Standard treatment for gastric ulcer. Peptic ulcer of the stomach and duodenum. Clinical protocol. Examination of feces for occult blood


Modern methods of treating duodenal ulcer

Standards for the treatment of duodenal ulcer
Treatment protocols for duodenal ulcer

Standards for the treatment of duodenal ulcer
Treatment protocols for duodenal ulcer

Duodenal ulcer

Profile: therapeutic.
Treatment stage: hospital
Purpose of the stage:
Eradication of H. pylori. "Relief (suppression) of active inflammation in the mucous membrane of the stomach and duodenum.
Healing of ulcerative defect.
Achieving stable remission.
Prevention of complications.
Duration of treatment: 12 days

ICD codes:
K25 Stomach ulcer
K26 Duodenal ulcer
K27 Peptic ulcer of unspecified localization
K28.3 Acute gastroduodenal ulcer without bleeding or perforation
K28.7 Gastroduodenal ulcer, chronic without bleeding or perforation
K28.9 Gastroduodenal ulcer, not specified as acute or chronic, without bleeding or perforation.

Definition: Peptic ulcer disease is a chronic recurrent disease, the main morphological substrate of which is an ulcerative defect in the stomach, 12 intestines or proximal jejunum, with frequent involvement in the pathological process of other organs of the digestive system and the development of various complications.
The etiological factor is Helicobacter pylori - a gram-negative spiral-shaped bacterium. Colonies live in the stomach, and the risk of infection increases with age. Helicobacter pylori infection in most cases is the cause of the development of gastric and duodenal ulcers, B-cell lymphoma and cancer of the distal stomach. About 95% of duodenal ulcers and about 80% of gastric ulcers are associated with Helicobacter pylori infection.
Separately, symptomatic ulcers associated with taking non-steroidal drugs are distinguished.
anti-inflammatory drugs (NSAIDs), steroid hormones.

Classification:
I. According to the localization of the ulcerative defect:
Gastric ulcer (cardiac, subcardial, antral, pyloric, along the greater or lesser curvature).

II. According to the phase of the disease:
1. Exacerbation
2. Faded exacerbation.
3.Remission

III. According to the flow: 1. Latent, 2. Light, 3. Moderate, 4. Heavy.

IV. By ulcer size: 1. Small, 2. Medium, 3. Large, 4. Giant, 5. Superficial, 6. Deep.

V. According to the stage of the ulcer: 1. Stage of open ulcer, 2. Stage of scarring, 3. Stage of scar.

VI. According to the condition of the mucous membrane of the gastroduodenal zone:
1. Gastritis of 1, 2, 3 degrees of activity (diffuse, limited).
2. Hypertrophic gastritis,
3. Atrophic gastritis,
4. Bulbit, duodenitis 1, 2, 3 degrees of activity.
5. Atrophic bulbitis, duodenitis,
6. Hypertrophic bulbitis, duodenitis.

VII. According to the state of the secretory function of the stomach:
1. With normal or increased secretory activity.
2. With secretory insufficiency.

VIII. Violations of the motor-evacuation function of the stomach and 12 fingers. intestines:
1. Hypertensive and hyperkinetic dysfunction,
2. Hypotonic and hypokinetic dysfunction,
3. Duodenogastric reflux.

IX. Complications:
1. Bleeding, posthemorrhagic anemia.,
2. Perforation,
3.Penetration,
4. Cicatricial deformation and pyloric stenosis of the 12th intestine (compensated,
subcompensated, decompensated),
5. Periviscerites,
6. Reactive pancreatitis,
hepatitis, cholecystitis,
7. Malignancy.

X. According to the timing of scarring:
1. Usual timing of scarring of an ulcer.
2. Long-term non-scarring (more than 8 weeks - for gastric localization, more than 4 weeks - for localization in the 12th p.c.).. 3. Resistant ulcer (more than 12 and more than 8 weeks, respectively.).

According to the degree of activity: 1st degree - moderately expressed, 2nd degree - pronounced, 3rd degree. - sharply expressed.
By size (diameter) of ulcers:
. Small: up to 0.5 cm
. Medium: 0.5-1 cm
. Large: 1.1-2.9 cm
. Giant: for stomach ulcers 3 cm or more, for duodenal ulcers 2 cm or more.

Risk factors:
. presence of Helicobacter pylori
. taking non-steroidal anti-inflammatory drugs, steroid hormones, family history, irregular medication intake (7), smoking, alcohol intake.

Admission: planned.

Indications for hospitalization:
. Peptic ulcer of the stomach and duodenum, complicated earlier.
. Peptic ulcer with a pronounced clinical picture of exacerbation: severe pain, vomiting, dyspeptic disorders.
. Severe peptic ulcer associated with H. pylori, not amenable to eradication.
. Gastric ulcer with a family history to exclude
malignancy.
. Peptic ulcer with mutual burden syndrome (concomitant disease).

The required scope of examinations before planned hospitalization:
1. EGDS, 2. General blood test, 3. Fecal occult blood test, 4. Urease test.

Diagnostic criteria:
1.Clinical criteria:
Pain. It is necessary to find out the nature, frequency, time of onset and disappearance of pain, and the connection with food intake.
. Early pain occurs 0.5-1 hour after eating, gradually increases in intensity, persists for 1.5 - 2 hours, decreases and disappears as the gastric contents move into the duodenum; characteristic of ulcers of the body of the stomach. When the cardiac, subcardial and fundic regions are affected, pain occurs immediately after eating.
. Late pain occurs 1.5-2 hours after eating, gradually intensifying as the contents are evacuated from the stomach; characteristic of ulcers of the pyloric stomach and duodenal bulb.
. “Hungry” (night) pains occur 2.5-4 hours after eating and disappear after the next meal, characteristic of ulcers of the duodenum and pylorus of the stomach.
. A combination of early and late pain is observed with combined or multiple ulcers. The severity of pain depends on the location of the ulcerative defect (minor pain - with ulcers of the body of the stomach, sharp pain - with pyloric and extra-bulb ulcers of the duodenum), age (more intense in young people), and the presence of complications. The most typical projection of pain, depending on the location of the ulcerative process, is considered to be the following:
. for ulcers of the cardial and subcardial parts of the stomach - the area of ​​the xiphoid process;
. for ulcers of the body of the stomach - the epigastric region to the left of the midline;
. for ulcers of the pylorus and duodenum - the epigastric region to the right of the midline.

2. History, objective examination.
3. The presence of an ulcerative defect on EGD; in case of a gastric ulcer, histological examination excludes malignancy.
4. Study of the presence of HP in the mucous membrane.
All persons with a confirmed diagnosis should be tested for the presence of Helicobacter Pylori.

Detection of Helicobacter Pylori:
Diagnosis of Helicobacter Pylori is mandatory for all patients with a history of gastric and duodenal ulcers, as well as a history of peptic ulcers and its complications (A).
Diagnostic interventions to identify Helicobacter Pylori must be carried out both before the start of eradication therapy and after its completion to assess the effectiveness of the measures.

Before starting treatment with NSAIDs, routine diagnosis of Helicobacter Pylori is not indicated.
Non-invasive diagnostic interventions are recommended for patients with uncomplicated symptoms of dyspepsia and a history of gastric and duodenal ulcers.

1. Breath test for urea - determination of C-13 isotopes in the exhaled air of a patient, which are released as a result of the breakdown of labeled urea in the stomach under the action of Helicobacter pylori urease (NICE 2004). It is used both for diagnosis and for the effectiveness of eradication (must be carried out at least 4 weeks after the end of treatment).
Detection of Helicobacter Pylori antigens (HpSA) in feces. The new test has comparable reliability to the urea breath test. It is used both for the diagnosis of Helicobacter Pylori and for the effectiveness of eradication therapy.
3. Serological test (determination of JgG to Helicobacter Pylori). It is characterized by lower sensitivity and specificity compared to the urea breath test and the detection of antigens to Helicobacter Pylori in stool. However, since the first 2 tests are characterized by high costs, the use of a serological test may be justified when the prevalence of Helicobacter Pylori is high, especially in the initial diagnosis of Helicobacter Pylori.
4. Invasive diagnostic interventions should be performed in all patients with symptoms: bleeding, obstruction, penetration and perforation. Empirical therapy cannot be started until diagnostic measures are completed.
5. Biopsy urease test. The sensitivity of this test increases if the biopsy is taken from the body and antrum of the stomach. However, compared to non-invasive measures, it is more expensive and traumatic.
6. The test is considered positive if the number of organisms is at least 100 in the field of view. Histological examination may be useful if the biopsy urease test is negative. For staining histological materials it is necessary to use hematoxylin and eosin.
7. Culture - should not be used to diagnose Helicobacter Pylori, since there are simpler and highly sensitive and specific methods for making the diagnosis. The use of culture is justified only if antibiotic sensitivity and resistance are detected in patients with 2 or more cases of unsuccessful eradication therapy.
4. At the moment, the most accessible rapid method for determining HP in saliva with subsequent confirmation by biopsy.

List of main diagnostic measures:
1. General blood test.
2. Determination of serum iron in the blood.
3. Fecal occult blood test.
4. General urine analysis.
5. EGD with targeted biopsy (according to indications).
6. Histological examination of the biopsy specimen.
7. Cytological examination of the biopsy specimen.
8. Test for No.

List of additional diagnostic measures:
1. Blood reticulocytes
2. Ultrasound of the liver, biliary tract and pancreas.
3. Determination of blood bilirubin.
4. Determination of cholesterol.
5. Determination of ALT, AST.
6. Determination of blood glucose.
7. Determination of blood amylase
8. X-ray of the stomach (according to indications).

Treatment tactics
NON-DRUG TREATMENT
. Diet No. 1 (1a, 15) with the exclusion of dishes that cause or enhance the clinical manifestations of the disease (for example, hot seasonings, pickled and smoked foods).
Meals are fractional, 5 times a day.

DRUG TREATMENT
Peptic ulcer of the stomach and duodenum associated with H. pylori
Eradication therapy is indicated.
Requirements for eradication therapy regimens:
. In controlled studies, it should lead to the destruction of H. pylori bacteria in at least 80% of cases.
. Should not cause forced discontinuation of therapy due to side effects (acceptable in less than 5% of cases).
. The regimen should be effective when the course of treatment lasts no more than 7~14 days.
Triple therapy based on a proton pump inhibitor is the most effective eradication therapy regimen.
When using triple therapy regimens, eradication is achieved in 85-90% of cases in adult patients and in at least 15% of cases in children.

Treatment regimens:
First line therapy.
Proton pump inhibitor (omeprazole 20 mg, rabeprazole 20 mg) or ranitidine bismuth citrate in standard dosage + clarithromycin 500 mg + amoxicillin 1000 mg or metronidazole 500 mg; All drugs are taken 2 times a day for 7 days.
The combination of clarithromycin with amoxicillin is preferable to clarithromycin with metronidazole, as it may help achieve a better outcome when prescribing second-line therapy. Clarithromycin 500 mg 2 times a day was more effective than taking drugs at a dose of 250 mg 2 times a day.
It has been shown that the effectiveness of ranitidine bismuth citrate and proton pump inhibitors is the same.

The use of second-line therapy is recommended in case of ineffectiveness of first-line drugs. Proton pump inhibitor in a standard dose 2 times a day + bismuth subsalicylate 120 mg 4 times a day + metronidazole 500 mg 3 times a day + tetracycline 100-200 mg 4 times a day.

Rules for the use of anti-Helicobacter therapy
1. If the use of a treatment regimen does not lead to eradication, it should not be repeated.
2. If the regimen used did not lead to eradication, this means that the bacterium has acquired resistance to one of the components of the treatment regimen (nitroimidazole derivatives, macrolides).
3. If the use of one and then another treatment regimen does not lead to eradication, then the sensitivity of the H. pylori strain to the entire range of antibiotics used should be determined.
4. If bacteria appear in the patient’s body a year after the end of treatment, the situation should be regarded as a relapse of the infection, and not as a reinfection.
5. If the infection recurs, it is necessary to use a more effective treatment regimen.
After the end of combined eradication therapy, it is necessary to continue treatment for another 5 weeks for duodenal ulcers and for 7 weeks for gastric ulcers using one of the antisecretory drugs (proton pump inhibitors, histamine H2 receptor blockers).

Peptic ulcer not associated with H. pylori
In case of peptic ulcer not associated with H. pylori, the goal of treatment is to relieve the clinical symptoms of the disease and scarring of the ulcer.
With increased secretory activity of the stomach, the prescription of antisecretory drugs is indicated.
. Proton pump inhibitors: omeprazole 20 mg 2 times a day, rabeprazole 20 mg 1-2 times a day.
. Histamine H-receptor blockers: famotidine 20 mg 2 times a day, ranitidine 150 mg 2 times a day.
. If necessary - antacids, cytoprotectors.

The effectiveness of treatment for gastric ulcers is monitored endoscopically after 8 weeks, for duodenal ulcers - after 4 weeks.

A. Continuous (for months and even years) maintenance therapy with an antisecretory drug at half the dose.
Indications:
1. Ineffectiveness of eradication therapy,
2. Complications of ulcer,
3. The presence of concomitant diseases requiring the use of NSAIDs,
4. Concomitant ulcerative reflux esophagitis,
5. Patients over 60 years of age with annually recurrent ulcerative disease.

B. On-demand therapy, which involves taking one of the secretory drugs in a full daily dose for 3 days when symptoms characteristic of an exacerbation of ulcer appear, then in half for 3 weeks. If the symptoms do not stop, then after endoscopy and detection of re-infection, repeated eradication therapy is carried out.

List of essential medications:
1. Amoxicillin 1000 mg, tablet
2. Clarithromycin 500 mg, tablet
3. Tetracycline 100-200 mg, tablet
4. Metronidazole 500 mg, tablet
3. Aluminum hydroxide, magnesium hydroxide
4. Famotidine 40 mg, tablet
5. Omeprazole 20 mg, tab.

List of additional medications:
1. Tripotassium bismuth dicitrate 120 mg, tablet
2. Domperidone 10 mg, tab.

Criteria for transfer to the next stage: relief of dyspeptic pain syndrome.
Patients require clinical observation.

Peptic ulcer disease (PU) is a fairly common pathology of the digestive tract. According to statistics, up to 10-20% of the adult population encounter it; in large cities the incidence rate is much higher than in rural areas.

This disease is associated with the formation of ulcers on the mucous membrane of the stomach and duodenum; in the absence of proper treatment, ulcers lead to serious complications and even death. The disease can be asymptomatic for a long time, but it is very dangerous during exacerbations. A correctly selected treatment regimen for stomach and duodenal ulcers ensures healing and prevents complications.

Causes of peptic ulcer

The main reason why the disease occurs is the activity of the bacterium Helicobacter Pylori: it provokes inflammation, which over time leads to the formation of ulcers on the mucous membrane. However, bacterial damage is aggravated by some additional factors:

  • Improper, irregular diet. Snacks on the go, lack of a full breakfast, lunch and dinner, an abundance of spices and over-salted dishes in the diet - all this negatively affects the stomach and creates a favorable environment for the growth of bacteria.
  • Bad habits. Peptic ulcers are especially common in those who smoke on an empty stomach; drinking alcohol also contributes to serious damage to the mucous membranes.
  • Stress and negative emotions. The development of an ulcer and its exacerbation is provoked by constant nervous excitement, as well as constant mental overload.
  • Hereditary factor. It has already been established that if there are cases of ulcers in the family, then the chance of a similar digestive disorder increases significantly.

The ulcer develops over a long period of time: at first, a person notices discomfort in the stomach and minor disturbances in the digestive process, over time they become more and more pronounced.

If measures are not taken in time, an exacerbation with serious complications is possible.

Main symptoms of ulcer

An exacerbation of ulcer occurs suddenly, the duration can reach several weeks.

Various factors can provoke an exacerbation: overeating with a serious violation of the diet, stress, overwork, etc. Symptoms vary depending on the location of the ulcer:

  1. If pain occurs immediately after eating and gradually decreases over the next two hours, this usually indicates that the ulcer is localized in the upper part of the stomach. The pain decreases as food gradually passes into the duodenum during digestion.
  2. If pain, on the contrary, occurs within 2 hours after eating, this indicates an ulcer located in the antrum of the stomach: from it food enters the duodenum, and it is in this area that a large accumulation of Helicobacter pylori is most often observed.
  3. Night pain, which also occurs during long breaks between meals, most often occurs with ulcerative lesions of the duodenum.
  4. In addition to pain of various types in the abdomen, a characteristic symptom of an ulcer is heartburn, which is associated with increased acidity of gastric juice. Heartburn occurs simultaneously with pain or appears before it. With sphincter weakness and reverse peristalsis, patients experience sour belching and nausea; these symptoms often accompany peptic ulcer disease.
  5. Another common symptom is vomiting after eating, and it brings significant relief to the patient. Appetite often decreases, some patients have a fear of eating due to fear of pain - because of this, significant exhaustion is possible.

Methods for diagnosing ulcers

To diagnose stomach and duodenal ulcers, you must consult a gastroenterologist; the sooner the patient comes for help, the higher the chance of recovery or long-term remission without exacerbations.

In case of a sharp exacerbation with bleeding, urgent surgical intervention is necessary, in this case it is necessary to urgently call an ambulance.

The main method of examining the stomach is fibrogastroduodenoscopy: it allows the doctor to see the condition of the mucous membrane in order to detect an ulcer and assess the advanced state of the disease. Not only the location of the ulcer is assessed, but also its condition: presence of scars, size.

At the same time, a tissue sample of the mucous membrane is taken to identify Helicobacter pylori and a more accurate diagnosis. A clinical blood test is also carried out, it allows you to evaluate deviations from the norm in the condition of the body.

Although FGDS is a rather unpleasant research method, it is the most informative, so it cannot be abandoned. In some cases, it is supplemented by x-ray examination.

Methods and regimens for treating peptic ulcers

The treatment regimen for peptic ulcer disease is based on taking antibiotics to get rid of Helicobacter pylori and avoid serious complications.

Three- and four-component treatment regimens are prescribed by a gastroenterologist; only a specialist can select specific drugs in accordance with the individual characteristics of the patient. Several groups of drugs are used to treat ulcers:

  • Antibiotics. Two drugs are prescribed at the same time, the doctor selects the drugs taking into account possible allergic reactions. Self-prescription of antibiotics is unacceptable; they should only be selected by a doctor. The course of treatment takes at least 7-10 days; even if you feel significantly better, you should not stop taking the pills.
  • Drugs that should neutralize the effect of gastric juice. These include Omeprazole, Pantoprazole and other common medications familiar to most patients with digestive disorders.
  • Substances that form a film on the surface of the mucous membrane. It protects it from the aggressive effects of gastric juice, which contributes to faster healing of the ulcer.
  • Antacids, the main purpose of which is to reduce the acidity of gastric juice. They significantly reduce heartburn and improve the well-being of patients; such drugs have an adsorbing effect.
  • Prokinetics (Cerucal, Motilium and others) are drugs designed to normalize the motility of the duodenum and ensure normal movement of food through the intestines. They are prescribed for a feeling of heaviness in the stomach or early satiety.

Complex therapy rarely takes more than two weeks. After this, it is only necessary to help the stomach recover faster; for this, special nutritional plans and additional treatment methods are used.

Diet for gastric ulcer

When diagnosing ulcer, patients are prescribed therapeutic nutrition, designed to provide a gentle regime for the stomach and duodenum with a reduction in load.

For this purpose, diet group No. 1 is used; they are prescribed during the acute phase of the disease. The diet prescribes the following restrictions for patients:

  1. Foods that irritate the stomach are completely excluded from the diet. These are spicy, sour, fatty dishes, pickles, marinades, etc.
  2. You should not eat vegetables containing large amounts of fiber - they can also have a negative effect on digestion during an exacerbation. You can only eat boiled vegetables; in the first days they can only be consumed pureed.
  3. You should not consume sour dairy products and salty cheeses; sour fruits and natural juices are also excluded from the diet.
  4. Alcohol and carbonated drinks are completely excluded; drinking coffee is undesirable.

All these restrictions prevent further negative effects on the digestive tract and prevent the development of complications.

Deviations from the diet can lead to serious complications, including bleeding and perforation of ulcers.

Additional treatments

In addition to drug treatment, methods of physiotherapy and physical therapy are added during the recovery stage.

They help strengthen the body and minimize the consequences of digestive disorders.

At home, as prescribed by a doctor, you can make warming alcohol compresses - the heat helps reduce pain and improve blood circulation.

Patients with peptic ulcer disease are prescribed sanatorium-resort treatment: in addition to health procedures and the climate at the resort, drinking mineral water “Borjomi”, “Smirnovskaya”, “Essentuki” has a beneficial effect.

Physical therapy exercises are aimed at improving blood circulation and preventing congestion, they improve secretory and motor function, and stimulate appetite. A set of therapeutic and health procedures in compliance with medical recommendations gives excellent results and helps eliminate the negative consequences of peptic ulcer disease.

The sooner the patient turns to specialists, the greater the chance of successful healing of the ulcer with normalization of well-being. It is important to take care of yourself in time and go to an appointment with a gastroenterologist at the first negative manifestations.

Complications of peptic ulcer

Peptic ulcer disease is dangerous due to serious complications during exacerbation, often requiring urgent surgery to prevent death. The following complications are common:

  • Gastric and intestinal bleeding. A characteristic symptom is vomit, which is the color of coffee grounds, and black stools.
  • Perforation of the ulcer. A rupture leads to the entry of the contents of the digestive tract into the abdominal cavity, resulting in a condition that threatens the patient’s life. Emergency surgery is required.
  • Penetration is a condition of the so-called hidden breakthrough, in which the contents of the intestine can enter other organs of the abdominal cavity. Only urgent surgery can save the patient.
  • When healing scars on the mucous membranes, the pylorus may narrow, which leads to disruption of the digestive tract. Treatment is only surgical.
  • Signs of complications from a peptic ulcer and internal bleeding are sudden weakness, fainting, a sharp drop in blood pressure, and severe abdominal pain. In case of vomiting blood and other signs of complications, it is necessary to take the patient to the hospital as soon as possible in order to prevent irreparable consequences.

Peptic ulcer disease is a disease that is largely associated with the irregular rhythm of life in a big city. It is necessary to find time to eat well; taking care of digestion will relieve discomfort and long-term complex treatment. If digestive problems have already arisen, there is no need to postpone a visit to the doctor until later. Timely diagnosis is an important factor in successful treatment.

How to treat peptic ulcers with antibiotics, watch the video:

Tell your friends! Share this article with your friends on your favorite social network using social buttons. Thank you!

Most often, exacerbation of duodenal ulcers occurs due to gross neglect of diet, abuse of alcohol and junk food that irritates the intestinal mucosa, as well as exposure to stress and fatigue.

Signs of exacerbation are mainly diagnosed in the off-season - spring and autumn. This is due to the deterioration of general immunity during this period. The course of the disease is characterized by cyclicity, when periods of stable remission alternate with exacerbations of the pathology.

Forms of the disease

Exacerbation of duodenal ulcer, its symptoms and treatment depend on the form of the disease.

The disease is classified according to the following criteria:

  • Is it possible to have pea soup during an exacerbation of an ulcer?
  • treatment of duodenal ulcers with propolis
  • symptoms treatment of colon ulcers

By relapse rate:

  • a form that has exacerbations from one to three times a year;
  • a disease that recurs more than three times in a year.

According to the location and depth of the lesion:

  • superficial or deep ulceration;
  • an ulcer located in the area of ​​the bulb or in the post-bulb area.

By the number of mucosal lesions:

  • single outbreak;
  • multiple foci.

Acute duodenal ulcer gives a very pronounced clinical picture with vivid symptoms, making it difficult to confuse it with any other disease. The chronic form of duodenal ulcer without exacerbation may not produce symptoms at all and proceed hidden.

Causes of duodenal ulcers

The causes of the disease may be due to family history, dietary habits and bad habits. In some cases, the disease is caused by the bacterium Helicobacter pylori, which affects the lining of the stomach and intestines.

Without adequate and timely treatment, the ulcer may undergo malignant degeneration.

The most likely factors for the occurrence of the disease are the following:

  • abuse of alcohol and tobacco products, which leads to impaired blood circulation in organs, as well as irritation of the mucous membranes of the gastrointestinal tract;
  • irregular meals with long intervals between meals, as well as a predominance in the diet of foods that are fried in fat, too sour, fatty and pickled. Food including canned, smoked foods and sauces;
  • prolonged and uncontrolled use of NSAIDs, which led to inflammation of the intestinal lining;
  • prolonged stress and fatigue can cause duodenal ulcers in people with an unbalanced psyche and mild excitability of the nervous system.

In the first stages, the disease does not always produce noticeable symptoms, so the patient often sees a doctor with an advanced form of the disease. The trigger mechanism for the disease can also be existing pathologies of the endocrine system, liver and kidneys, and infectious diseases.

Tuberculosis, diabetes, hepatitis, pancreatitis lead to intestinal irritation and can provoke duodenal ulcer. The causes of the disease can also be mechanical damage due to surgery.

Symptoms of relapse of the disease

Clinical symptoms of duodenal pathology do not appear immediately; often, at the very beginning, the disease proceeds latently. An advanced form of peptic ulcer disease can suddenly manifest itself with life-threatening symptoms. In a third of people with this pathology, the presence of the disease is determined after a post-mortem autopsy.

The main diagnostic signs of duodenal ulcers:

  • epigastric pain;
  • symptoms of gastrointestinal dysfunction;
  • neurological symptoms.

The main symptom of the disease is pain in the pit of the stomach or in the upper part of the navel. Relapse often provokes pain in the back and heart area. This is due to the fact that it can radiate from its localization site to other parts of the body, distorting ideas about the real source of pain. Therefore, gastroenterologists primarily focus on discomfort in the navel area.

All painful sensations occur on an empty stomach, and immediately after eating the abdominal pain subsides. But if the patient overeats or consumes foods prohibited by the nutritionist, the pain may intensify.

Often, the symptoms of exacerbation of a duodenal ulcer exhaust the patient, not allowing him to fully rest at night. This occurs due to excessive production of acid, which irritates the diseased area of ​​the intestinal mucosa.

Even during stable remission, a stressful situation, a violation of the diet and the use of pharmacological drugs (hormones or NSAIDs) can lead to a worsening of the condition, pain and nausea.

The second most important sign of duodenal ulcer is gastrointestinal dysfunction, characterized by the ability to bring relief to the patient:

  • constant long-term constipation;
  • bloating, belching and flatulence;
  • dark stool indicating the presence of blood.

The third most important are neurological symptoms. Signs of exacerbation of duodenal ulcer may include: irritability, sleep disturbance, depressed mood, and weight loss.

Diet for exacerbation of duodenal ulcers

Nutrition for gastrointestinal pathologies is of paramount importance. In the first days of the disease, nutrition is limited to a small amount of pureed food. Vegetable and bakery products are excluded.

After 5 days, you are allowed to eat vegetarian soups in which white crackers can be soaked. In addition, puree or soufflé from boiled poultry and fish fillets is allowed; for dessert you can eat fruit jelly.

In the second week, meat dishes are added to the treatment menu, which must be steamed; these can be poultry or fish meatballs. In addition, you should eat eggs in the form of an omelet or boiled, milk porridge with a small amount of butter, as well as mashed carrots or potatoes.

Contraindicated in case of exacerbation of duodenal ulcer:

  • mushroom, meat broth;
  • confectionery and baked goods;
  • dishes that were fried in fat;
  • too fatty foods;
  • fresh fruits and vegetables;
  • fatty sea fish;
  • alcohol-containing products;
  • any lean meat;
  • spices, sauces and marinades.

To neutralize the aggressive effects of hydrochloric acid, you should eat little and often. It is better to treat duodenal ulcers in a hospital setting, and dietary table No. 1-a or 1-b is indicated; such nutrition should last 4 months. After discharge, you can follow diet No. 5.

Pathology therapy

Duodenal ulcers, depending on the severity of clinical manifestations, can be treated conservatively and surgically.

The impact method includes the following set of measures:

  • therapeutic nutrition;
  • pharmacological agents (antibiotics, antacids and antisecretory drugs);
  • herbal decoctions;
  • Surgical treatment is indicated only if conventional methods are ineffective. Most often, the patient needs surgical help after constant exacerbations of the disease, with impaired ulcer healing and severe scarring.

When Helicobacter pylori is detected, treatment should include a complex of several antibiotics with antiprotozoal and bactericidal effects:

  • Amoxicillin;
  • Tetracycline;
  • Clarithromycin;
  • Metronidazole.

In order to neutralize the acidity of gastric juice, antacids are used:

  • Maalox;
  • Rennie;
  • Phosphalugel;
  • Almagel;
  • Gastal.

To improve the healing of the duodenal membrane, antiulcer drugs are prescribed:

  • De-nol;
  • Venter;
  • Misoprostol.

In addition, antisecretory agents are prescribed:

  • Rabeprozole;
  • Omeprazole;
  • Esomeprazole;
  • Lanzoprazole.

When, after taking medications for a long time under the supervision of a doctor, the patient does not feel any improvement, then it is advisable to agree to surgical intervention, which will consist of removing the affected area or suturing the duodenum.

Complications of duodenal ulcers

If duodenal ulcers are treated incorrectly, the pathology can periodically worsen and ultimately cause serious complications.

  • If blood vessels are involved in the process, the disease can be complicated by hemorrhage. Hidden bleeding can be identified by such a characteristic sign as anemia. If the hemorrhage is abundant, then it can be determined by the type of stool (they turn black).
  • Perforation of an ulcer is the appearance of a hole in the wall of the duodenum. This complication can be determined by the occurrence of acute pain during palpation or a change in body position.
  • Narrowing of the duodenal lumen occurs as a result of edema or scar. Identified by bloating, uncontrollable vomiting, and lack of stool.
  • Ulcer penetration – penetration into neighboring organs through a defect in the duodenum. The main symptom is pain radiating to the back.

A duodenal ulcer can worsen during the off-season (autumn, spring) and is most often triggered by poor diet or stress. The main symptom is pain in the navel area. To avoid this, you need to remember about preventive measures, compliance with all the conditions prescribed by a specialist, including strengthening the immune system and following a diet.

Recommended
Expert advice
RSE at the RVC "Republican Center"
healthcare development"
Ministry of Health
and social development
Republic of Kazakhstan
dated December 10, 2015
Protocol No. 19

Protocol name: Perforated ulcer of the stomach and duodenum.

Perforated ulcer- this is the occurrence of a through defect in the wall of the stomach, duodenum or area of ​​gastrojejunal anastomosis in the center of a chronic or acute ulcer, which opens into the free abdominal cavity, omental bursa, and retroperitoneal space.

Protocol code:

ICD-10 code(s):
K25-Stomach ulcer
K25.1 - Acute with perforation
K25.2 - Acute with bleeding and perforation
K25.5 - Chronic or unspecified with perforation
K26-Dodenal ulcer
K26.1 - Acute with perforation
K26.2 - Acute with bleeding and perforation
K26.5 - Chronic or unspecified with perforation
K28 - Gastrojejunal ulcer
K28.1 - Acute with perforation
K28.2 - Acute with bleeding and perforation
K28.5 - Chronic or unspecified with perforation

Abbreviations used in the protocol:
BP - Blood pressure
D-observation - Dispensary observation
Duodenum VIZHZH - Duodenum
ELISA - Enzyme-linked immunosorbent assay
CT - Computed tomography
NSAIDs - Nonsteroidal anti-inflammatory drugs
ACVA - Acute cerebrovascular accident
CBC - Complete blood count
OAM - General urine analysis
AKI - Acute renal failure
LOE -Level of Evidence
Ultrasound - Ultrasound examination
CRF - Chronic renal failure
HR - Heart rate
ECG - Electrocardiography
EFGDS - Esophagofibrogastroduodenoscopy
ASA - American Association of Anesthesiologists
H.pylori -Helicobacter pylori

Date of development of the protocol: 2015

Protocol users: surgeons, anesthesiologists-resuscitators, ambulance doctors and paramedics, general practitioners, therapists, endoscopists, radiology department doctors.

Recommendation Methodological quality of supporting documents Note
Class 1A - Strong recommendation, high quality of evidence RCTs without important limitations and compelling evidence from observational studies
Class 1B - Strong recommendation, moderate quality of evidence
Strong recommendation, can be applied to most patients in most cases without reservation
Class 1C - Strong recommendation, weak evidence
Observational studies or case series Strong recommendation, but may change when higher quality evidence becomes available
Class 2A - Weak recommendation, high quality of evidence RCTs without important limitations and compelling evidence from observational studies
Class 2B - Weak recommendation, moderate quality of evidence
RCTs with important limitations (inconsistent results, methodological flaws, indirect or imprecise) or exceptionally strong evidence from observational studies Weak recommendation, depending on circumstances, patients or social values
Class 2C - Weak recommendation, poor quality evidence Observational studies and case series Very weak recommendations, there may be other alternatives equally
GPP Best Pharmaceutical Practices

CLASSIFICATION

Clinical classification V.S., Savelyeva, 2005:

by etiology:
perforation of a chronic ulcer;
· perforation of an acute ulcer (hormonal, stress, etc.);

by localization:
· stomach ulcers (lesser and greater curvature, anterior and posterior walls in the antrum, prepyloric, pyloric, cardiac, in the body of the stomach);
· duodenal ulcers (bulbar, postbulbar);

according to clinical form:
· perforation into the free abdominal cavity (typical, covered);
· atypical perforation (into the omental bursa, lesser or greater omentum - between the layers of the peritoneum, into the retroperitoneal tissue, into a cavity isolated by adhesions);
combination of perforation with bleeding in the gastrointestinal tract;

by peritonitis phase (by clinical periods):
· phase of chemical peritonitis (period of primary shock);
phase of bacterial peritonitis and systemic syndrome
inflammatory reaction (period of imaginary well-being);
phase of diffuse purulent peritonitis (period of severe
abdominal) sepsis.

It is necessary to take into account the peculiarities of the clinical course of a perforated ulcer depending on the period of the disease and the location of the ulcer (diagnostic errors are made during the period of imaginary well-being, as well as with covered and atypical perforation!).
During the course of the disease there are:
· period of shock - first 6 hours - severe pain syndrome - “dagger” pain, bradycardia, “board-shaped” tension of the abdominal muscles);
· period of imaginary prosperity - from 6 to 12 hours after perforation - in contrast to the period of shock, the pain syndrome is not pronounced, patients subjectively note an improvement in well-being, tachycardia, and no “board-like” tension in the abdominal muscles;
· period of widespread peritonitis - 12 hours after perforation - signs of progressive peritonitis appear.
The clinical picture of atypical (perforation into the retroperitoneal space, omental bursa, thickness of the lesser and greater omentum) and covered perforation is characterized by a less pronounced pain syndrome without clear localization, and the absence of “board-like” tension in the abdominal muscles.

Diagnostic criteria:

Complaints and anamnesis:

Complaints: sudden « “dagger” pain in the epigastrium, severe weakness in some cases to the point of loss of consciousness, cold sweat, dry mouth.

History taking if a perforated ulcer is suspected, it has great diagnostic value and should be especially careful:
· sudden acute onset of the disease - “dagger” pain - Dieulafoy’s symptom, radiating to the left shoulder and shoulder blade (perforation of a stomach ulcer), to the right shoulder and shoulder blade (perforation of a duodenal ulcer) - Eleker’s symptom (Eleker - Brunner);
· presence of an instrumentally confirmed ulcer history, D-observation in the clinic for a peptic ulcer; previous operations for perforated ulcers, ulcerative gastroduodenal bleeding, pyloroduodenal stenosis; seasonal pain, pain after eating, night pain, “hunger” pain;
· a history of risk factors that provoked this complication: long-term therapy with NSAIDs for heart disease, joints, trauma, neurological diseases, uremia due to chronic renal failure or acute renal failure, hormone therapy, bad habits, poor diet.

Physical examination:
During the first period (up to 6 hours) physical examination reveals shock. The patient is in a forced position with his legs adducted to his stomach, does not change his body position, is pale, covered in cold sweat, with a frightened expression on his face.
Objectively: bradycardia (vagal pulse), hypotension, tachypnea.
The tongue is clean and moist. The abdomen does not participate in the act of breathing, is tense like a board, sharply painful in the epigastrium, in the projection of the right lateral canal;
percussion - disappearance of hepatic dullness in the patient's supine position - Spizharny's (Jobert) symptom. Symptoms of peritoneal irritation are positive: Shchetkin-Blumberg, Razdolsky's symptom; rectal and vaginal examination reveals pain in the projection of the pouch of Douglas - Kullenkampf's symptom.
Second period (from 6 to 12 hours). The patient's face acquires a normal color. The pain becomes less intense, the patient subjectively notes a significant improvement, and is reluctant to allow himself to be examined. That is why the second period is called the period of imaginary well-being.
Objectively: bradycardia is replaced by moderate tachycardia. The tongue becomes dry and coated.
The abdomen is painful on palpation in the epigastrium, in the projection of the right lateral canal, but the board-like tension disappears.
Percussion: dullness is determined in sloping areas - Querven's symptom (De Querven), liver dullness is not determined (Spizharny's symptom). Auscultation: peristalsis is weakened or absent. Symptoms of peritoneal irritation are positive, the definition of Kullenkampf’s symptom is especially informative.
The third period of abdominal sepsis (12 hours from the moment of illness).
The patient's condition is progressively worsening. The patient is restless. The first symptom of progressive peritonitis is vomiting, vomiting can be repeated and congestive. There is dry skin and mucous membranes, the tongue is dry, coated with a brown coating. The abdomen is swollen, sharply painful in all parts, tense; percussion: dullness in sloping areas due to fluid accumulation; Auscultation: no peristalsis. Symptoms of peritoneal irritation are positive.

Most often, patients present in the first period of the disease, which is characterized by the classic triad of symptoms:
· Dieulafoy's sign(Dieulafoy) - sudden intense « “dagger” pain in the epigastrium;
· ulcer history;
· plank-shaped tension of the abdominal muscles.

The following symptoms are also identified:
Spizharny (Jobert) symptom - disappearance of hepatic dullness upon percussion;
Frenicus-Eleker's symptom(Eleker - Brunner) - pain radiating to the right shoulder girdle and right shoulder blade;
Quervain's sign(DeQuerven) - pain and dullness in the right lateral canal and in the right iliac fossa;
Kullenkampf's sign (symptom of irritation of the pelvic peritoneum) - rectal and vaginal examination reveals sharp pain in the projection of the pouch of Douglas;
Symptoms of peritoneal irritation (Shchetkin-Blumberg, Razdolsky).
With the development of abdominal sepsis(see Appendix 1) local manifestations (abdominal pain, muscle tension, positive symptoms of peritoneal irritation) are accompanied by 2 or more criteria for systemic inflammatory response syndrome:
body temperature is determined to be above ≥ 38C or ≤ 36C,
tachycardia ≥ 90/min, tachypnea > 20/min,
leukocytes> 12 x10 9 /l or< 4 х 10 9 /л, или наличие >10% immature forms).

For severe abdominal sepsis and septic shock(see Appendix developing organ dysfunction):
Hypotension (SBP)< 90 мм рт. ст. или ДАД < 40 мм рт. ст.),
hypoperfusion (acute change in mental status, oliguria, hyperlactic acidemia).

To objectively assess the severity of the condition, the integral scales APACHE, SAPS, SOFA, MODS, as well as specific scales - Mannheim Peritonitis Index, Prognostic Relaparotomy Index (see Appendices) are used.

List of basic and additional diagnostic measures

Basic (mandatory diagnostic tests carried out on an outpatient basis if the patient goes to the clinic): no.

Additional diagnostic tests performed on an outpatient basis: are not carried out.

Minimum list of studies that must be carried out when referring for planned hospitalization: there is no planned hospitalization.

Basic (mandatory) diagnostic studies carried out at the hospital level:
Implementation of the “Sepsis Screening” program if the perforation is more than 12 hours old and there are signs of widespread peritonitis: examination by an anesthesiologist-resuscitator to assess the state of hemodynamics, early diagnosis of abdominal sepsis, determine the scope of preoperative preparation (if there are signs of sepsis, hemodynamic disorders, the patient is immediately transferred to the intensive care unit where further diagnostic and therapeutic measures are carried out);
Laboratory research:
· general blood analysis;
· general urine analysis;
· microreaction;
· blood test for HIV;
· blood type and RH factor;
· biochemical blood test: (glucose, urea, creatinine, bilirubin, ALT, AST, total protein);
· electrolytes;
· KSH;
· coagulogram 1 (prothrombin time, fibrinogen, APTT, INR).
Instrumental research in compliance with the following algorithm:
EFGDS (Recommendations 1B);
Absolute contraindications: agonal state of the patient, acute myocardial infarction, stroke.
· plain radiography of the abdominal cavity in a vertical position (Recommendations 1A) (with preliminary EGD, there is no need for pneumogastrography in doubtful cases);
· ECG, consultation with a therapist;
· bacteriological examination of peritoneal exudate;
· histological examination of the resected organ;
· in the absence of an endoscopic service with round-the-clock operation (district hospitals), it is permissible to limit ourselves to a survey radiography of the abdominal cavity with capture of the diaphragm.

Additional diagnostic measures carried out at the hospital level (according to indications to clarify the diagnosis):
· pneumogastrography (in the absence of the possibility of emergency endoscopy, the presence of a clear clinical picture of a perforated ulcer during physical examination and the absence of radiological signs of pneumoperitoneum);
Abdominal ultrasound (to confirm the presence of free fluid) (Recommendations 1B);
· plain radiography of the chest (to exclude diseases of the lungs and pleura);
· vaginal examination;
· in the absence of radiological evidence of pneumoperitoneum - CT (if CT is available in the medical institution) (Recommendations 1B);

N.B.! - consider the risk of radiation exposure during CT for young patients!
· in the absence of CT sign of pneumoperitoneum - CT with oral contrast - triple contrast (if CT is available in the medical institution) (Recommendations 1B);
· laparoscopy (Recommendations 1B);
· biopsy from a stomach or duodenal ulcer;
· determination of tumor markers using ELISA (if technically possible);
lactate level determination;
· procalcitonin test in blood plasma (quantitative immunoluminometric method or semi-quantitative immunochromatographic express method);
· determination of central venous pressure;
· determination of hourly diuresis;
· determination of HBsAg in blood serum;
· determination of total antibodies to hepatitis C virus (HCV) in blood serum by ELISA.

Diagnostic measures carried out at the stage of emergency care:
· collection of complaints, medical history and life history;
· physical examination (examination, palpation, percussion, auscultation, determination of hemodynamic parameters - heart rate, blood pressure).

Instrumental studies:
Instrumental studies allow us to determine the undoubted signs of the disease: 1) the presence of an ulcer, 2) the presence of a perforation, 3) the presence of pneumoperitoneum, 4) the presence of free fluid in the abdominal cavity.
EGD - the presence of an ulcer with a perforated hole (in some cases, a perforated ulcer may not be visualized) (Recommendations 1B);
· Plain radiography of the abdominal cavity - the presence of pneumoperitoneum (Recommendations 1A) ;
Ultrasound of the abdominal cavity - the presence of free fluid in the abdominal cavity (Recommendations 1B);
CT with oral contrast - the presence of contrast in the stomach, duodenum and abdominal cavity, detection of ulcers and perforations (Recommendations 1B);
CT with oral contrast - the presence of free gas and free fluid in the abdominal cavity, detection of ulcers and perforations (Recommendations 1B);
Laparoscopy - presence of free fluid, free gas, perforation (Recommendations 1B).

Indications for consultation with specialists:
consultation with a therapist: exclusion of the abdominal form of myocardial infarction and concomitant somatic pathology
consultation with an oncologist if malignancy is suspected;
consultation with an endocrinologist for concomitant diabetes mellitus;
consultation with a nephrologist if there are signs of chronic renal failure.
consultation with a gynecologist (to exclude gynecological pathology);
consultation with a nephrologist (if there are signs of chronic renal failure);
consultation with an endocrinologist (if you have diabetes).

Laboratory criteria:
· general blood test: increasing leukocytosis, lymphocytopenia, shift of the leukocyte formula to the left;
· biochemical blood test: increased levels of urea, creatinine;
· hyperlactic acidemia (in shock);
· increased procalcitonin levels (see Appendix 2);
· coagulogram: DIC syndrome (with the development of abdominal sepsis).

Differential diagnosis carried out with acute appendicitis, acute pancreatitis, rupture of aneurysm of the retroperitoneal aorta, myocardial infarction (Table 2). table 2 Differential diagnosis of perforated ulcer

Disease General clinical symptoms Distinctive clinical symptoms
Acute appendicitis · pain in the epigastrium, in the right iliac region; · reflex vomiting. · absence of the classic triad of symptoms of a perforated ulcer; · absence of ulcer during endoscopy; · movement and localization of pain in the right iliac region.
Pancreatitis · absence of the classic triad of symptoms of a perforated ulcer; · absence of ulcer during endoscopy; · absence of clinical and radiological signs of pneumoperitoneum; · presence of a triad of symptoms: girdling pain, repeated vomiting, flatulence; · history of cholelithiasis, presence of ultrasound signs of cholelithiasis, pancreatitis; · increased levels of amylase in the blood and urine, possibly increased levels of bilirubin and glucose in the blood.
Ruptured aneurysm of the retroperitoneal aorta · sudden intense pain in the epigastrium. · absence of the classic triad of symptoms of a perforated ulcer; · absence of ulcer during endoscopy; · absence of clinical and radiological signs of pneumoperitoneum; · elderly age; · presence of cardiovascular pathology; presence of an abdominal aortic aneurysm; · unstable hemodynamics with a tendency to decrease blood pressure, tachycardia; Auscultation: systolic murmur in the epigastrium; · Doppler ultrasound: aneurysm in the projection of the abdominal aorta; · anemia.
Myocardial infarction · sudden intense pain in the epigastrium. · absence of the classic triad of symptoms of a perforated ulcer; · absence of ulcer during endoscopy; · absence of clinical and radiological signs of pneumoperitoneum; · elderly age; · presence of cardiovascular pathology, recurring angina pectoris; · ECG: pathological Q wave, ST segment elevation; · presence of markers of cardiomyocyte damage (troponin test, CK-MB isoenzyme) in the blood.

Treatment goals:
elimination of perforation;
carrying out complex treatment of peritonitis;
carrying out complex treatment of gastric and duodenal ulcers.

Treatment tactics:
A perforated ulcer is an absolute indication for emergency surgery (Recommendations 1A) .
The basic principles of treatment of abdominal sepsis, severe sepsis, septic shock that developed against the background of a perforated ulcer are set out in the clinical protocol “Peritonitis”.

Non-drug treatment:
mode - bed;
diet - after diagnosis before surgery and the 1st day after surgery - table 0, in the postoperative period - early fractional tube enteral nutrition in order to protect the gastrointestinal mucosa and prevent bacterial translocation.

Drug treatment:

Drug treatment provided on an outpatient basis: is not carried out.

Drug treatment , provided at the stationary level:
N.B.! HNon-narcotic analgesics for ulcers are contraindicated!


p/p
INN name dose multiplicity method of administration duration of treatment note level of evidence
strictly
sti
Narcotic analgesics (1-2 days after surgery)
1 Morphine hydrochloride 1%-1 ml every 6 hours first day IM 1-2 days IN
2 Trimeperidine injection solution 2% - 1 ml every 4-6 hours i/m 1-2 days Narcotic analgesic for pain relief in the postoperative period IN
Opioid narcotic analgesic (1-2 days after surgery)
3 Tramadol 100 mg - 2 ml 2-3 times i/m within 2-3 days Analgesic of mixed type of action - in the postoperative period A
Antibacterial drugs
(recommended schemes are given in clause 14.4.2)
6 Ampicillin orally, single dose for adults - 0.25-0.5 g, daily - 2-3 g. IM 0.25-0.5 g every 6-8 hours 4-6 times a day inside, intravenously, intramuscularly from 5-10 days to 2-3 weeks or more A
7 Amoxicillin adults and children over 10 years old (body weight more than 40 kg) - orally, 500 mg 3 times a day (up to 0.75-1 g 3 times a day for severe infections); maximum daily dose - 6 g 2-3 times a day Inside, intramuscularly, intravenously 5-10 days Broad-spectrum semisynthetic penicillin antibiotic A
8 Cefuroxime 0.5-2 g each 2-3 times a day i/m, i/v 7-14 days 2nd generation cephalosporins A
9 Ceftazidime 0.5-2 g each 2-3 times a day i/m, i/v 7-14 days 3rd generation cephalosporins A
10 Ceftriaxone the average daily dose is 1-2 g once a day or 0.5-1 g every 12 hours. 1-2 times i/m, i/v 7-14 (depending on the course of the disease) 3rd generation cephalosporins A
11 Cefotaxime 1 g every
12 hours, in severe cases the dose is increased to 3 or 4 g per day
3-4 times i/m, i/v 7-14 days 3rd generation cephalosporins
for initial empirical antibiotic therapy
A
12 Cefoperazone the average daily dose for adults is 2-4 g, for severe infections - up to 8 g; for children 50-200 mg/kg every 12 hours i/m, i/v 7-10 days 3rd generation cephalosporins
For initial empirical antibiotic therapy
A
13 Cefepime 0.5-1 g (for severe infections up to 2 g). 2-3 times i/m, i/v 7-10 days or more 4th generation cephalosporins
For initial empirical antibiotic therapy
A
14 Gentamicin single dose - 0.4 mg/kg, daily - up to 1.2 mg/kg, for severe infections single dose - 0.8-1 mg/kg. Daily - 2.4-3.2 mg/kg, maximum daily - 5 mg/kg 2-3 times i.v., i.m. 7-8 days Aminoglycosides IN
15 Amikacin 10-15 mg/kg. 2-3 times i.v., i.m. with intravenous administration - 3-7 days, with intramuscular administration - 7-10 days. Aminoglycosides
A
16 Ciprofloxacin 250mg-500mg 2 times inside, intravenously 7-10 days Fluoroquinolones IN
17 Levofloxacin orally: 250-750 mg 1 time per day. IV: 250-750 mg slowly by drip every 24 hours (a dose of 250-500 mg is administered over 60 minutes, 750 mg over 90 minutes). inside, intravenously 7-10 days Fluoroquinolones A
18 Moxifloxacin 400 mg 1 time per day IV (infusion over 60 min) IV generation fluoroquinolones A
19 Aztreons 0.5-1.0 g i.v. or i.m.
3.0-8.0 g/day in 3-4 administrations;
for Pseudomonas aeruginosa infection - up to 12.0 g/day;
Monobactam, monocyclic β-lactam
20 Meropenem 500 mg, for nosocomial infections - 1 g every 8 hours IV 7-10 days Carbapenems A
21 Imipenem 0.5-1.0 g every 6-8 hours (but not more than 4.0 g/day) 1 time per day IV 7-10 days Carbapenems A
22 Ertapenem 1g 1 time per day i.v., i.m. 3-14 days Carbapenems
23 Doripenem 500 mg every 8 hours IV 7-10 days Carbapenems A
24 Azithromycin 500 mg/day 1 time per day inside 3 days Azalids A
25 Clarithromycin 250-500 mg each 2 times a day inside 10 days Macrolides A
26 Tigecycline 100 mg IV for the first injection, 50 mg every 12 hours IV 7 days Glycylcycline IN
27 Vancomycin 0.5 g every 6 hours or 1 g every 12 hours 2-4 times inside, intravenously 7-10 days Glycopeptides IN
28 Metronidazole a single dose is 500 mg, the rate of IV continuous (jet) or drip administration is 5 ml/min. every 8 hours intravenously, inside 7-10 days Nitroimidazoles IN
29 Fluconazole 2 mg/ml - 100ml 1 time per day IV slowly over 60 minutes once Antifungal agent of the azole group for the prevention and treatment of mycoses A
30 Caspofungin On the 1st day, a single loading dose of 70 mg is administered, on the 2nd and subsequent days - 50 mg per day. 1 time per day IV slowly
within 60 minutes
The duration of use depends on the clinical and microbiological effectiveness of the drug A
31 Micafungin 50mg 1 time per day IV
slowly
within 60 minutes
7-14 days Antifungal agent of the echinocandin group for the prevention and treatment of mycoses A
Antisecretory drugs (used to reduce gastric secretion
- treatment of ulcers and prevention of stress ulcers, one of the following drugs is prescribed)
32 Pantoprozole 40 - 80 mg/day 1-2 times inside,
IV
2-4 weeks Antisecretory drug - proton pump inhibitor A
33 Famotidine 20 mg 2 times a day or 40 mg 1 time per day at night inside,
IV
4-8 weeks Antisecretory drug - histamine receptor blocker A
Direct acting anticoagulants (used for treatment and prevention
and treatment of coagulopathies in peritonitis)
34 Heparin initial dose - 5000 IU, maintenance: continuous intravenous infusion - 1000-2000 IU/hour (20000-40000 IU/day) every 4-6 hours IV 7-10 days A
35 Nadroparin 0.3 ml 1 time per day i.v., s.c. 7 days Direct anticoagulant (for the prevention of thrombosis) A
36 Enoxaparin 20mg 1 time per day PC 7 days Direct anticoagulant (for the prevention of thrombosis) A
Antiplatelet agent (used to improve microcirculation in peritonitis)
37 Pentoxifylline 600 mg/day 2-3 times inside, intramuscularly, intravenously 2-3 weeks Antiplatelet agent, angioprotector IN
Proteolysis inhibitor (used in the complex treatment of peritonitis, coagulopathy)
38 Aprotinin
as an auxiliary treatment - in an initial dose of 200,000 units, followed by 100,000 units 4 times a day with an interval of 6 hours IV slowly Proteolysis inhibitor - for the prevention of post-operative
tional pancreatitis
IN
initial dose 300,000 units, subsequent - 140,000 units every 4 hours IV (slow) until the clinical picture of the disease and laboratory test indicators are normalized Proteolysis inhibitor - for bleeding IN
Diuretic (used to stimulate diuresis)
39 Furosemide 20-80 mg/day 1-2 times a day intravenously, inside Loop diuretic A
40 Aminophylline 0.15 mg each 1-3 times a day inside up to 14-28 days Antispasmodic myotropic action IN
0.12-0.24 g each (5-10 ml of 2.4% solution) according to indications slowly (over 4-6 minutes) as the spasm subsides Antispasmodic myotropic action IN
Means for stimulating the intestinal tract for paresis
41 Neostigmine methyl sulfate 10-15 mg per day, maximum single dose - 15 mg, maximum daily dose - 50 mg. 2-3 times a day inside, intramuscularly, intravenously The duration of treatment is determined strictly individually depending on the indications, severity of the disease, age, and the patient’s response to treatment Anticholinesterase agent for the prevention and treatment of intestinal atony IN
42 Metoclopramide orally - 5-10 mg 3 times a day before meals; IM or IV - 10 mg; the maximum single dose is 20 mg, the maximum daily dose is 60 mg (for all routes of administration). 3 times a day inside, intramuscularly, intravenously according to indications Prokinetic, antiemetic IN
43 Sorbilact 150-300 ml (2.5-5 ml/kg body weight) once IV drip repeated infusions of the drug are possible every 12 hours during the first 2-3 days after surgery -
stva
Regulator of water-electrolyte balance and acid-base balance WITH
Antiseptics
44 Povidone - iodine An undiluted 10% solution is lubricated and washed with infected skin and mucous membranes; for use in drainage systems, the 10% solution is diluted 10 or 100 times. daily externally as needed Antiseptic, for treating skin and drainage systems IN
45 Chlorhexidine 0.05% aqueous solution externally once Antiseptic A
46 Ethanol solution 70%; for processing the surgical field, surgeon's hands externally once Antiseptic A
47 Hydrogen peroxide 3% solution for wound treatment externally as needed Antiseptic IN
Solutions for infusions
48 Sodium chloride 0.9% - 400ml 1-2 times IV
drip
depending on indication Solutions for infusions, regulators of water-electroite balance and acid-base balance A
49 Dextrose 5%, 10% - 400 ml, 500 ml; solution 40% in ampoule 5 ml, 10 ml 1 time IV
drip
depending on the indication Solution for infusion, for hypoglycemia, hypovolemia, intoxication, dehydration A
50 Aminoplaz-
mal
10% (5%) solution - up to 20 (40)
ml/kg/day
1 time IV
drip
depending on the patient's condition Parenteral nutrition product B
51 Hydroxy-
ethyl starch (HES) 6%, 10% - 400ml
250 - 500 ml/day 1-2 times IV Plasma replacement agent IN
Blood products
52 Leukofiltered erythrocyte suspension, 350 ml according to indications 1-2 times IV
drip
according to indications Blood components A
53 Apheresis leukofiltered virus-inactivated platelet concentrate, 360 ml according to indications 1-2 times IV
drip
according to indications Blood components A
54 Fresh frozen plasma, 220 ml according to indications 1-2 times IV
drip
according to indications Blood components A

Drug treatment , provided at the emergency stage:
No. INN name Dose Multiplicity Method of administration Continue
duration of treatment
Note Level of evidence
1 Sodium chloride 0.9% solution - 400ml 1-2 times IV
drip
depending on indication Solution for infusion A
2 Dextrose 5%, 10% - 400 ml,
500 ml; solution 40% in ampoule 5 ml, 10 ml
1 time IV
drip
depending on indication Solution for infusion,
for hypoglycemia, hypovolemia, intoxication, dehydration
A
3 Hydroxyethyl starch (HES) 6%, 10% - 400ml 250 - 500 ml/day 1-2 times IV
drip
The duration of treatment depends on the indication and blood volume. Plasma replacement agent IN

Other treatments

DOther types of treatment provided on an outpatient basis: are not carried out.

DOther types of treatment provided at the hospital level (according to indications):
plasmapheresis;
hemodiafiltration;
enterosorption;
ILBI.

DOther types of treatment provided at the emergency stage: are not carried out.

Surgical intervention:

Surgical intervention performed on an outpatient basis:
Surgical intervention is not performed on an outpatient basis.

Surgical intervention performed in an inpatient setting:
Anesthetic management: general anesthesia.
The purpose of surgery for a perforated ulcer:
elimination of perforated ulcer;
evacuation of pathological exudate, sanitation and drainage of the abdominal cavity;
source control (for abdominal sepsis);
gastric decompression or nasointestinal intubation for paresis due to peritonitis;
determination of further tactics in the postoperative period (for abdominal sepsis).

Scope of preoperative preparation
The scope of preoperative preparation depends on the severity of the patient’s condition (the presence or absence of abdominal sepsis).
1. Preoperative preparation of a patient with a perforated ulcer in the absence of abdominal sepsis:
1) antibiotic prophylaxis 60 minutes before the intravenous incision:
· 1.2 g amoxicillin/clavulanate,
· or 1.5 g ampicillin/sulbactam;
or 1.5 g cefuroxime,
· or cephalosporins (in the dosage indicated above) + 500 mg of metronidazole - with a high risk of contamination with anaerobic bacteria;
· or 1 g of vancomycin - if you are allergic to beta-lactams or have a high risk of wound infection;
2) correction of dysfunctions caused by concomitant pathologies;



2. Intensive preoperative preparation of a patient with a perforated ulcer and signs of abdominal sepsis, severe abdominal sepsis and septic shock - carried out over 2 hours (Recommendation 1A):
A patient with a perforated ulcer and signs of abdominal sepsis is immediately transferred to the intensive care unit (Recommendation 1A)!
1) effective hemodynamic therapy after central vein catheterization - EGDT with monitoring (adequacy criteria: blood pressure>65 mm Hg, CVP - 8-12 mm Hg, ScvO2> 70%, diuresis>0.5 ml/kg /h):
· administration of crystalloids not less than 1000 ml within 30 minutes(Recommendation 1A);
· or 300-500 ml of colloids for 30 minutes;
· according to indications (hypotension, hypoperfusion): vasopressors (norepinephrine, vasopressin, dopamine), corticosteroids - drugs and doses are selected by the resuscitator according to indications, taking into account monitoring data;
2) early (within the first hour from the moment the patient is admitted to the hospital) maximum starting empirical broad-spectrum antibiotic therapy one of the following drugs in monotherapy or in combination with metronidazole:
in monotherapy:
· piperacillin/tazobactam - 2.25 g x every 6 hours intravenously in a slow stream (over 3-5 minutes) or drip (over at least 20-30 minutes);
· or carbapenems: imipenem/cilastatin, meropenem, doripenem - 500 mg every 8 hours, ertapenem - 1 g x 1 time per day IV for 30 minutes;
· or tigecycline - 100 mg IV for the first injection, 50 mg every 12 hours;
· or moxifloxacin - 400 mg x 1 time per day intravenously for 60 minutes;
in combination with metronidazole, if the source is destruction of the appendix, colon, terminal ileum:
· or cefepime - 1-2 g per day IV (or 3rd generation cephalosporins 1-2 g x 2 times a day) + metronidazole 500 mg x 2 times a day IV;
· or aztreonam - 1-2 g per day IV + metronidazole 500 mg x 2 times a day IV;
3) a nasogastric tube into the stomach to evacuate the stomach contents;
4) bladder catheterization;
5) hygienic preparation of the surgical area.

Surgery
perforated ulcer is performed as a palliative or radical operation on the stomach and duodenum using an open and minimally invasive method.
Palliative operations:
· suturing the ulcer;
· excision of the ulcer followed by drug treatment;

· tamponade of the perforated hole using the Oppel-Polikarpov method (Cellan-Jones) (for large callous ulcers, when there are contraindications to gastric resection, and suturing leads to the cutting of sutures).
Radical operations:
· gastric resection;
· excision of the ulcer with vagotomy.
Factors influencing the volume of the operation:
· type and location of the ulcer;
· time elapsed since perforation;
· nature and prevalence of peritonitis;
· presence of a combination of complications of peptic ulcer;
· patient's age;
· technical capabilities of the operating team;
· degree of surgical and anesthetic risk.
Palliative surgery is indicated (Recommendation 1A) :
· if the perforation is more than 12 hours old;
· in the presence of widespread peritonitis;
· with a high degree of surgical and anesthetic risk (age, concomitant pathology, hemodynamic disorders).
Gastric resection is indicated (Recommendation 1B):
· for large callous ulcers (more than 2 cm);
· for ulcers with a high risk of malignancy (ulcers of the cardiac, prepyloric and greater curvature of the stomach);
· in the presence of a combination of complications (pyloroduodenal stenosis, bleeding).
Contraindications to gastric resection:
· perforation is more than 12 hours old;
widespread fibrinous-purulent peritonitis;
· high degree of surgical and anesthetic risk (according to ASA> 3);
old age;
· lack of technical conditions for performing the operation;
· insufficient qualification of the surgeon.
For large callous ulcers, when there are contraindications for gastric resection, and suturing leads to the cutting of sutures and an increase in the size of the perforation hole, the following are indicated:
· tamponade of the perforated hole using the Oppel-Polikarpov method (Cellan-Jones);
tamponade of the perforation with an isolated section of the greater omentum using the Graham method;
· insertion of a Foley catheter into the perforated hole with fixation of the greater omentum around the drainage.
Vagotomy:
not recommended for urgent surgery.
Minimally invasive operations(laparoscopic ulcer suturing, omental tamponade, ulcer excision) are indicated (Recommendations 1A) :
· with stable hemodynamic parameters in the patient;
· when the perforation hole size is less than 5 mm;
· when the perforation is localized on the anterior wall of the stomach or duodenum;
· in the absence of widespread peritonitis.
Contraindications to daparoscopic interventions:
· the dimensions of the perforation hole are more than 5 mm with pronounced periprocess;
widespread peritonitis;
· hard-to-reach localization of the ulcer;
· patients have at least 2 risk factors out of 3 on the Boey scale (see Appendix 7) (hemodynamic instability on admission, late hospitalization (more than 24 hours), the presence of serious concomitant diseases (ASA more than ≥ 3).
If the patient categorically refuses surgical treatment(after talking with the patient and warning about the consequences of refusal, it is necessary to obtain a written refusal from the patient from the operation), and also in the presence of absolute contraindications to surgical treatment, conservative treatment of a perforated ulcer is carried out as an option of despair:
· Taylor method - gastric drainage with constant aspiration, antibacterial, antisecretory, detoxification therapy and analgesia (Recommendations 1A) .
Postoperative therapy
The volume of therapy in the postoperative period depends on the severity of the patient’s condition (the presence or absence of abdominal sepsis).
1. Therapy of the postoperative period of a patient with a perforated ulcer in the absence of abdominal sepsis:
1) antibiotic therapy:
1.2 g amoxicillin/clavulanate + 500 mg metronidazole every 6
hours;
or 400 mg IV ciprofloxacin every 8 hours + 500 mg metronidazole
every 6 hours;
· or 500 mg IV levofloxacin once a day + 500 mg metronidazole
every 6 hours;
2) antifungal therapy:



3) antisecretory therapy:


4) adequate pain relief in the “on demand” mode (1 day - narcotic analgesic, 2-3 days - opioid narcotic analgesics - see P. 14.2.2 - Table) N.B.! Do not prescribe non-steroidal anti-inflammatory drugs - there is a risk of bleeding from the ulcer!);
5) infusion therapy for 2-3 days (crystalloids, colloids);
6) intestinal stimulation according to indications: enema +



7) early fractional tube enteral nutrition.
2. Intensive therapy of the postoperative period of a patient with a perforated ulcer in the presence of abdominal sepsis, severe abdominal sepsis, septic shock:
1) continuation of empirical broad-spectrum antibiotic therapy
actions according to the selected initial therapy regimen until receiving an antibiogram;
2) continuation of antibacterial therapy in de-escalation mode, taking into account
antibiograms 48-72 hours after the start of empirical therapy;
3) antifungal therapy:
· 400 mg of fluconazole x 1 time IV slowly over 60 minutes;
· or caspofungin 50 mg x 1 time IV slowly over 60 minutes;
· or micafungin 50 mg x 1 time IV slowly over 60 minutes;
4) effective hemodynamic therapy - EGDT with monitoring (BP>65 mmHg, CVP - 8-12 mmHg, ScvO2>70%, diuresis>0.5 ml/kg/h) to avoid intra-abdominal syndrome hypertension: crystalloids (Recommendation 1A), colloids, vasopressors (norepinephrine, vasopressin, dopamine - drugs and doses are selected by the resuscitator according to indications taking into account monitoring data), corticosteroids (for refractory septic shock 200-300 mg/day hydrocortisone or its equivalent bolus or continuously for at least 100 hours) ;
5) antisecretory therapy:
Pantoprozole 40 mg IV x 2 times a day - for the period of hospitalization;
· or famotidine 40 mg IV x 2 times a day - for the period of hospitalization;
6) prosthetics of external respiration function;
7) intra- and extracorporeal detoxification (forced diuresis, plasmapheresis, hemodiafiltration);
8) adequate pain relief “on demand” (narcotic, opioid narcotic analgesics - see P. 14.2.2 - Table., Do not prescribe non-steroidal anti-inflammatory drugs - there is a risk of bleeding from the ulcer!), prolonged epidural anesthesia;
9) prevention and treatment of coagulopathy under the control of a coagulogram (anticoagulants, agents that improve microcirculation, fresh frozen plasma, aprotinin - see P. 14.2.2 - Table);
10) correction of water and electrolyte disorders;
11) correction of hypo- and dysproteinemia;
12) blood transfusion for septic anemia (recommended hemoglobin level is at least 90 g/l);
13) intestinal stimulation: enema +
· neostigmine methyl sulfate 10-15 mg IM or IV x 3 times a day;
· or metoclopramide 10 mg/m or IV x 3 times a day;
· or/and sorbilact 150 ml IV;
14) nutritional support of at least 2500-3000 kcal per day (including early fractional tube enteral nutrition);
15) recombinant human activated protein C (drotrecoginA, rhAPC) not recommended for patients with sepsis.

Surgical intervention performed at the stage of emergency medical care: is not executed.

Indicators of treatment effectiveness:
relief of peritonitis;
absence of purulent-inflammatory complications of the abdominal cavity.

Indications for hospitalization

Indications for planned hospitalization: No.

Indications for emergency hospitalization:
A perforated ulcer is an absolute indication for emergency hospitalization in a specialized hospital.

Preventive actions:

Primary prevention:
· early diagnosis of gastric and duodenal ulcers;
· combating bad habits (smoking, alcohol abuse);
· adherence to diet and nutrition;
· carrying out eradication of HP infection with control of eradication;
Prescription of gastroprotectors when taking NSAIDs and anticoagulants;
· sanatorium-resort treatment, carried out no earlier than 2-3 months after the exacerbation subsides in specialized sanatoriums.

Prevention of secondary complications:
· prevention of the progression of peritonitis, intra-abdominal purulent complications, wound complications: adequate choice of the volume of surgery, method of eliminating the perforation, thorough sanitation and drainage of the abdominal cavity, timely determination of indications for programmed relaparotomy, antibiotic prophylaxis and adequate initial antibiotic therapy (Recommendations 1A) ;
· detoxification therapy (including extracorporeal detoxification);
· combating intestinal paresis to prevent SIAH;
· prevention of thrombohemorrhagic complications;
· prevention of pulmonary complications;
· prevention of stress ulcers.

Further management:
· differentiated therapy of the postoperative period (for perforated ulcers without sepsis and perforated ulcers with sepsis) - in P. 14.
· daily assessment of the severity of the condition (for assessment systems, see the Appendices);
· daily dressings;
· control of drainage (function, nature and volume of discharge), removal in the absence of exudate, if the volume of discharge is more than 50.0 ml, removal of drainage is not recommended in order to avoid the formation of an abdominal abscess;
· care of the nasogastric or nasointestinal tube by passively washing with saline solution (100-200 ml x 2-3 times a day) to ensure its drainage function, removal after the appearance of peristalsis;
· Ultrasound, plain radiography of the chest and abdominal cavity (if indicated);
· laboratory tests in dynamics (UAC, OAM, BHAK, coagulogram, lactate level, procalcitonin level - according to indications);
· the issue of suture removal and discharge is decided individually;
Recommendations after discharge:
· observation by a surgeon and gastroenterologist in a clinic (the duration of outpatient treatment and the issue of work ability are decided individually);
· diet No. 1 according to M.I. Pevzner, frequent, fractional, gentle meals;
· eradication therapy after suturing and excision of the ulcer - Maastricht-4 recommendations (Florence, 2010): if clarithromycin resistance rates in the region do not exceed 10%, then standard triple therapy is prescribed as a first-line regimen without prior testing. If resistance rates are in the range of 10-50%, then sensitivity to clarithromycin is first determined using molecular methods (real-time PCR).
One of the following schemes is selected:
The first line scheme is triple:
pantoprozole (40 mg x 2 times a day, or 80 mg x 2 times a day)
clarithromycin (500 mg 2 times a day)
amoxicillin (1000 mg 2 times a day) - 7-14 days
Second line diagram:
1 option- quad therapy:
bismuth tripotassium dicitrate (120 mg 4 times a day)

Tetracycline (500 mg 4 times a day)
Metronidazole (500 mg 3 times a day)
Option 2- triple therapy:
pantoprozole (40 mg x 2 times a day)
Levofloxacin (at a dose of 500 mg 2 times a day)
amoxicillin (at a dose of 1000 mg 2 times a day)
Third line diagram is based on determining the individual sensitivity of H. pylori to antibiotics.
Control of eradication after a course of treatment: rapid urease test + histological method + polymerase chain reaction to detect H. pylori in stool.

  1. Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
    1. References: 1. Guyatt G, Gutterman D, Baumann MH, Addrizzo-Harris D, Hylek EM, Phillips B, Raskob G, Lewis SZ, Schunemann H: Grading strength of recommendations and quality of evidence in clinical guidelines: report from an American college of chest physicians task force. Chest 2006, 129:174-181. 2. Brozek JL, Akl EA, Jaeschke R, Lang DM, Bossuyt P, Glasziou P, Helfand M, Ueffing E, Alonso-Coello P, Meerpohl J, Phillips B, Horvath AR, Bousquet J, Guyatt GH, Schunemann HJ: Grading quality of evidence and strength of recommendations in clinical practice guidelines: part 2 of 3. The GRADE approach to grading quality of evidence about diagnostic tests and strategies. Allergy 2009, 64:1109-1116. 3. Guide to emergency surgery of the abdominal cavity. // Edited by V.S. Savelyev. - M., Publishing house "Triada-X". 2005, - 640 p. 4. Diagnosis and treatment of perforated or bleeding peptic ulcers: 2013 WSES position paper Salomone Di Saverio, #1 Marco Bassi, #7 Nazareno Smerieri, 1,6 Michele Masetti, 1 Francesco Ferrara, 7 Carlo Fabbri, 7 Luca Ansaloni, 3 Stefania Ghersi ,7 Matteo Serenari,1 Federico Coccolini,3 Noel Naidoo,4 Massimo Sartelli,5 Gregorio Tugnoli,1 Fausto Catena,2 Vincenzo Cennamo,7 and Elio Jovine1 5. ASGE Standards of Practice Committee, Banerjee S, Cash BD, Dominitz JA, Baron TH, Anderson MA, Ben-Menachem T, Fisher L, Fukami N, Harrison ME, Ikenberry SO, Khan K, Krinsky ML, Maple J, Fanelli RD, Strohmeyer L. The role of endoscopy in the management of patients with peptic ulcer disease. GastrointestEndosc. 2010 Apr;71(4):663-8 6. Zelickson MS, Bronder CM, Johnson BL, Camunas JA, Smith DE, Rawlinson D, Von S, Stone HH, Taylor SM. Helicobacter pylori is not the predominant etiology for peptic ulcers requiring surgery. Am Surg. 2011;77:1054-1060. PMID: 21944523. 7. Svanes C. Trends in perforated peptic ulcer: incidence, etiology, treatment, and prognosis. WorldJ Surg.2000;24:277-283. 8. Møller MH, Adamsen S, Wøjdemann M, Møller AM. Perforated peptic ulcer: how to improve outcome/Scand J Gastroenterol. 2009;44:15-22. 9. Thorsen K, Glomsaker TB, von Meer A, Søreide K, Søreide JA. Trends in diagnosis and surgical management of patients with perforated peptic ulcer. J Gastrointest Surg. 2011;15:1329-1335. 10. Gisbert JP, Legido J, García-Sanz I, Pajares JM. Helicobacter pylori and perforated peptic ulcer prevalence of the infection and role of non-steroidal anti-inflammatory drugs. DigLiverDis. 2004;36:116-120. 11. Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal anti-inflammatory drugs, Helicobacter pylori, and smoking. J ClinGastroenterol. 1997;24:2-17. PMID: 9013343. 12. Manfredini R, De Giorgio R, Smolensky MH, Boari B, Salmi R, Fabbri D, Contato E, Serra M, Barbara G, Stanghellini V, Corinaldesi R, Gallerani M. Seasonal pattern of peptic ulcer hospitalizations: analysis of the hospital discharge data of the Emilia-Romagna region of Italy. BMC Gastroenterol. 2010;10:37. PMID: 20398297. 13. Janik J, Chwirot P. Perforated peptic ulcer-time trends and patterns over 20 years. MedSci Monit.2000;6:369-372. PMID:11208340. 14. D.F. Skripnichenko Emergency surgery of the abdominal cavity. Kiev - 1986 15. Yaitsky N.A., Sedov V.M., Morozov V.P. Ulcers of the stomach and duodenum. - M.: MEDpress-inform. - 2002. - 376 p. 16. Bratzler DW, Dellinger EP, Olsen KM, Perl TM, Auwaerter PG, Bolon MK, Fish DN, Napolitano LM, Sawyer RG, Slain D, Steinberg JP, Weinstein RA. Clinical practice guidelines for antimicrobial prophylaxis in surgery. Am J Health Syst Pharm. 2013 Feb 1;70(3):195-283. 17. Malfertheiner P., Megraud F., O’Morain C. et al. Management of Helicobacter pylori infection - the Maastricht IV Florence Consensus report // Gut. - 2012. - Vol.61. - P.646-664. 18. LuneviciusR, MorkeviciusM. Systematic review comparing laparoscopic and open repair for perforated peptic ulcer. Br J Surg. 2005;92:1195-1207. 19. 2013 WSES guidelines for management of intra-abdominal infections. Massimo Sartelli 1*, Pierluigi Viale 2, Fausto Catena 3, Luca Ansaloni 4, Ernest Moore 5, Mark Malangoni 6, Frederick A Moore 7, George Velmahos 8, Raul Coimbra 9, Rao Ivatury 10, Andrew Peitzman 11, Kaoru Koike 12, Ari Leppaniemi 13, Walter Biffl 5, Clay Cothren Burlew 5, Zsolt J Balogh 14, Ken Boffard 15, Cino Bendinelli 14, Sanjay Gupta 16, Yoram Kluger 17, Ferdinando Agresta 18, Salomone Di Saverio 19, Imtiaz Wani 20, Alex Escalona 21 , Carlos Ordonez 22 , Gustavo P Fraga 23 , Gerson Alves Pereira Junior 24 , Miklosh Bala 25 , Yunfeng Cui 26 , Sanjay Marwah 27 , Boris Sakakushev 28 , Victor Kong 29 , Noel Naidoo 30 , Adamu Ahmed 31 , Ashraf Abbas 32 , Gianluca Guercioni 33, Nereo Vettoretto 34 , Rafael Díaz-Nieto 35 , Ihor Gerych 36 , Cristian Tranà 37 , Mario Paulo Faro 38 , Kuo-Ching Yuan 39 , Kenneth Yuh Yen Kok 40 , Alain Chichom Mefire 41 , Jae Gil Lee 42 , Suk-Kyung Hong 43, Wagih Ghnnam 44, Boonying Siribumrungwong 45, Norio Sato 11, Kiyoshi Murata 46, Takayuki Irahara 47, Federico Coccolini 4, Helmut A Segovia Lohse 48, Alfredo Verni 49 and Tomohisa Shoko 50 20. Recommendations of the Russian Gastroenterological Association for the diagnosis and treatment of Helicobacter pylori infection in adults // Ross. magazine gastroenterol. hepatol., coloproctol. - 2012. - No. 1. - P.87-89.

List of protocol developers:
1) Akhmedzhanova Gulnara Akhmedzhanovna - Candidate of Medical Sciences, RSE at the PCV “Kazakh National Medical University named after S.D. Asfendiyarov”, Associate Professor of the Department of Surgical Diseases No. 1.
2) Medeubekov Ulugbek Shalharovich - Doctor of Medical Sciences, Professor, JSC National Scientific Surgical Center named after A.N. Syzganova”, Deputy Director for Scientific and Clinical Work.
3) Tashev Ibrahim Akzholuly - Doctor of Medical Sciences, Professor, JSC National Scientific Medical Center, Head of the Department of Surgery.
4) Izhanov Ergen Bakhchanovich - Doctor of Medical Sciences, JSC National Scientific Surgical Center named after A.N. Syzganov", chief researcher.
5) Elmira Maratovna Satbaeva - Candidate of Medical Sciences, RSE at the PHE "Kazakh National Medical University named after S.D. Asfendiyarov", head of the Department of Clinical Pharmacology.

Conflict of interest: absent.

Reviewers: Tuganbekov Turlybek Umitzhanovich - Doctor of Medical Sciences, Professor, Astana Medical University JSC, Head of the Department of Surgical Diseases No. 2.

Conditions for reviewing the protocol: review of the protocol 3 years after its publication and from the date of its entry into force and/or in the presence of new methods with a high level of evidence.

Annex 1


Clinical classification of sepsis:
Pathological process Clinical and laboratory signs
SIRS (System inflammatory response syndrome) - syndrome of a systemic inflammatory response of a macroorganism to a powerful damaging effect (infection, injury, surgery) body temperature above ≥ 38C or ≤ 36C
tachycardia (heart rate ≥ 90/min)
Tachypnea (RR> 20/min)
or hyperventilation
(PaCO2 ≤ 32 mm Hg)
· leukocytes> 12 x10 9 /l
or< 4 х 10 9 /л
or the presence of >10% immature
forms
Sepsis (abdominal): the body's systemic response to infection (infection + SIRS)
presence of an infectious focus (peritonitis)
· presence of 2 or more SIRS criteria
· establishing bacteremia is not necessary
Severe sepsis organ dysfunction
impaired perfusion (lactic acidosis, oliguria, impaired consciousness) or hypotension (SBP< 90 ммрт.ст. или ДАД < 40 мм.рт.ст.)
Septic shock
Hypotension resistant to BCC replacement
tissue and organ hypoperfusion
Additional definitions
Multiple organ dysfunction syndrome (MODS) Dysfunction of 2 or more body systems
Refractory septic shock Hypotension, resistant to BCC replacement, inotropic and vasopressor support

Appendix 2


Clinical interpretationresults of determining procalcitonin concentration
Concentration
procalcitonin
Interpretation Tactics
< 0,5 Sepsis, severe sepsis and septic shock are excluded.
However, it is necessary to exclude the presence of a localized infection.
· Observation
· Appointment of additional
laboratory and instrumental studies
0,5 - 2,0 Infection and sepsis are possible.
Severe sepsis and septic
shock is unlikely. Dynamic research needed
Search for the source of infection
· Establish the reason for the increase in procalcitonin concentration
· Consider the need
antibacterial therapy
2 - 10 High probability
SVR syndrome associated with a bacterial infectious complication
Intensive search for the source of infection
· Establish the reason for the increase in PCT concentration
· Start specific and supportive therapy
Antibacterial therapy required
> 10 High probability
severe sepsis and
septic shock. High risk
development of multiple organ dysfunction
Search for the source of infection
· Start a specific and
maintenance therapy
Intensive treatment is strictly necessary

Appendix 3


Mannheim peritonitis index(M. Linder et al., 1992)
MPI values ​​can range from 0 to 47 points. The MPI provides three grades of peritonitis severity. With an index of less than 21 points (first degree of severity), mortality is 2.3%, from 21 to 29 points (second degree of severity) - 22.3%, more than 29 points (third degree of severity) - 59.1%.
Billing et al. in 1994, a formula was proposed to calculate predicted mortality based on MPI:
Mortality (%) = (0.065 x (MPI - 2) - (0.38 x MPI) - 2.97.

Appendix 4


Assessment of functional organ-system capacity in sepsis can be carried out according to A. Baue criteria or the SOFA scale.
Criteria for organ dysfunction in sepsis(A.Baue, E. Faist, D. Fry, 2000)
System/organ Clinical and laboratory criteria
The cardiovascular system Blood pressure ≤ 70 mm Hg. for at least 1 hour, despite correction of hypovolemia
urinary system Diuresis< 0,5 мл/кг/ч в течение часа при адекватном волемическом восполнении или повышение уровня креатинина в 2 раза от нормального значения
Respiratory system Respiratory index (PaO2/FiO2) ≤ 250, or the presence of bilateral infiltrates on the radiograph, or the need for mechanical ventilation
Liver An increase in bilirubin content above 20 µmol/l for 2 days or an increase in transaminase levels by 2 times or more from normal
Blood coagulation system Platelet count< 100 000 мм 3 или их снижение на 50% от наивысшего значения в течение 3-х дней
Metabolic dysfunction
pH ≤7.3, base deficiency ≥ 5.0 mEq/L, plasma lactate 1.5 times higher than normal
CNS Glasgow scale score less than 15

Appendix 5


The severity of the condition depending on the severitysystemic inflammatory response and multiple organ dysfunction

Appendix 6


ANESTHETIC RISK ASSESSMENT
ASA classification of anesthetic risk(American Society of Anesthesiologists)
ASA 1
The patient has no organic, physiological, biochemical or mental disorders. The disease for which surgery is proposed is localized and does not cause systemic disorders.
ASA 2
Mild and moderate systemic disorders caused either by the disease for which surgery is planned or by other pathophysiological processes. Mild organic heart disease, diabetes, mild hypertension, anemia, old age, obesity, mild manifestations of chronic bronchitis.
ASA 3
Limitation of the usual lifestyle. Severe systemic disorders associated either with the underlying disease or due to other causes, such as angina pectoris, recent myocardial infarction, severe diabetes, heart failure.
ASA 4
Severe systemic disorders, life-threatening. Severe heart failure, persistent angina, active myocarditis, severe pulmonary, renal, endocrine or liver failure, which is not always amenable to surgical correction.
ASA 5
Extreme severity of the condition. There is little chance of a favorable outcome, but a “desperation” operation is performed.

Appendix 7


Boey Prognostic Scale
Consists of 3 factors:
· hemodynamic instability upon admission (systolic blood pressure less than 100 mmHg) - 1 point
Late hospitalization (over 24 hours) - 1 point
presence of serious concomitant diseases (ASA more than ≥ 3) - 1 point
In the absence of all risk factors, postoperative mortality is 1.5% (OR = 2.4), in the presence of 1 factor - 14.4% (OR = 3.5), in the presence of 2 factors - 32.1% (OR = 7.7). When all three factors are present, mortality increases to 100% (P< 001, Пирсона χ 2 тест).

Clinical protocols for diagnosis and treatment are the property of the Ministry of Health of the Republic of Kazakhstan

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2007 (Order No. 764)

Stomach ulcer (K25)

general information

Short description

Peptic ulcer- a chronic relapsing disease, the main morphological substrate of which is an ulcerative defect in the stomach, duodenum or proximal jejunum, with frequent involvement in the pathological process of other organs of the digestive system and the development of various complications.


The etiological factor is Helicobacter pylori (HP), a gram-negative spiral-shaped bacterium. Colonies live in the stomach, and the risk of infection increases with age. HP infection in most cases is the cause of the development of gastric and duodenal ulcers, B-cell lymphoma and cancer of the distal parts of the stomach. About 95% of duodenal ulcers and about 80% of gastric ulcers are associated with HP infection. Separately, there are symptomatic ulcers associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs) and steroid hormones.

Protocol code: H-T-029 "Peptic Ulcer"

For therapeutic hospitals
ICD-10 code(s):

K25 Stomach ulcer

K26 Duodenal ulcer

K27 Peptic ulcer of unspecified localization

K28.3 Acute gastroduodenal ulcer without bleeding or perforation

K28.7 Gastroduodenal ulcer, chronic without bleeding or perforation

K28.9 Gastroduodenal ulcer, not specified as acute or chronic without bleeding or perforation

Classification

Classification (Grebenev A.L., Sheptulin A.A., 1989, 1995)


According to nosological independence

1. Peptic ulcer.

2. Symptomatic gastroduodenal ulcers:

2.1 “Stress” ulcers:

A) with widespread burns (Curling ulcers);

B) with traumatic brain injuries, cerebral hemorrhage, neurosurgical operations (Cushing's ulcer);

C) for myocardial infarction, sepsis, severe injuries and abdominal operations.

2.2 Drug-induced ulcers.

2.3 Endocrine ulcers:

A) Zollinger-Ellison syndrome;

B) gastroduodenal ulcers with hyperparathyroidism.

2.4 Gastroduodenal ulcers in certain diseases of internal organs:

A) for nonspecific lung diseases;

B) for liver diseases (hepatogenic);

C) for diseases of the pancreas (pancreatogenic);

D) with chronic renal failure;

D) for rheumatoid arthritis;

E) for other diseases (atherosclerosis, diabetes mellitus, erythremia, etc.).


By location of the lesion

1. Stomach ulcers:

Cardiac and subcardial sections;

Body and angle of the stomach;

Antrum;

Pyloric canal.


2. Duodenal ulcers:

Duodenal bulbs;

Postbulbar region (intrabulb ulcers).


3 Combination of gastric and duodenal ulcers. Projection of damage to the stomach and duodenum:

Small curvature;

Greater curvature;

Front wall;

Back wall.

By number and diameter of ulcers:

Singles;

Multiple;

Small (up to 0.5 cm);

Average (0.6-1.9);

Large (2.0-3.0);

Giant (> 3.0).


According to clinical form:

Typical;

Atypical (with atypical pain syndrome, painless, asymptomatic).

According to the level of gastric acid secretion:

Elevated;

Normal;

Reduced.


According to the nature of gastroduodenal motility:

Increased tone and increased peristalsis of the stomach and duodenum;

Decreased tone and weakened peristalsis of the stomach and duodenum;

Duodenogastric reflux.


According to the phase of the disease:

Exacerbation phase;

Scarring phase;

Remission phase.


According to the timing of scarring:

With the usual terms of scarring (up to 1.5 months for duodenal ulcers and up to 2.5 months for gastric ulcers);

Hard-to-heel ulcers;

By the presence or absence of post-ulcer deformity;

Cicatricial ulcerative deformity of the stomach;

Cicatricial ulcerative deformity of the duodenal bulb.

According to the nature of the disease:

Acute (first identified ulcer);

Chronic: with rare exacerbations (once every 2-3 years); with monthly exacerbations (2 times a year or more often).

Risk factors and groups

Availability of HP;

Taking non-steroidal anti-inflammatory drugs, steroid hormones;

Presence of a family history;
- irregular intake of medications;
- smoking;

Drinking alcohol.

Diagnostics

Diagnostic criteria

Complaints and anamnesis
Pain: it is necessary to find out the nature, frequency, time of onset and disappearance of pain, connection with food intake.


Physical examination

1. Early pain occurs 0.5-1 hour after eating, gradually increases in intensity, persists for 1.5-2 hours, decreases and disappears as the gastric contents move into the duodenum; characteristic of ulcers of the body of the stomach. When the cardiac, subcardial and fundic regions are affected, pain occurs immediately after eating.

2. Late pain occurs 1.5-2 hours after eating, gradually intensifying as the contents are evacuated from the stomach; characteristic of ulcers of the pyloric stomach and duodenal bulb.


3. “Hungry” (night) pains occur 2.5-4 hours after eating, disappear after the next meal, characteristic of duodenal ulcers and pyloric stomach.


4. A combination of early and late pain is observed with combined or multiple ulcers. The severity of pain depends on the location of the ulcerative defect (minor pain - with ulcers of the body of the stomach, sharp pain - with pyloric and extra-bulb ulcers of the duodenum), age (more intense in young people), and the presence of complications.

The most typical projection of pain, depending on the location of the ulcerative process, is considered to be the following:

For ulcers of the cardial and subcardial parts of the stomach - the area of ​​the xiphoid process;

For ulcers of the body of the stomach - the epigastric region to the left of the midline;

For ulcers of the pylorus and duodenum - the epigastric region to the right of the midline.

Laboratory research

In the general blood test: posthemorrhagic anemia, reticulocytosis, increased amylase activity in the blood serum and urine (with penetration of the ulcer into the pancreas or reactive pancreatitis).
Changes in biochemical liver tests are possible (increased activity of ALT, AST in nonspecific reactive hepatitis, direct bilirubin when the papilla of Vater is involved in the inflammatory-destructive process).

When bleeding from an ulcer, the reaction to occult blood in the stool becomes positive.
The presence of HP is confirmed by microscopic, serological tests and the urease breath test (see below).

Instrumental studies


1. Presence of an ulcerative defect on endoscopy. In case of gastric localization of ulcers, it is necessary to conduct a histological examination to exclude malignancy.


2. Study of the presence of HP in the mucous membrane. Diagnosis of HP is mandatory for all patients with a history of gastric and duodenal ulcers, as well as a history of peptic ulcers and its complications. Diagnostic interventions to identify HP should be carried out both before the start of eradication therapy and after its completion to assess the effectiveness of the measures.


Invasive and non-invasive methods for detecting HP are used. According to the recommendations of Maastricht-3 (2005), in cases where endoscopy is not performed, it is preferable to use a urease breath test, determination of HP antigens in stool or a serological test for primary diagnosis. If endoscopy is performed, then a quick urease test (in a biopsy) is performed to diagnose HP; if it is impossible to perform it, a histological examination of the biopsy with Romanovsky-Giemsa, Warthin-Starry, hematoxylin-eosin, fuchsin or toluidine blue staining can be used to identify HP.

To monitor eradication, 6-8 weeks after the end of eradication therapy, it is recommended to use a breath test or study of HP antigens in the stool, and if this is impossible, a histological examination of biopsy specimens for HP.


Indications for consultation with specialists: according to indications.

List of main diagnostic measures:

General blood analysis;

Determination of serum iron in the blood;

General urine analysis;

Endoscopy with targeted biopsy (according to indications);

Histological examination of the biopsy;

Cytological examination of biopsy specimen;

HP test.


List of additional diagnostic measures:

Blood reticulocytes;

Ultrasound of the liver, biliary tract and pancreas;

Determination of blood bilirubin;

Determination of cholesterol;

Determination of ALT, AST;
- determination of blood glucose;

Determination of blood amylase;

X-ray of the stomach (if indicated).

Differential diagnosis

Signs

Functional (non-ulcer)

dyspepsia

Peptic ulcer
Daily rhythm of pain

Uncharacteristic (pain at any time of the day)

Characteristic
Seasonality of pain Absent Characteristic

Multi-year rhythm

pain

Absent Characteristic

Progressive course

illnesses

Not typical Characteristic
Duration of illness More often 1-3 years Often over 4-5 years
Onset of the disease

Often even in childhood and

adolescence

More often in young adults

of people

Pain relief after eating

Not typical

Characteristic when

duodenal ulcer

Night pain Not typical

Characteristic when

duodenal ulcer

Relationship between pain and

psycho-emotional

factors

Characteristic Occurs
Nausea Occurs frequently Rarely
Chair Mostly normal More often constipation
Weight loss Not typical Mostly moderate

Symptom of local

palpation

soreness

Not typical Characteristic

Related

neurotic manifestations

Characteristic

They meet, but not

natural and not so

significantly expressed, as in non-ulcer dyspepsia

Data

X-ray

research

Revealed motor

evacuation dyskinesia

stomach

An ulcerative “niche”, periduodenitis, perigastritis is revealed

FEGDS

Normal or increased gastric tone, pronounced vascular

pattern, distinct folds

Ulcer, post-ulcer scar,

gastritis

Complications

Bleeding;
- perforation;
- penetration;
- perigastritis;
- periduodenitis;
- cicatricial ulcerative pyloric stenosis;
- malignancy.

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment Goals

Eradication of H. pylori. “Relief (suppression) of active inflammation in the mucous membrane of the stomach and duodenum;

Healing of ulcerative defect;

Achieving stable remission;

Prevention of complications.


Non-drug treatment

Diet No. 1 (1a, 15) with the exclusion of foods that cause or enhance the clinical manifestations of the disease (for example, hot seasonings, canned, pickled and smoked foods).

Meals are split, 5~6 times a day.

Drug treatment

For gastric and duodenal ulcers associated with H. pylori, eradication therapy that meets the following requirements is indicated:

In controlled studies, HP eradication should occur in at least 80% of cases;

Should not be canceled due to side effects (acceptable in less than 5% of cases);


First line therapy (triple therapy) includes: proton pump inhibitor (omeprazole* 20 mg, pantoprazole* 40 mg, rabeprazole* 20 mg) + clarithromycin* 500 mg + amoxicillin* 1000 mg or metronidazole* 500 mg; All drugs are taken 2 times a day. The combination of clarithromycin with amoxicillin is preferable to clarithromycin with metronidazole due to the rapid development of resistance of HP strains to metronidazole.

Second line therapy(quad therapy) is recommended if first-line drugs are ineffective. Prescribed: proton pump inhibitor in a standard dose 2 times a day + bismuth B preparations 120 mg 4 times a day + metronidazole** 500 mg 3 times a day + tetracycline** 500 mg 3 times a day.

As an alternative, the above first-line therapy with the addition of bismuth preparations (480 mg per day) can be prescribed.

In case of ineffectiveness of first- and second-line eradication regimens, according to Maastricht-3 (2005), amoxicillin is proposed at a dose of 0.75 g 4 times a day in combination with high (quadruple) doses of proton pump inhibitors for 14 days. Another option may be to replace metronidazole with furazolidone at a dose of 100-200 mg 2 times a day.

Rules for anti-Helicobacter therapy:

1. If the use of a treatment regimen does not lead to eradication, it should not be repeated.

2. If the above regimens did not lead to eradication, this means that the bacteria previously had or acquired resistance to one of the components of the treatment regimen (nitroimidazole derivatives, macrolides).

3. If bacteria appear in the patient’s body a year after the end of treatment, the situation should be regarded as a relapse of the infection, and not as a reinfection.

After completion of combined eradication therapy according to indications (persistence of symptoms of hyperacidism, large and deep ulcers, complicated course, need to take ulcerogenic drugs for concomitant diseases), treatment should be continued with one of the antisecretory drugs on an outpatient basis for up to 4 weeks in case of duodenal and up to 6 weeks - for gastric localization of ulcers with subsequent histological monitoring.

In cases where HP cannot be detected, one should keep in mind the possible false negative results of the tests used. The reasons for this may be an incorrectly taken biopsy (for example, from the bottom of an ulcer), the use of antibacterial or antisecretory drugs by the patient, insufficient qualifications of morphologists, etc.

Severe peptic ulcer associated with H. pylori, not amenable to eradication;

Peptic ulcer with mutual burden syndrome (concomitant diseases).


The required scope of examinations before planned hospitalization:
- EGDS;
- general blood analysis;

Fecal occult blood test;
- urease test.

Information

Sources and literature

  1. Protocols for diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 764 of December 28, 2007)
    1. 1. Prodigy guidance – Dyspepsia – proven DU, GU, or NSAID-associated ulcer. NICE 2004 Management of Helicobacter pylori Infection. MOH Clinical Practice Guidelines 9/2004 2. I.N. Denisov, Yu.L. Shevchenko. Clinical guidelines plus pharmacological reference. M.2004. 3. New Zealand guidelines group/ Management of dyspepsia and heartburn, June 2004.) 4. Management of Helicobacter pylori infection. Ministry of health clinical practice guidelines 9/2004/ 5. Guidelines for clinical care. University of Michigan health system. May 2005. 6. Practice guidelines. Guidelines for the Management of Helicobacter pylori Infection/ THE AMERICAN JOURNAL OF GASTROENTEROLOGY Vol. 93, No. 12, 1998. 7. National Committee for Clinical Laboratory Standards/ Methods for Dilution Antimicrobial Susceptibility Tests for Bacteria That Grow Aerobically-Fift Edition/ Approved Standard NCCLS Document M7-F5, Vol.20, NCCLS, Wayne, PA, January 2000. 8 V.T. Ivashkin. Recommendations for the diagnosis and treatment of peptic ulcer. A manual for doctors. Moscow., 2005 9. Diagnosis and treatment of acid-dependent and Helicobacter-associated diseases. Ed. R.R. Bektaeva, R.T. Agzamova. Astana, 2005 10. A.V. Nersesov. Clinical classifications of the main diseases of the digestive system Educational and methodological manual, Astana, 2003.
    2. The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
    3. The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
    4. The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.

Classification.

  1. By etiology: peptic ulcer (chronic, callous ulcer), symptomatic ulcers (stress, NSAID-induced).
  2. By localization: stomach ulcers, ulcers of the pyloroduodenal zone.
  3. According to clinical forms: perforation into the abdominal cavity, covered perforation, atypical perforation (into the retroperitoneal space, omental bursa, into the pleural cavity).
  4. According to the stages of the course: initial stage, stage of limited peritonitis, stage of widespread peritonitis.

Diagnostics.

The diagnostic algorithm for suspected perforation of a gastroduodenal ulcer includes: establishing the fact of perforation of a hollow abdominal organ, identifying a history of ulcers, identifying complications, and assessing concomitant pathologies.

In the emergency department, a general clinical blood test, a biochemical blood test, a coagulogram, and a general urinalysis are urgently performed; determine blood type and Rh factor; An ECG, chest x-ray in direct projection and survey x-ray of the abdominal cavity (in bedridden patients - in the later position), ultrasound of the abdominal cavity (assessment of the presence of gas and liquid in the abdominal cavity) are performed; According to indications, consultations are carried out by doctors of therapeutic specialties.

The diagnosis of a perforated ulcer is established on the basis of: characteristic complaints (intense pain in the epigastrium), anamnestic data (history of peptic ulcer disease, taking NSAIDs, sudden appearance of sharp “dagger” pain in the epigastrium), physical signs of peritonitis and the absence of hepatic dullness on percussion, radiological signs free gas in the abdominal cavity.

In the absence of radiological signs of pneumoperitoneum, esophagogastroduodenoscopy (EGDS) is performed. During endoscopy, the location, nature and size of the ulcerative defect are determined, signs of perforation are identified, and combined complications of the ulcer are identified (bleeding, stenosis of the pylorobulbar zone, penetration). After endoscopy, a repeat radiography of the abdominal cavity is performed.

If there is no need for preoperative preparation and a verified diagnosis of perforation of a gastric or duodenal ulcer, the patient is subject to emergency surgery within 1 hour from the moment of diagnosis.

Patients with severe symptoms of intoxication, syndromic disorders and severe concomitant diseases are recommended to undergo short-term (within 1.5-2 hours) preoperative preparation in the intensive care unit. The question of the need and scope of preoperative preparation of the patient for surgery is decided jointly by the surgeon and anesthesiologist.

Surgical tactics.

A diagnosed perforated gastroduodenal ulcer is an absolute indication for surgical intervention. In the event of a patient’s categorical refusal to undergo surgery or the objective impossibility of performing surgical intervention established by the council due to the severity of the patient’s general condition, treatment using the Taylor method (aspiration and gastric lavage drainage) is used against the background of antiulcer, antibacterial, and infusion therapy.

Antibiotic therapy should begin immediately before surgery (the first administration of antibiotics is made 30 minutes before the start of surgery) and should be continued in the postoperative period. Empirical antibacterial therapy is carried out with third generation cephalosporins (2 g x 2 times a day) in combination with metronidazole (2 g per day).

Scope of surgery.

The priority surgical method for perforated gastroduodenal ulcers is suturing the perforated hole using video laparoscopic access.

Contraindications to endosurgical suturing are:

1. Widespread fibrinous and fibrinous-purulent peritonitis.

2. Severe inflammatory infiltration of the wall in the area of ​​perforation in combination with a large (more than 1.0 cm) perforation diameter.

3. A combination of several complications of peptic ulcer (perforation + stenosis, bleeding, penetration).

4. Severe cardiovascular and respiratory failure.

5. Pronounced adhesions in the abdominal cavity.

6. Rough scarring on the anterior abdominal wall due to previous operations.

If there are contraindications to the endosurgical method of suturing, the surgical procedure is performed from the upper-middle laparotomy approach.

Features of the perforation hole suturing technique:

1. If the size of the wall defect (stomach or duodenum) is 2 mm or less, and there is no perifocal inflammation, suturing the perforation with one U-shaped suture is indicated.

2. If the size of the perforation (stomach or duodenum) is from 2 to 5 mm, suturing is carried out with 3-4 separate gray-serous sutures in 1 row.

3. A wall defect of 5 mm to 1 cm is sutured with separate double-row sutures.

4. If the perforation is localized on the anterior wall of the stomach, it is possible to suturing defects more than 1 cm in diameter, but in these cases the decision is made individually.

5. In case of pronounced infiltration of the edges of the perforation, the use of the Welch-Polikarpov method (closing the perforation with a strand of the greater omentum) is indicated.

When performing suturing using video laparoscopic access, the first stage of the operation is the evacuation of exudate from the abdominal cavity.

After suturing perforated ulcers, it is mandatory to install a nasogastric tube and check the tightness of the sutures by insufflating air into the tube.

Sanitation of the abdominal cavity is carried out according to the accepted method (see Peritonitis) depending on the distribution of gastroduodenal contents and exudate.

Indications for performing distal gastrectomy for perforated gastroduodenal ulcers:

  1. The presence of complications of peptic ulcer combined with perforation - bleeding (including from a “mirror ulcer”), penetration, stenosis;
  2. Reasonable suspicion of malignancy or primary malignancy of a perforated gastric ulcer;
  3. Formation of decompensated stenosis after suturing large (one-third to half the diameter) pyloroduodenal perforated ulcers;
  4. Impossibility of reliable suturing of the perforation due to wall infiltration, including the Welch-Polikarpov method.

Postoperative management.

To prevent failure of sutures when suturing a perforated hole, patients are advised to undergo continuous decompression of the stomach through a nasogastric tube until postoperative paresis resolves.

In the postoperative period, patients are prescribed intensive therapy with inhibitors of gastric secretion: esomeprazole, omeprazole - initially 80 mg IV bolus, then as a drip infusion of 8 mg/hour, after resolution of the digestive tube paresis - switch to tablet forms as part of Helicobacter eradication therapy .

Loading...Loading...