological pathology is not determined, but after 2 hours there is a delay in the evacuation of the contrast mass. At
endoscopic examination reveals a pylorus closed in the form of a gap, through which it is always possible to pass with an endoscope, which makes it possible 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 comply with the sleep and wakefulness regimen, as well as keeping 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 if regurgitation occurs.
Of the medicinal preparations, 0.5-1.0 ml of a 2% solution of papaverine hydrochloride or a 2% solution of no-shpy *, 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% solution of atropine sulfate - 0.25-1.0 mg s / c, / m or / in 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 region No. 5-10; paraffin applications on the abdomen No. 5-6 every other day.
Forecast
The prognosis is favorable, by 3-4 months of life, the phenomena of pylorospasm usually disappear.
pyloric stenosis
ICD-10 codes
Q40.0. Pediatric pyloric stenosis.
K31.8. Other specified diseases of the stomach and duodenum: gastric constriction 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 muscle layer of the pylorus, its thickening associated with impaired innervation, as a result of which the pylorus takes the form of a white tumor-like formation resembling cartilage. In adolescents and adults, pyloric stenosis is considered as a complication of gastric ulcer or tumors of this department.
The incidence is 1 in 300 infants aged 4 days to 4 months. In boys, compared with girls, the defect occurs 4 times more often.
Etiology and pathogenesis
The main etiopathogenetic factors in children are as follows:
Violation of innervation, underdevelopment of the ganglion gatekeeper;
Intrauterine delay in the opening of the pyloric canal;
Hypertrophy and edema of the muscles of the pyloric 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 the result of severe scarring from ulcerative disease or malignancy.
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 a defect appear in the first days after birth, but more often in the 2-4th week of life. The skin becomes dry, facial features are sharpened, a hungry expression appears, the child looks older than his age.
The first and main symptom of pyloric stenosis is vomiting with a fountain, which occurs between feedings, at first rare, then more frequent. The volume of vomit, consisting of curdled milk with a sour smell, without an admixture of bile, exceeds the dose of a single feeding in quantity. The child becomes restless, malnutrition and dehydration develop, urination becomes rare, and there is a tendency to constipation.
When examining the abdomen in the epigastric region, bloating and increased, visible to the eye, segmented
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 looks like a dense tumor of a plum-like shape, shifting from top to bottom.
In the later stages, dehydration and a violation of water-salt metabolism develop. Due to the loss of chlorine and potassium with vomiting, their level in the blood decreases, metabolic alkalosis and other severe water-electrolyte and metabolic disorders develop. Possible aspiration syndrome. Of the late manifestations, deficiency anemia, an increase in hematocrit as a result of blood clotting, are noted.
Diagnostics
To confirm the diagnosis of pyloric stenosis, ultrasound is used, in which a long, thickened pylorus is revealed. 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 liquid 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. In pyloric stenosis, endoscopy reveals pinpoint
Rice. 3-11. Pyloric stenosis: a - a schematic representation of the place of transition of the stomach into the duodenum; b - a visible increase in the pylorus and peristalsis in the form of an hourglass; c - X-ray examination: retention of a 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. When insufflated with air, the pylorus does not open, it is impossible to pass the endoscope into the duodenum. With an 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 vegetative somatic 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, 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 nutrient enemas.
Forecast
As a rule, surgery contributes to a complete recovery.
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Job title: Education |
Doctor's answer: Hello! It is necessary for you to address to the neuropathologist, pains are possible or probable are connected with a stress.
Medical services in Moscow:
Question: Hello! After FGS, I was diagnosed with Atrophic-Hyperplastic Atrium Gastritis. Also in the conclusion it is written: "The stomach contains a clear liquid, foamy mucus. The tone of the walls is reduced, the peristalsis is sluggish. The relief of the folds is smoothed. The mucosa in the antrum is moderately thinned, a vascular pattern is visible, the relief of the mucosa is like a "cobblestone pavement"". In addition, a positive reaction to Helicobacter pylori was found.
To be honest, I was even a little surprised by the diagnosis, because. at the moment, the stomach practically does not bother me (and did not bother me before). Unless often after eating there is rumbling and discomfort in the stomach (as if something is pressing inside the stomach, then in one place then in another, while the food is being digested). Discomfort lessens when gas is released. But there is no such thing as pain.
In connection with this diagnosis, I have two questions:
1. Is it true that this is some kind of dangerous type of gastritis that can lead to oncology? If so, how urgently should I start worrying?
2. How effective are drugs for removing Helicobacter pylori at present? What is the probability of getting rid of it?
Doctor's answer: Hello. Yes, complications are possible. It is possible to estimate their probability only by seeing all survey data. Helicobacter treatment is effective. You should consult with a gastroenterologist.
Question: Hello. Around December 7-8, 2005, there were pains in the stomach (constant, but more after eating), belching with air, heartburn, I turned to a gastroenterologist, did an ultrasound of the liver, gallbladder, pancreas and FGDS. Ultrasound results: sagittal size of the pr. 15.1 cm, the lower edge of the left lobe at an angle of -45 degrees, the contours are even, the echogenicity is normal, the structure is homogeneous (I did not make out the rest of the words), the bile ducts are 04, see. The gallbladder is not deformed, the dimensions are 6.4 *2.4, wall thickness-02, contents-homogeneous. Pancreatic head-2.4, body-1.4, tail-2.3, smooth contours, homogeneous structure. we pass, the mucous membrane is pink, smooth. The cardia closes. There is mucus and bile in the stomach. The gastric mucosa is thickened with a hyperplastic elevation up to 0.1-0.2 cm, spotted in the outer body (? not legible), the folds are edematous. Peristalsis active, bulb 12p. the intestines are not deformed, the mucosa is patchy, moderately edematous. Conclusion: focal hyperplastic gastritis, moderately pronounced bulbitis. The doctor prescribed treatment - Ultop 1 per day - 10 days, Trichopolum 1 * 3r - 7 days, Malaox, Mezim, diet. I did not complete the course of treatment, I did not finish drinking Trichopolum, but my health improved, the pain became less intense, usually after eating. By the New Year, for several days, the stomach did not hurt even after eating. For the New Year, I had errors in my diet (alcohol, smoked meats, heavy salads, etc.). medicines in a pharmacy (ultop, trichopol, mezim, almagel) and started a course of treatment. After 4 days it became easier, but the pain does not go away completely, there is an eructation of air, rumbling in the stomach. I do not eat fatty, spicy, smoked, etc. But I remembered something that I did not tell at the reception of the gastroenterologist. A week before the first pain in the stomach, I had my period (1 day, as always painful). On this day, I had a strong physical load, I strained my abdominal muscles very much (I had to saw off something, I didn’t succeed, I made every effort for a long time). As a result, pains began in my stomach, but not below, but in the middle and above, there was a feeling that I had been hit hard in the stomach and everything was on fire there, even my head was spinning. She attributed all the sensations to menstruation (although the lower abdomen did not hurt) and drank pentalgin, it became better. At this time, I noticed that I can’t lift the bag, the child (the stomach starts to hurt and it’s like the stomach), I can’t even laugh because in the stomach immediately burning, pain, radiates to the stomach, now even homework causes discomfort. Now (on the 6th day of treatment) severe pains have disappeared, but after eating they remained, and in general I feel depressed, bad thoughts about my health come into my head, suddenly something terrible is in me, the doctors just didn’t find it. Tell me, please, 1) is there a connection between the “tear” of the abdomen and gastritis, or are these different diseases and should I tell a gastroenterologist or consult a surgeon or other doctor? annotations to the ultop it is written the need to exclude stomach tumors before starting treatment, is there a chance that the doctor may not detect a tumor with EGD? 4) how long can pain last during treatment and diet with this diagnosis (gastritis). Please answer my questions, thanks in advance.
Doctor's answer: Hello. During physical exertion, muscles hurt, and there may also be problems with the spine. In this case, the pains are reflected in nature and the abdominal area may hurt. The nature of pain in gastritis is different. The tumor is visible on EGDS. The diet is followed for a long time, until complete recovery. Gradually expand the diet of products. For abdominal pain, do not self-medicate. Seek immediate medical attention.
Question: Hello!
Therapist from polycl. quit and need advice. Stomach constantly RUMBLING..
Please advise on preventive treatment, diet and in general how to behave with such conclusions (below).---
Conclusion: Bulboduodenitis. Follicular bulbitis Superficial gastritis
Endoscopic signs of sliding HH. (10/29/2004) -----
Conclusion: Endoscopic signs of HH
Reflux esophagitis stage I Atrophic hyperplastic gastritis. Bultitis. DGR.
(14.04.2005)
Vladimir.
Doctor's answer: Hello. Treatment of gastritis should be comprehensive. Includes diet. Means that reduce the acidity of gastric juice (with hyperacid gastritis), vitamin preparations are used. In the treatment of this disease, it is important to choose the right drugs that protect the gastric mucosa. The diet is developed based on the clinical picture of the underlying disease. Typically based on table #2 or #1. When prescribing treatment, it is necessary to take into account all the features of the clinical picture of the disease. Unfortunately, without examination it is impossible to establish a diagnosis and recommend treatment. You should consult with a gastroenterologist.
Question: For a year and a half, I have been suffering from pain in the abdomen (I feel it under the left rib, closer to the middle of the abdomen.) The pain practically does not depend on food intake, it is constant, sometimes it disappears, but not for long. According to the beginning, they don’t bother me much, when I sleep, I don’t feel it. Sometimes there is a slight heartburn. The chair is different - sometimes normal, sometimes a little disorder. For a year now, I have been feeling a burning sensation of the tongue (on the left side and the tip). I was examined three times (ultrasound of the abdominal organs, endoscopic examination of the stomach, a cardiogram was taken, irrigoscopy, general tests were taken and a biochemical blood test was done). Twice diagnosed moderately severe gastritis, one chronic hyperplastic antral gastritis. Violations from other organs were not revealed, the tests were normal (at least they said so). Gastritis was treated (metronidazole + ranitidine + NEO almagel). She also drank medication to calm the nervous system. There is little sense. The pain was the same as it was. What do you think it could be? The worst comes to mind.
Doctor's answer: Hello. These symptoms can be observed in many diseases - chronic pancreatitis, enterocolitis, gastritis, duodenitis and others. Unfortunately, without examination it is impossible to establish a diagnosis and prescribe treatment. You should consult with a gastroenterologist. If necessary, an additional examination will be carried out, treatment will be prescribed or consultation of other specialists will be recommended.
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Or giant fold gastritis - a disease associated with inflammation of the stomach, a characteristic feature of which is an increase in the cells of the mucous membrane of this organ. The first researcher of her clinical picture in 1888 was the French physician P. E. Menetner, after whom she is named.
Other names for this disease are chronic hypertrophic polyadenomatous gastritis, exudative gastropathy, giant hypertrophic gastritis, excess gastric mucosa, adenopapillomatosis, tumor-like gastritis.
In hypertrophic gastritis, the gastric mucosa thickens.
With this disease, it thickens, its folds reach a height of more than 3 centimeters. Localization of such manifestations is most often in the region of the greater curvature of the stomach.
The hypertrophy of the folds is rarely limited, in many cases the changes affect a large part of the mucosa.
There are fewer chief and parietal cells, and mucus-forming cells increase mucus production and themselves increase in size. As a result, the gastric glands increase in size and turn into cysts. Multiple cysts lead to polyadenomatosis.
Folds of mucous are exposed to focal inflammatory process. The lining of the stomach becomes permeable to gastric juice and protein. When the inflammatory process passes to the vessels of the mucous membrane, gastric bleeding appears.
Reasons for the appearance
Metabolic disorders can be the cause of hypertrophic gastritis.
Insufficiently studied pathology does not make it possible to establish the exact causes of Menetrier's disease. Possible causes of hypertrophic gastritis:
- Metabolic disorders.
- Intoxication with alcohol, nicotine and industrial hazards (lead).
- Lack of vitamins in the diet.
- The consequences of past infections (, dysentery, typhoid fever).
- hereditary factors.
- Hypersensitivity to.
- Anomalies of development at the stage of the embryo.
- Consequences of the inflammatory process of the gastric mucosa.
- The tumor is benign.
For more information about gastritis with mucosal hypertrophy, see the video:
Clinic of the disease
The development of the disease is slow, periods of exacerbation alternate with periods of prolonged remission.
In some patients, the clinic of manifestations of this disease subsides, turning to clinical manifestations, becomes a precancerous condition. Symptoms of giant fold gastritis:
- Pain in the epigastric region after eating, have different duration and intensity.
- Feeling of heaviness and fullness in the stomach.
- Diarrhea, .
- Loss of appetite and a sharp weight loss associated with this symptom (by 10-20 kg), turning into anorexia in advanced cases.
- Peripheral edema due to protein loss.
- Slight stomach bleeding, anemia.
For patients with this type of gastritis, the optimal prevention of relapses will be a timely visit to the doctor, following his recommendations, and regular diagnostic procedures.
Menetrier's disease is a rare inflammatory disease of the stomach, when its mucosa develops excessively, hypertrophies into giant folds. The reasons for this are not well understood, diagnostic methods make it possible to determine an accurate diagnosis and prescribe adequate treatment.
In children, Menetrier's disease is extremely rare, proceeds without complications, responds well to treatment. In adults, complicated forms of the disease that are not amenable to drug therapy lead to surgical intervention.
Even more than 140 years ago, anatomists observed cases of significant thickening of the folds of the gastric mucosa. In 1888, Menetrier described in detail the pathohistological picture of the gastric mucosa in 2 cases of a sharp thickening of its folds: “... the mucosa is a diffuse glandular hyperplasia; extending to a larger or smaller area of the stomach - a sharp hyperplasia of the glands, in some places the expansion of their lumens up to the formation of real cysts, as well as the replacement of the differentiated epithelium with an indifferent one. In subsequent years, descriptions of isolated cases of this pathology periodically appeared in the literature, and only in the last 10-15 years, interest in it has increased significantly; descriptions of patients with gastritis, or Menetrier's disease, as such a condition has recently been designated, have become more frequent. We found in the literature a description of 314 observations treated by the authors as Menetrier's disease. And yet it is currently difficult to give an exact answer to the question of what constitutes this disease. Three main points - the difficulty of diagnosis, the lack of pathohistological evidence in many of the cases described, and the conflicting interpretation by different authors of the histological essence of changes in the gastric mucosa - are the reason for such significant uncertainty in all matters related to the study of Menetrier's disease (statistics, clinic, diagnosis, prognosis and etc.).
In view of the fact that the study of Menetrier's disease is of undoubted interest, from the 314 descriptions of this pathology we collected, we selected 123 observations, confirmed by histological examination, in which the picture was similar to that observed by Menetrier. Among these patients there were 106 men and 17 women (6:1). The age of the patients ranged from 40 to 70 years. Apparently, Menetrier's disease is a rare pathology. Sapkas and Pavaris (1970) emphasize that in their clinic from 1939 to 1966, for 6400 resections of the stomach, produced for various reasons, only 1 case of Menetrier's disease was identified. PV Vlasov (1963) describes 112 observations, however, histological confirmation of the diagnosis is available only in 25 cases.
An analysis of the literature data does not allow us to draw definite conclusions about the etiology of the disease. Menetrier associated the occurrence of the changes in the gastric mucosa described by him with chronic intoxication (in one of the cases he observed, chronic intoxication with lead and alcohol was noted). Scherer et al. (1930) attach importance to hormonal disorders in these changes. The cause of mucosal hyperplasia is explained by sclerosis of the tunica muscularis mucosae, food trauma to "paralyzed mucosa and its reactive hyperplasia." Some researchers believed that "excessive mucosa" occurs as a result of systematic overeating and constant overdistension of the stomach. Although glandular cystic hyperplasia in case of excessive mucosa is usually not accompanied by inflammatory infiltration and sclerotic signs, which are considered characteristic of inflammation, a number of authors still associate the pathogenesis of the disease with inflammation. PV Vlasov believes that the thickening of the folds of the gastric mucosa is due to changes not only in the surface layers of the mucosa, but also in its muscular layer; this author explains the changes noted at the same time by functional and morphological reorganization. Scherer, N. G. Shulyakovskaya, Yu. N. Sokolov and others consider changes in the gastric mucosa as an anomaly in its development. This view, however, is contradicted by the rarity of finding such changes in the stomach in childhood: only 7 cases of Menetrier's disease in children have been described. We also did not find descriptions of the detection of such changes in the mucous membrane among the relatives of patients. Many authors attribute Menetrier's disease to chronic hypertrophic gastritis, Schiindler (1962) defines it as "chronic atrophic proliferative gastritis". N. S. Smirnov (1958) adheres to the view of the polyetiology of Menetrier's disease. A number of authors consider it as an angiomatosis of the gastric mucosa and refer to benign tumors.
The clinical picture of Menetrier's disease is more studied. The most common symptoms of this disease are pain in the epigastric region, observed in 74% of cases, weight loss (60%), vomiting (42%), gastric bleeding (20%), diarrhea (10%).
According to clinical signs, many authors distinguish three variants of the course of Menetrier's disease: dyspeptic, pseudotumor, and, less often, asymptomatic. Indications of the presence of an ulcer-like variant of the disease need to be verified: in many cases, with careful examination in such patients, it is possible to detect a peptic ulcer, usually in the duodenal bulb. Anemia and hypoproteinemia are rare. Hypoproteinemia was previously considered one of the characteristic symptoms of the disease and was explained by the loss of protein from gastric juice. However, P. V. Vlasov (1963) comes to the fair conclusion that the data on the frequency of hypoproteinemia in this disease cited in the literature are overestimated, since usually the authors studied the content of protein and protein fractions of serum only in cases where there were clinical signs of hypoproteinemia (edema and etc.). So, Keppeu (1930) observed 20 patients with Menetrier's gastritis, however, the study of blood serum proteins was carried out only in 6 cases - in patients with obvious edema. Hypoalbuminemia (albumin content 1-3.1 g%) was revealed in 5 of them. A number of researchers have studied the exchange of albumin in patients with hypertrophic gastritis of the Menetrier type using radioactive iodine. None of the examined patients had hypoalbuminemia. However, the rate of albumin catabolism, as measured by 1311 labeled albumin, was increased. Subtotal gastrectomy was accompanied by a marked decrease in the fractional catabolic rate of albumin.
Opinions of authors about gastric secretion relatively coincide. Most emphasize a decrease in the concentration and secretion of hydrochloric acid, an increase in primary alkalinity and mainly in the buffering capacity of gastric juice. Charles et al. (1963) explain the absence of free hydrochloric acid by a combination of edema with an inflammatory reaction that prevents the passage of this acid into the stomach cavity. Other authors explain these changes by the presence in the gastric juice of the patient of a large amount of protein (albumin, gamma globulin), mucus, as well as metaplasia of the epithelium of the glands (replacement of the main and parietal cells with mucoid ones). It should be noted that some authors describe cases of Menetrier's disease with a high content of hydrochloric acid in the gastric juice, however, histological confirmation of the diagnosis in such cases, as a rule, is absent.
X-ray examination usually reveals in the region of the body of the stomach and, less often, in the subcardial region, local or diffuse thickening of the folds, which are dense, rigid, difficult to palpate. Tortuosity, uneven relief, deformation of the folds can give the impression of their breakage, the presence of filling defects that are observed in malignant tumors. More accurate information is given by parietography, which consists in the imposition of pneumoperitoneum and the introduction of 300-400 ml of air into the stomach cavity, followed by "impregnation" of the mucous membrane with barium sulfate. Parietography allows not only to determine the wall thickness and contours of the stomach, but also to study in detail the relief of the mucous membrane. Parietography should be performed in all cases where Menetrier's disease and gastric neoplasms are suspected, if the diagnosis remains unclear after plain x-ray examination.
By the method of gastroscopy, Menetrier's disease is diagnosed 2-3 times more accurately; the use of flexible gastrofibroscopes helps to obtain additional data for differential diagnosis with other types of diseases accompanied by thickening of the folds of the gastric mucosa.
Summarizing our gastrofibroscopic observations and comparing them with those described in the literature, it can be noted that the endoscopic picture of Menetrier's disease is characterized by sharply thickened "brain-shaped" folds of the gastric mucosa, which often take the form of a "cobblestone pavement", look pale, edematous or have a normal color, and sometimes intense red. The mucous membrane is easily vulnerable, often erosions are detected along the tops of the folds. With simultaneous instrumental "palpation" and additional introduction of air, some elasticity of the folds is noted.
Gastroscopic diagnosis is difficult if the mucous membrane is hypertrophied locally, swells into the lumen of the stomach in the form of a dark red limited "tumor", sometimes covered with ulcers, erosions. In these cases, it is impossible to exclude carcinoma or lymphosarcoma. It is possible to clarify the diagnosis after a histological examination of the targeted biopsy material, and in some cases only after a pathohistological examination of the entire thickness of the gastric wall during diagnostic laparotomy.
It should be noted that in the assessment of the gastroscopic picture in Menetrier's disease, there is a certain subjectivity, since during the study, an arbitrary amount of air is usually introduced into the stomach cavity, which causes a different degree of stretching of the gastric folds, and consequently, a different picture of the gastric mucosa during the study. In addition, factors such as the size of the stomach cavity, the elasticity of its walls, the tone of the abdominal press, the functional efficiency of the cardiac and pyloric sphincters are of no small importance. Jamada et al. (1972) consider it necessary in case of a gastroscopic picture of "giant folds" to produce a dosed inflation of the stomach, introducing 1700 ml of air or more into it, while in the stomach a pressure of at least 15 mm Hg is reached, sufficient to straighten the normal folds of the mucous membrane; with Menetrier's disease, the "giant" folds of the mucosa do not straighten out.
A targeted biopsy, unfortunately, has no diagnostic value in Menetrier's disease, since the biopsy device allows you to take pieces for research only from the most superficial part of the mucous membrane; altered glands of the gastric mucosa usually do not enter the drug. Therefore, targeted biopsy in diagnostically difficult cases is used not so much to clarify the diagnosis of Menetrier's disease, but as a method to identify the tumor (with the exception of cases of its submucosal growth). The method of aspiration biopsy makes it possible to obtain large areas of the mucous membrane for histological examination, including often those layers where the gastric glands end, which in some cases allows histological confirmation of Menetrier's disease, but as a "blind" biopsy method, it gives a significant percentage of errors due to taking biopsy material not from those areas where a pathological process is expected.
In cases where it is not possible to immediately establish an accurate diagnosis based on clinical data and examination results, it is necessary either to re-examine the patient after 1-1.5 months with an assessment of the dynamics of the process, or immediately perform a trial laparotomy so as not to miss a stomach tumor (differential diagnosis between the disease Menetria and gastric cancer in many cases is extremely difficult). An operative biopsy makes it possible to take sections of the stomach wall of sufficient size for examination and, therefore, provides an accurate diagnosis.
There are also many conflicting interpretations regarding the course, prognosis and treatment of the disease. Most foreign researchers indicate the need for surgical intervention. In their opinion, the only method of treatment is total gastrectomy, since even after subtotal resection of the stomach, relapses of the disease are possible. Gastrectomy in cases with severe disorders of protein metabolism can also eliminate hypoproteinemia caused by damage to the gastric mucosa. The opinion about the expediency of gastrectomy in Menetrier's disease is also confirmed by observations of a significant incidence of gastric cancer in such patients. For example, Martini et al. (1962) noted that out of 155 descriptions of Menetrier's disease found in the literature in 10% of cases, gastric cancer was observed or developed subsequently (among the entire population, the frequency of gastric cancer is 0.5-2%). AV Melnikov (1953) considers it possible to monitor patients only for 2-3 months, and then it is necessary to raise the question of the operation. L. K. Sokolov (1964), Ts. G. Masevich (1969) refer Menetrier's disease to precancerous diseases of the stomach. However, Cabanne et al. (1970) indicate that in some cases, in the absence of severe symptoms of the disease, there is no need for a mandatory operation, provided that a systematic x-ray and gastroscopic examination of patients is carried out in order to timely detect a cancerous tumor if it occurs. Frank and Kern (1967) observed a case of Menetrier's disease for 8 years without resorting to surgical intervention. At first, the patient had giant gastric folds, severe hypoproteinemia, and a large loss of serum albumin from the gastric mucosa. After 5 years, hypertrophic gastritis began to regress and atrophy of the gastric mucosa was revealed. The edema disappeared, the content of serum albumin returned to normal, the patient did not complain. The content of protein in the gastric juice did not exceed the norm.
Our work was based on observations of 110 patients referred to the clinic with a diagnosis of hypertrophic gastritis in 1971-1974. A thorough examination made it possible to establish giant hypertrophic gastritis in 36 patients. All patients underwent studies: general clinical, targeted X-ray with a mandatory multi-axial study of the relief and contours of a tightly filled stomach on a series of sighting images, endoscopic with the use of dosed inflation of the stomach cavity with air according to the Yamada scheme modified by us, determination of the amount of protein and pepsin in the gastric contents, study of secretory function stomach by methods of intragastric pH-metry and fractional sounding with the use of submaximal stimulation with histamine, determination of the hourly tension of secretion and debit-hour of free hydrochloric acid, as well as the study of motor activity of the stomach by electrogastrographic and balloon kymographic methods.
For the purpose of differential diagnosis with other diseases, primarily with tumors of the stomach, as well as to clarify the diagnostic value of oral biopsy methods (aiming through the gastrofibroscope channel and aspiration) in this pathology, the histograms obtained by these methods were studied and the results were compared. Based on the data literature, according to which, until now, histological confirmation of Menetrier's giant hypertrophic gastritis by oral biopsy is not always possible, and dynamic observation is of primary importance, we re-examined 21 patients who were in our clinic in 1963-1964 for this disease. was carried out, in addition, for all 36 patients with a confirmed diagnosis of giant hypertrophic gastritis Menetrier.
The age of the patients with giant hypertrophic gastritis examined by us ranged from 20 to 67 years; the majority (34) were aged 30-50; of them 26 men, 10 women, (3:1). Given the variety of factors that may play a role in the etiology and pathogenesis of Menetrier type gastritis, we carefully analyzed the living conditions of patients, identified their bad habits, past and concomitant diseases. In the anamnesis of the surveyed diseases of the gastrointestinal tract and various infections prevailed. Typhoid fever suffered 7 patients, Botkin's disease - 2, dysentery - 2, malaria - 1 patient; 4 Menetrier's diseases were accompanied by polyposis of the rectum. It should be noted the frequent combination of several concomitant diseases: their number (65) exceeded the number of observations (36).
Possible etiological factors include smoking (21 patients), irregular diet (18), infections (16). food poisoning (13). Frequent intake of excessive amounts of alcohol was noted in 5 patients, medications - in 2.
A thorough study of the anamnesis of our patients made it possible to establish that, due to the difficulty of differential diagnosis with polypoid cancer and lymphosarcoma, 21 patients (out of 36) were examined in oncological or surgical institutions before admission to the clinic; 6 of them were operated on with suspected gastric tumor. We did not observe family cases of the disease; The first symptoms of the disease appeared already at the age of over 20 years.
Development of archival material of the clinic of propaedeutics, internal diseases of the I Moscow Medical Institute. I. M. Sechenova for 10 years showed that Menetrier's giant hypertrophic gastritis is a rather rare pathology. According to our data, the ratio of the number of patients with this pathology to the total number of those on treatment is 1: 1178, to patients with stomach diseases - 1: 342. gastritis - 1: 150, hypertrophic gastritis - 1: 10.
The study of the clinical symptoms of giant hypertrophic gastritis showed that most of the data obtained during an objective examination of patients with this pathology are also found in other diseases of the abdominal organs, so a correct diagnosis is possible only by comparing complaints, anamnesis and objective results.
Depending on the originality of clinical symptoms, we identified three groups of patients. Most often (16 patients); a “pseudotumor-like” type of disease was observed, characterized by aching pains in the epigastric region, a feeling of heaviness, fullness in the abdomen, weight loss, loss of appetite, fatigue, and weakness. Less common were "dyspeptic" (10 patients) and "dyskinetic" (9 patients), i.e., occurring with symptoms of intestinal dyskinesia, types of the disease. The asymptomatic course of the disease was exceptionally rare. When comparing the morphological changes in the mucous membrane in different clinical groups, we did not reveal any clearly defined pattern.
The hourly tension of basal secretion in 12 examined patients was significantly reduced (less than 50 ml/h) and only in 6 exceeded it (101-150 ml/h), which may have been due to the nature of concomitant diseases (2 patients had peptic ulcer with localization of the process in duodenal bulb). Indicators of hourly tension of secretion after histamine stimulation were reduced in 11 patients, remained within the normal range in 14 patients, and slightly exceeded the norm in 11 patients.
In the study of the basal flow rate of free hydrochloric acid, its significant decrease was noted in 35 patients, and in 23 this indicator was 0, in 11 it did not exceed 1 meq/h and in 1 it was 2.64 meq/h. Debit-hour of free hydrochloric acid after histamine stimulation was below normal in all cases; its maximum level was 10.3 meq/h. In the study of secretion by intragastric pH-metry, a persistent decrease in secretory function was detected in 22 cases (in 12 cases pH> 6.0, in 10 cases it was 3.0), in 5 cases a moderate decrease in acidity was noted (pH 3.7 ± 0, 1) and in 7 - normacid state; only in 2 cases hypersecretion was detected (pH< 1,0). У 30 больных содержание пепсина было менее 21 мг% (у 6 - в пределах 10-23 мг%, у 14 - менее 10мг%, у 9 -менее 1 мг%, у 1 больного - 0), у 4 больных оно было нормальным и лишь у 2 - повышенным.
Quantitative determination of protein in gastric contents was carried out by the biuret method, similar to the determination in blood serum. If the normal content of protein in the gastric contents is, according to various authors, from 6-10 mg% to 280 mg%, then in most of our patients a clear increase was noted. Thus, in 23 examined patients, the protein content in gastric juice was 280-715 mg%, and in 7 - from 280 to 350 mg%, in 13 - from 360 to 600 mg% and in 3 - from 610 to 715 mg%. Only in 13 patients, the protein content in the gastric contents did not exceed the norm. From all of the above, it follows that this pathology is characterized by a significant decrease in the acid- and pepsin-forming functions of the stomach. Along with this, most patients showed an increase in the amount of protein and mucus in the gastric contents.
X-ray examination is of great importance in the diagnosis of giant hypertrophic gastritis. However, at the first fluoroscopy, it is far from always possible to find out and correctly assess the nature of changes in the gastric mucosa. The first errors occur during X-ray examination, when the picture of coarse thickening of the folds is often mistaken for polyposis or even cancer. However, with a purposeful and methodically correctly conducted x-ray examination, its reliability is significantly increased. X-ray examination of patients was carried out by us on diagnostic X-ray machines and on an X-ray television installation equipped with an electron-optical amplifier. With the help of this method, pronounced hyperplasia of the gastric mucosa by the type of excess was detected in 41 patients. Thus, overdiagnosis occurred only in 5 cases during the examination of 110 patients who were referred with a diagnosis of hypertrophic gastritis established in various medical institutions during a conventional X-ray examination.
To clarify the X-ray semiotics of Menetrier's disease, to determine the significance of this method in making a diagnosis, as well as for the purpose of dynamic monitoring of 36 patients with a confirmed diagnosis, X-ray examination was repeated after 3, 6 and 12 months. It was established that in terms of prevalence, the process was predominantly diffuse in nature (32 cases) and was localized along the greater curvature of the stomach: the body of the stomach was involved in the process in 12 cases, the body and sinus - in 7, the sinus - in 6, the upper and middle third - in 4 , upper third - in 3 cases. Scalloped and serrated contours of the greater curvature, most common in excess gastric mucosa, were found in 20 patients; in 8, rough thickened folds of the mucosa gave the impression of filling defects, which, however, straightened out during the study; in the remaining patients, the contours of the stomach remained smooth, unchanged. In 12 patients, the initial x-ray examination failed to exclude a tumor, which necessitated a second study after a course of anti-inflammatory therapy and repeated endoscopy. In 4 patients, a localized form of Menetrier's disease was detected, which presented especially great difficulties for differential diagnosis with a cancerous tumor of the stomach.
Our observations confirm that with a targeted x-ray examination, the accuracy of diagnosis is much higher. So, with a conventional X-ray examination, the diagnosis turned out to be correct in 32.7% of cases (all 110 patients were referred with an X-ray conclusion about mucosal hyperplasia, and giant hypertrophic gastritis was established only in 36), with a targeted one - in 87.8%.
The radiographic picture of the local lesion is very characteristic. More often, the body of the stomach at the greater curvature is selectively affected (Fig. 5 and 6). The folds of the mucous membrane in a limited area are sharply thickened, tortuous, but their location retains a certain rhythm, there is no break in the folds of the mucous membrane, they are elastic. The wall of the stomach, corresponding to the lesion of the mucous membrane, is elastic, peristalsis is clearly visible. In other parts of the stomach, the relief of the mucosa may not be changed (Fig. 7). In the affected area, the folds of the mucous membrane can be so hypertrophied that they create a filling defect when the stomach is tightly filled with barium suspension and mimic the picture of a tumor lesion. Despite such a vivid and seemingly very characteristic picture, in some cases it is necessary to carry out a differential diagnosis with a tumor process in the stomach (cancer, sarcoma, hemangioma). In such cases, it is advisable to repeat the study after a course of anti-inflammatory therapy. However, sometimes clarification of the nature of the lesion requires the use of the pneumogastrography technique described above with the introduction of air and barium suspension through a probe.
The widespread or diffuse form is less common and is also characterized by a bright x-ray picture: the folds of the mucous membrane are thickened, tortuous, edematous, the interfold spaces are expanded in all parts of the stomach. However, its walls retain elasticity, peristalsis is clearly visible along both curvatures. When the stomach is stretched with an additional portion of barium suspension, and sometimes two, as well as in the study after taking breakfast, it is possible to see how the mucosal folds are stretched, the volume of the stomach increases. This makes it possible to differentiate the diffuse form of Menetrier's disease with a "frozen" relief of the mucous membrane with submucosal spread of the tumor process. However, the exact diagnosis of this form of Menetrier's disease is not always easy and it has to be differentiated from non-epithelial tumors of the stomach, as well as from its defeat in lymphogranulomatosis.
All 110 patients underwent gastrofibroscopic examination. 5 patients with localization of the process in the upper part of the stomach additionally underwent a study of the mucous membrane of the upper part of the stomach using an esophagofibroscope. In 47 patients, the study was carried out many times (2-4 times) for the purpose of dynamic observation and in terms of differential diagnosis. Endoscopic examination made it possible to establish Menetrier's disease in 36 patients, in 20 - the phenomena of banal chronic gastritis, in 17 patients - a picture of moderate hyperplasia of the mucous membrane (the folds were easily straightened by air), in 12 the mucous membrane was normal. Changes characteristic of peptic ulcer disease were detected in 12 patients, in 6 - a tumor lesion of the stomach, in 3 - polyposis, in 1 - an isolated lesion of the stomach with reticulosarcoma. The final differential diagnosis of Menetrier's disease with a tumor lesion of the stomach could not be carried out in 2 patients (this was the reason for the surgical intervention) and in 1 patient the endoscopic picture of the gastric mucosa indicated pronounced hyperplasia, and subsequently hemangioma was diagnosed during the operation.
To date, there are no clear criteria to distinguish between various forms of hypertrophic gastritis. Diagnosis is aided by endoscopic examination using the method of dosed inflation of the stomach with air, with the help of which it is possible to control intragastric pressure at a certain level and objectify the results. We attributed to giant folds those that did not straighten out at a pressure in the stomach of more than 15 mm Hg. Art. These data have pathological confirmation. The endoscopic picture of giant hypertrophic gastritis is characterized by the presence of sharply thickened mucosal folds in the body of the stomach along the greater curvature, taking the form of cerebral convolutions or "cobblestone pavement", their slight vulnerability, erosions, hemorrhages, and a large amount of mucus were often found. More often, the folds were located in parallel, less often - transversely or chaotically, the degree of their hypertrophy in all cases was at least 2-3 cm. thickened (2) and significantly thickened folds hanging into the lumen of the stomach (1). Our observations showed the predominance of the diffuse form of giant hypertrophic gastritis and the absence of damage to the mucous membrane of the antrum in this disease.
For the purpose of differential diagnosis of Menetrier's disease with various diseases (usual hypertrophic gastritis, polyposis, polypoid cancer, familial polyposis, Peutz-Touraine-Jeghers syndromes, Cronkhite-Canada), we studied histological material obtained by targeted (endoscopic) gastrobiopsy and by aspiration biopsy. We also studied the data of surgical gastrobiopsy in patients operated on for a suspected neoplasm, which was difficult to exclude during examination, and Menetrier's disease was diagnosed during gastrotomy. A total of 164 histological preparations were studied.
Histological examination of the material taken by the method of targeted and aspiration biopsy, in no case revealed the characteristic features of Menetrier's gastritis, and the histological picture of the mucous membrane was varied: from normal to characteristic of various forms of gastritis (in 20 patients - atrophic, in 7 - superficial, in 5 - a picture of normal mucosa, in 4 - it was not possible to judge the nature of the changes due to unsuccessful biopsy taking). The picture characteristic of Menetrier's gastritis was revealed only by studying the histograms obtained by the method of surgical biopsy. However, targeted gastrofibrobiopsy proved to be very valuable in the differential diagnosis of this pathology with tumor lesions of the stomach: it made it possible to exclude the blastomatous process in 15 cases and to detect it in a timely manner - in 2.
During the dynamic observation of our patients, the relative constancy of the data was noted, although the results of longer observations indicate their lability. Dynamic examination of 21 patients who were under observation in the clinic in 1963-1964. with a diagnosis of tumor-like gastritis, confirmed the diagnosis in 2 patients. In 7 patients, the gastric mucosa was of a normal appearance, 5 had peptic ulcer, 3 had often pronounced hypertrophy of the mucosa, 2 had gastric cancer, and 2 had atrophic gastritis. Thus, our observations have shown that the diagnosis of Menetrier's gastritis should be based on a comprehensive examination of patients, including the most modern diagnostic methods (X-ray television, gastrofibroskonia with targeted biopsy). The leading diagnostic method is endoscopic using the method of dosed inflation of the stomach cavity with air, the auxiliary one is the study of secretory function.
The prognosis of the disease is relatively favorable. This is evidenced by the long-term remissions observed in our patients during dynamic observation and the duration of the disease from 10 to 33 years. In the vast majority of patients with Menetrier's giant hypertrophic gastritis, the disease proceeded for a long time, more or less monotonously.
The observations showed that patients with Menetrier's gastritis need dynamic monitoring (at least 2 examinations per year) with mandatory X-ray endoscopic control, which allows timely detection of cases of malignant degeneration, as well as avoiding unreasonable surgical intervention. Subject to systematic dispensary observation, patients with Menetrier's gastritis can be treated conservatively. In therapeutic measures, compliance with a sparing diet and the periodic use of drugs that have an astringent and enveloping effect, metabolic agents, and replacement therapy are of primary importance.
The need for surgical intervention may be caused by the presence of severe bleeding, refractory hypoproteinemia, pain, and uncertainty in the diagnosis, especially in cases of local forms of the disease.
Recently, there have been reports in the literature about the effectiveness of long-term treatment of Menetrier's disease with high doses of the anticholinergic drug - propaneline bromide, antifibrinolytic agents, cimetidine, but these data need further verification.
The main indications for diagnostic gastroduodenoscopy are the following symptoms:
recurrent vomiting;
Recurrent and chronic abdominal pain;
Gastrointestinal bleeding.
In the structure of morbidity of the digestive system, gastritis occupies the first place. Among diseases of the stomach, it is 60-85%.
Chronic gastritis is a clinical and anatomical concept, characterized by certain pathomorphological changes in the gastric mucosa - a nonspecific inflammatory process. Currently adhere to the following endoscopic classification:
superficial gastritis,
atrophic gastritis,
hypertrophic gastritis,
mixed gastritis,
Hemorrhagic gastritis.
Any of these forms of gastritis can be limited (localized) or widespread (generalized).
With superficial gastritis, the gastric mucosa is edematous, shiny from an excess amount of mucus, with areas of diffuse, moderately pronounced hyperemia and intramucosal hemorrhages. Often on the mucous membrane there are fibrin overlays and microrelief changes. In patients with concomitant duoditgastric reflux, the gastric mucosa is pasty, diffusely bright red with bile staining and mucous overlays. As a result of inflammatory edema, the gastric fields flatten, the gastric pits are compressed, and the grooves between the gastric fields are filled with exudate and fibrin, becoming small and narrow. As a result, the microrelief of the gastric mucosa acquires a peculiar appearance: delicate light fibrin overlays border the bright pink gastric fields. In the remission phase, the endoscopic picture changes somewhat: edema and pastosity decrease or disappear, the mucous membrane turns pale.
Atrophic gastritis is more often observed in elderly and senile people. Changes in the gastric mucosa may be focal or diffuse. With a generalized form of atrophic gastritis, the mucous membrane is pale gray, dull, smooth; its folds are weakly expressed and mainly along the greater curvature of the stomach in the upper section. The folds are low, easily straightened with air insufflation. The mucous membrane is thinned, through it the vessels lying in the submucosal layer are clearly visible. With a focal form of atrophic gastritis, it has a spotty appearance. Against the background of normal preserved areas, there are foci of atrophy of the mucous membrane of a rounded shape of a grayish-white color. In some places, on the contrary, foci of hyperplasia of the mucous membrane can occur.
Often, gastroscopy reveals areas characteristic of superficial and atrophic gastritis. In such cases, we are talking about mixed gastritis.
Hypertrophic gastritis is characterized by large, wide, rigid folds of the gastric mucosa, closely adjacent to each other and poorly straightened with air insufflation. The microrelief of the folds is uneven, bumpy, as a result of proliferation, it can be granular (granular gastritis - the mucous membrane takes the form of a cobblestone pavement), warty (warty gastritis - in the form of larger grains or papillae located separately from each other), and pump-like gastritis - with the presence of pump-like formations.
Convoluted, wide, covered with thick mucus, uneven folds of the mucous membrane resemble the cerebral gyrus or cobblestone pavement. Such changes in the mucous membrane can be observed both in limited areas and throughout. In the literature, hypertrophic gastritis is known under various names: Menetrier's disease, rigid, hyperplastic, tumor-like gastritis.
Most often, these formations are located in the antrum and distal body of the stomach. X-ray picture in hypertrophic gastritis used to be taken for cancer. Endoscopic and morphological examination makes it possible to exclude such errors in clinical practice.
Hemorrhagic gastritis develops under the influence of various factors of a general and local order (stress, severe infection and other toxic diseases, mechanical irritation of the gastric mucosa, damage to it by drugs).
The endoscopic picture of hemorrhagic gastritis is characterized by all the signs of superficial gastritis, but more pronounced. In some cases, in the mucous membrane and submucosal layer with hemorrhagic gastritis, hemorrhages are observed in the form of non-techial rashes, in others, numerous traces of injections are found. Erosions can be large (0.2-0.5 cm in diameter) and of various shapes, bordered by a narrow strip of hyperemia, covered with a coating of different shades (gray, brown, brown).
At the height of bleeding, the mucous membrane appears to be strongly edematous, bleeding. When washed with a stream of water, it is cleansed, and then again covered with blood. At the end of the acute period of bleeding, the endoscopic picture is characterized by the presence of inflammatory changes - edema and hyperemia of the mucous membrane, a large amount of viscous mucus. Usually, erosion of the gastric mucosa is a defect in the epithelium of a rounded shape, 1-5 mm in diameter, it may also have an irregular shape, covered with a grayish or hemorrhagic coating, bordered by a halo of hyperemic mucous membrane.
There are also "complete" or "chronic" erosions (warty erosive gastritis, pox-like gastritis). "Complete" erosions are single and multiple, they do not disappear for many months and even years, they are difficult to treat. "Complete" erosions are called a superficial defect of the mucous membrane with the presence of an inflammatory shaft that raises the erosive surface above the surrounding mucosa. The sizes of "full" erosions range from 0.5 to 1.0 cm. They are most often located on the tops of the folds of the mucous membrane and are most clearly detected when the folds are straightened, achieved by air insufflation into the stomach. All patients with "complete" erosions morphologically show signs of gastritis, mostly superficial.
Sometimes erosions reach large sizes, and it is not possible to differentiate them visually from acute ulcers. It is likely that in such cases it is possible to observe the stage of acute ulceration.
Acute ulcers occur in people of all age groups, but more often in elderly and senile patients, who, as a rule, suffer from numerous concomitant diseases of the cardiovascular and respiratory systems. Acute ulcers are divided into flat and crater-shaped, but this division is conditional, since the same ulcer can turn from superficial to deep within 2-3 days and vice versa. Acute gastric ulcers can be single or multiple, often combined with erosions.
Chronic ulcers (benign) are localized mainly on the lesser curvature of the stomach in the antrum at the level of the angle, in the prepyloric region, less often in the pylorus and subcardiac and cardiac regions. The endoscopic picture of a chronic gastric ulcer is characteristic, but very variegated and depends on the stage of the disease, the localization of the ulcer, the duration of the process, the frequency of exacerbations, etc.
In the acute stage, chronic gastric ulcers are usually round or oval. Its edges are even, sometimes undermined, often rise above the surrounding mucous membrane as a result of inflammatory edema.
The depth of the ulcer is different - from superficial to penetrating through all layers of the stomach wall. The ulcerated surface is called the bottom of the ulcer, which is represented by necrotic or granulation tissue, has fibrin overlays. More often the bottom is painted yellowish, sometimes gray. When an ulcer is complicated by bleeding, the bottom, in whole or in separate fragments, is covered with dark brown hemorrhagic overlays or fixed blood clots. In a chronic ulcer, the mucous membrane surrounding it is hyperemic, edematous, easily injured.
There are also indirect signs of an ulcer of the gastric mucosa, which are not pathognomotic, but contribute to the correct diagnosis. These are signs such as the presence in the stomach of an increased amount of secretion, sometimes cloudy with an admixture of greenish (stale) bile, multiple petechiae, a pronounced gag reflex, and active peristalsis. All this (together with the data of the anamnesis) serves as a reason for a more thorough search for the cause of the disease. The ulcer can be detected either in the region of the cardia on the back wall, or at the corner of the stomach, using the technique of inversion endoscopy, increasing air insufflation.
In the process of ulcer healing, the visual characteristics of the ulcer itself and the surrounding mucosa change. Gradually, inflammation around the ulcer decreases, edema and hyperemia of the mucous membrane disappear, fibrin deposits disappear, the amount of contents in the stomach decreases and its character changes. The stomach becomes "cleaner", peristalsis - less violent. Against this background, the patient's well-being improves, pain stops, sleep normalizes. The ulcer changes shape, becomes oblong, its bottom is cleared, covered with granulation tissue (sometimes in the form of islets), scarring and epithelization of the ulcer occurs. Depending on the size and depth of the ulcer, signs of deformation of the stomach wall appear during the healing process with convergence to the scar of the folds of the mucous membrane, shortening of the lesser curvature, narrowing of the pylorus and a change in its shape. It should be remembered that even in the absence of a tendency to heal, the visual picture of gastric ulcer (and duodenal ulcer) during each study (no matter how often they are repeated) is different. Therefore, one should not be surprised when completely new data are recorded in the protocol of endoscopic examination of the same patient, especially when examined by another doctor.
According to observations, in 7% of patients suffering from chronic gastric ulcer, ulcer malignancy occurs.
Endoscopy also makes it possible to diagnose various neoplasms, both benign and malignant. The duplicating diagnostic method is fluoroscopic. The advantage of endoscopy over X-ray diagnostics in this case is obvious and lies in the possibility of histological examination of biopsy material.
Benign gastric tumors are of epithelial origin (adenomatous polyps) and non-epithelial origin, which, in turn, are divided into mesenchymal (lipomas, liomyomas, neurinomas) and endothelial (hemangiomas, endotheliomas).
The most common among benign tumors of the stomach are adenomatous polyps, the growth and development of which occurs mainly due to the mucous membrane. They can be single (solitary) and multiple. When there are many polyps and they are located in all parts of the stomach, they speak of total polyposis. There are polyps of cylindrical, pear-shaped, spherical and other shapes, their sizes range from 0.3 to 5 cm or more. Their surface is smooth, sometimes granular. In some cases, polyps consist of many lobules, in others they have a villous structure. Distinguish the base, leg, body and top of the polyp. The base can be wide, and the length of the legs is different.
If a polyp with a long stalk is located near the cardia or pylorus, it may prolapse into the esophagus or into the duodenum or infringement. Such polyps are often subjected to mechanical trauma, ulcerate, and cause bleeding. The mucous membrane over benign adenomatous polyps is usually with atrophic changes. The presence of ulceration, proliferation of the mucous membrane, a change in its color, the appearance of inflammatory processes make it possible to suspect the degeneration of the polyp, its malignancy.
There are no pathognomonic clinical symptoms of gastric polyposis. The observed symptoms are mostly due not to the presence of polyps, but to concomitant diseases (gastritis, cholecystitis, etc.). Basically, these are aching pains in the abdomen without a specific localization, stool disorders, loss of appetite. These patients often present with gastrointestinal bleeding.
Practice shows that today one hundred percent diagnosis of polyps of those parts of the digestive tract that can be examined visually with an endoscope is possible.
However, the problem of timely diagnosis of polyposis can be successfully solved only if endoscopy is used in the clinic, with mass preventive endoscopic examinations.
Other benign tumors of the stomach (more often mimyoma, less often lipoma, nevranoma, etc.) are usually located in the submucosal layer, covered with unchanged mucous membrane, have a spherical shape on a broad base protruding into the lumen of the stomach. The tumor is inactive; when examined with a probe, it appears to be malelastic. It is not possible to capture such a tumor with its significant size with a loop for removal, as is done with a polyp. Above such a tumor, the mucous membrane is atrophic, sometimes with areas of ulceration, hyperemia, and fibrin overlays. In rare cases, there is bleeding into the lumen of the stomach. An important result of the biopsy is the absence of indications for the presence of signs of a malignant tumor.
Of the malignant tumors of the stomach, cancer is the most commonly diagnosed. Its early diagnosis is important. Clinicians began to detect early gastric cancer more often due to the widespread use of fabroendoscopes, since radiological diagnosis in such cases is unusually difficult.
A decisive role in the diagnosis of early cancer is played by the histological examination of biopsy material, for this it is necessary to conduct multiple biopsies (5-10 biopsies) or the so-called loop biopsy, which allows obtaining material for research ten times larger than with conventional endoscopic biopsy.
The diagnosis of stage I-II cancer is finally established only after surgery and histological examination of the macropreparation. Before surgery, in the vast majority of cases, early cancer can only be suspected. An exception to this rule are gastric polyps, which are removed using an endoscope without laparotomy, and the prevalence of malignant growth is determined by subsequent morphological examination.
The endoscopic semiotics of cancer is diverse. In the vast majority of cases, endoscopic detection of gastric cancer on the basis of visual data is easy. This is explained primarily by the fact that diagnosis is usually carried out in the later stages of the disease. Visually, cancer is often represented by a spherical tumor protruding into the lumen of the stomach on a wide base, the surface of which can be smooth, bumpy with or without ulcerations of various shapes and sizes. Such a tumor can reach 7-8 cm. Single or multiple, it does not occupy large areas of the stomach and belongs to the polypoid form of cancer. The color of the tumor usually differs from the unchanged mucous membrane and may be light pink, dirty gray with a yellowish tint, or even red. This tumor is most often located in the antrum of the stomach.
Often, gastric cancer is a deep ulceration (non-infiltrative cancerous ulcer) of irregular shape with jagged edges and with a shaft of uneven width, height and color that rises above the adjacent mucous membrane. The ulcer reaches 3 4 cm and more. The ulcerated surface of such an ulcer with raised, irregularly shaped edges turned outward from the ulcer resembles the shape of a bowl or saucer - a “saucer-shaped tumor”. Its edges are easily injured, moderately bleed and are devoid of elasticity, rigid, easily crumble.
More often it is necessary to meet with an infaltrative cancerous ulcer. This form of cancer is a more mature tumor with a bumpy bottom and different colors. It is more correct to say that an ulcer or multiple ulcerations are located on a cancerous tumor that infiltrates the wall of the stomach in the form of a bumpy massive formation without clear boundaries. The mucous membrane adjacent to the tumor is rigid, devoid of the usual structure, inelastic, immobile, bleeding on biopsy, there is no peristalsis, and does not straighten out with air insufflation.
Malignant tumors of the stomach of non-epithelial origin (sarcoma, localized forms of reticulosis, etc.) are rare, but it is impossible to visually distinguish them from a cancerous tumor. In this regard, targeted biopsy is of decisive importance, without which it is also impossible to differentiate cancer and ulcers of a specific genesis (tuberculosis, syphilis, etc.).
Rare gastric diseases diagnosed during gastroscopy include gastric varicose veins and diverticulosis. Varicose veins of the stomach, like the veins of the esophagus, are a consequence of portal hypertension. The localization of the process is the cardial part of the stomach, mainly on the lesser curvature. Their classification and endoscopic signs are the same as for varicose veins of the esophagus. More often, varicose veins of the stomach and esophagus are combined, but an isolated lesion of the cardiac part of the stomach can also occur. These veins are a source of intense gastric bleeding.
Diverticula are located in any of the departments of the stomach, but more often at the weekend. Endoscopic diagnosis of gastric diverticulum requires experience. The illusion of additional exit from the stomach or fistula is visually created. Ulceration of the mucosa (diverticulitis with ulceration or peptic ulcer) may form in or near the diverticulum.