Perforated gastric ulcer is an acute surgical disease, which is a complication of peptic ulcer. The term "perforated" means the occurrence of a through hole in the wall of a hollow organ. In medicine, to determine this condition, the synonym “perforative” (perforacio, which is translated from Latin as “drill”) is used.
Worldwide, ulcer perforation is considered one of the most dangerous conditions in emergency surgery with a high mortality rate.
Perforation is the formation of an opening in the wall of the stomach that opens into the abdominal cavity. Predominantly (up to 85%), a perforated ulcer develops against the background of an increase in inflammatory and destructive processes in the focus of a chronic or acute ulcer. And in 20%, perforation is noted in people without previously observed symptoms of peptic ulcer.
The mechanism of the development of the disease
Exacerbation of the chronic destructive process in the tissues of the ulcer without signs of regeneration leads to a gradual defeat of all layers of the gastric wall. At the bottom of the ulcer, new foci of necrosis appear, the size of the ulcer increases in depth and in width, which leads to the formation of a through opening in the wall of the organ.
From the hole formed, gastric juice flows into the free abdominal cavity. All organs of the abdominal cavity are covered with a special protective sheath - the peritoneum. The gastric secret has a physical, chemical, and later bacterial effect on the peritoneum. The body reacts to perforation with a state of shock as a result of a burn of the serous membrane with acidic gastric juice. Then comes the stage of sero-fibrous peritonitis with the transition to purulent diffuse or local peritonitis.
Sometimes perforation of the ulcer occurs unexpectedly against the background of health in young people with no connection with gastric ulcer. This is due to the development of autoimmune processes in the body, when the produced antibodies show aggression to their own cells.
In the lesion, an inflammatory response is activated with the release of a large number of inflammatory mediators (serotonin, prostaglandins). The aggressive acidic environment of the gastric chyme contributes to the destruction of the gastric wall, which leads to the formation of a hole.
It is still not possible to fully elucidate the mechanisms of ulcer perforation.
Varieties of perforated ulcer
In addition to cases of typical perforation into the abdominal cavity, which make up 80-90%, there are other types of perforations.
Covered perforation observed in 5–8% of cases when the opening in the stomach is closed by the wall of the adjacent adjacent organ, part of the omentum, fibrin film or a piece of food bolus. The clinical picture has a two-phase course: an acute onset, as in a typical case, then the extinction of symptoms, as the hole closes, and gastric juice no longer enters the abdominal cavity.
Atypical perforation(0.5%) occurs in the case of outflow of gastric secretions into a closed zone, limited by fibrous adhesions.
Combined variant. In 10% of all cases of perforated ulcers, a combination of perforation and internal bleeding occurs. This significantly alters the symptoms, leading to late diagnosis and poor outcome.
Risk of gastric ulcer perforation
Perforated gastric ulcer is a serious condition, even with timely surgery, the mortality rate is 5–18%. With delayed diagnosis and treatment, mortality reaches 60-70%.
A conditionally favorable result is observed in young people under 45 years of age without concomitant pathologies of other organs and systems.
A conditionally unfavorable outcome of the disease awaits elderly patients, people suffering from systemic diseases (diabetes, AIDS, autoimmune pathologies).
With the development of peritonitis occurs:
- blood poisoning - sepsis;
- the formation of purulent abscesses in the abdominal cavity;
- mesenteric thrombosis and intestinal necrosis.
Massive internal bleeding leads to hemolytic shock with neurological symptoms and the transition of the patient into a coma.
Complications in the postoperative period:
ICD-10 code
Perforated gastric ulcer according to ICD-10 (International Classification of Diseases 10th revision) has code K25 with clarifications depending on the stage of the process and the presence or absence of bleeding.
- acute forms with perforation only, or with perforation and bleeding: K25.1; K25.2.
- chronic or unspecified forms with perforation, or a combination of ulcer perforation with bleeding: K25.5; K25.6.
Causes and risk factors
The condition can provoke:
The causes of gastric ulcer perforation are diverse, but there is not always a direct relationship between the incidence of pathology and risk factors.
Useful video
Why a perforated ulcer occurs and how it is diagnosed is voiced in this video.
Diagnostics
A perforated stomach ulcer is an acute surgical condition, and immediate surgery is the only way to save the patient's life.
For diagnosis, laboratory and instrumental methods of examination are used.
Criteria confirming the diagnosis of ulcer perforation:
- In the clinical analysis of blood - leukocytosis, accelerated ESR.
- X-ray shows free gas under the dome of the diaphragm. X-rays are performed with the patient in an upright position or in a lateral position.
- Ultrasound reveals gas and effusion in the abdomen.
- FGDS is performed in the absence of characteristic symptoms of peritonitis and with suspicion of a covered perforated ulcer.
- Computed tomography shows the location of the ulcer, signs of perforation: free gas and liquid, thickening of the gastric wall.
- With unclear clinical symptoms in the case of atypical forms of perforated gastric ulcer, diagnostics is carried out by the laparoscopic method. A miniature video camera not only allows you to visually determine the perforation, assess the degree of spread of the pathological process in the abdominal cavity, but also take photos and videos. This may be necessary for a collegial decision on the issue of further therapeutic tactics in relation to the patient.
- Be sure to do an ECG to assess the state of cardiac activity and exclude myocardial infarction, which, in the abdominal form, has symptoms similar to the clinical picture of an "acute" abdomen.
Gastric ulcer or gastric ulcer is a common pathology of the digestive system, occurring in almost 1/10 of the population. More than 70% of patients are men, mostly young - from 20 to 45 years. Although this disease is much less common than duodenal ulcer, it has a more severe course, is more difficult to treat and is fraught with the development of serious complications.
Peptic ulcer of the stomach has its own general code according to ICD10 - K25, which is divided into subparagraphs, depending on the type and stage of the ulcer:
What is a stomach ulcer?
Peptic ulcer is a defect in the gastric mucosa, which is formed under the influence of various external and internal factors. It is considered not as a disease of a separate organ of the stomach, but as a whole organism for two reasons:
- the development of an ulcer contributes to a number of disorders in the body;
- the presence of an ulcer has a negative impact on other organs and systems, leads to the development of complications and deterioration of health.
From these considerations, it is more correct to speak not about an ulcer - a defect in the mucous membrane, but about a peptic ulcer - a pathology of the body as a whole.
What are the causes and risk factors for developing the disease?
The inner shell of the stomach is covered with a layer of mucus, which protects against damage by gastric juice, food. It becomes unprotected when, for any reason, the function of the mucous glands is insufficient. There are many such reasons.
- The presence in the stomach of a pathogenic bacillus of Helicobacter is detected in 80% of patients with an ulcer. This bacterium invades the mucous membrane and destroys its cells. The infection can enter the stomach with saliva and mucus when using shared utensils, close contact. This allows us to classify the ulcer as a contagious disease.
- Stress leading to impaired blood circulation in the stomach.
- Systematic exposure to alcohol, tobacco smoke products.
- Long-term use of drugs from the NSAID group (aspirin, paracetamol, ibuprofen, diclofenac and other analogs).
- Rough and spicy food, dry food.
Predisposing factors that increase the risk of developing the disease are heredity, chronic hyperacid gastritis, especially with the presence of erosions, as well as diseases of other organs - the liver, pancreas, intestines, diabetes mellitus, tuberculosis, cancer, decreased immunity.
Development mechanism
The pathogenesis of the development of peptic ulcer occurs as follows. Damaged by bacteria or other factors, the mucous membrane is constantly exposed to hydrochloric acid, the protein enzyme pepsin and food. Initially, superficial ulceration is formed, which gradually deepens, forming an ulcer.
In response to this, a pain reaction occurs, a spasm of smooth muscles, the process of digestion and evacuation from the stomach is disturbed. As a result, the entire gastrointestinal tract (gastrointestinal tract) suffers, duodenitis, enterocolitis may develop. Reflex occurs biliary dyskinesia, pancreatic ducts, cholecystitis, pancreatitis may develop.
Varieties of the disease
Classification of peptic ulcer is carried out according to several criteria.
According to the nature of the secretion of the stomach:
- with high and normal acidity;
- with reduced acid-forming function;
According to the localization of the ulcer:
According to the duration of the disease:
- acute stomach ulcer;
- chronic ulcer;
According to the phase of the disease:
- acute stage;
- subacute;
- remission.
According to the severity of the flow:
- latent(hidden);
- lung(exacerbations less than 1 time per year);
- moderate(exacerbations 1-2 times a year);
- heavy(exacerbations 3 or more times a year, the presence of complications).
Why is a stomach ulcer dangerous?
The disease leads to indigestion and gradually developing changes in all organs and systems associated with a lack of protein, vitamins, iron, and a decrease in hemoglobin levels. Such a pathology is especially dangerous during pregnancy - both for the mother and for the unborn child, and an exacerbation can provoke a miscarriage.
A threat to health and life are complications of peptic ulcer:
- perforation (perforation);
- bleeding;
- pyloric stenosis (pylorus);
- malignancy.
perforation
When the ulcer is deep, a through hole may appear in the wall of the stomach. Through it, gastric contents flow into the abdominal cavity, inflammation of the peritoneum develops - peritonitis.
Bleeding
If vessels are located in the defect zone, they can be corroded by gastric juice and burst, blood is poured into the stomach. Especially dangerous are ulcers of lesser curvature, where large vessels extend from the celiac artery - branches of the abdominal aorta. Such blood loss is very massive, often they are fatal.
Pyloric stenosis
Repeatedly scarred ulcer in the area of the outlet of the stomach causes its stenosis - narrowing. Food stagnates in the stomach, inflammation develops.
Malignization
Long-term non-healing gastric ulcers, especially those with reduced or no acid-forming function, tend to turn into cancer. A dense tissue shaft is formed around the defect - the so-called callous ulcer, in which malignant degeneration of cells occurs.
Clinical symptoms
How a stomach ulcer is clinically manifested depends on its shape and location, the nature of gastric secretion, and the presence of complications. Common characteristic symptoms are:
- heartburn 1.5-2 hours after eating;
- epigastric pain after eating;
- belching after eating with sour contents, food;
- nausea 30-60 minutes after eating, vomiting;
- a feeling of heaviness in the epigastric region, a feeling of fullness in the abdomen;
- bloating, stool retention.
In the latent course, these manifestations are not expressed, and in the acute phase, the clinical picture can be very dramatic.
If there is a perforation of the ulcer, there is a strong "dagger" pain, tension in the abdominal muscles, vomiting, and the general condition is disturbed. With bleeding, pain is not characteristic, vomiting occurs like coffee grounds (blood mixed with gastric juice), there is a sharp pallor, dizziness, pressure decreases, and the pulse quickens. Hemorrhagic shock may develop.
With pyloric stenosis, frequent vomiting and rapid weight loss appear. A malignant ulcer causes constant pain in the abdomen, vomiting, loss of appetite, a sharp decrease in weight, enlarged lymph nodes (metastases) may appear on the neck on the left and above the collarbone.
Diagnostics
When examining the patient, attention is drawn to a white thick coating on the tongue, bloating, palpation pain in the epigastrium. An x-ray of the stomach with contrast is preliminarily prescribed, this allows you to identify a mucosal defect, deformation by scars, and the presence of a tumor.
The most reliable is FGDS - fiberoptic gastroscopy, when the entire stomach is examined from the inside with a probe with a video camera, it is possible to take a biopsy.
The diagnosis includes the study of gastric secretion by probing, clinical blood and urine tests, all biochemical studies. Be sure to test for the presence of Helicobacter by one of the methods (endoscopic, respiratory, laboratory).
Useful video
What causes the development of the disease and how to treat it are told by experienced specialists in this matter.
Treatment Methods
Treatment of peptic ulcer disease is complex, it includes:
- diet therapy;
- medicinal preparations;
- physiotherapy.
The diet should consist of well-digestible food that does not irritate the stomach, with multiple intake 5-6 times a day in small portions. The diet includes a sufficient amount of protein, vitamins, coarse fiber, spicy seasonings, salty, fried and canned foods are excluded.
The medical program is compiled individually. If Helicobacter is detected, antimicrobial drugs are prescribed. With increased acidity, antacids are given, with reduced acidity, hydrochloric acid, pepsin. In all cases, gastroprotectors, vitamins, biostimulants are prescribed to accelerate the epithelialization of the defect.
Of the physiotherapeutic procedures, magnetotherapy, iontophoresis, galvanization, electrosleep are prescribed, laser therapy gives a good effect - stimulating irradiation through a probe. The treatment course is carried out until the onset of scarring, which is detected at the control endoscopy.
Surgical treatment is indicated in cases of complications. In case of bleeding, perforation, the operation is performed according to vital indications. With pyloric stenosis, the patient is prepared and operated on in a planned manner. Malignant ulcers are treated in oncology.
Forecast and prevention
It is difficult to achieve a complete cure for an ulcer, with proper treatment it is possible to achieve long-term remissions, so the prognosis for health is relatively favorable. For life, it is unfavorable in the event of the development of severe complications that have a high mortality rate. Surviving patients after surgery often become disabled.
With regard to military service, depending on the nature and stage of the disease, a delay may be given, and after a second examination, the question of fitness for service is decided. Most often, in peacetime, such patients are not called up for service.
Prevention of peptic ulcer disease consists in proper nutrition, getting rid of bad habits, observing the rules of personal hygiene, and timely treatment of existing chronic diseases.
Penetration is the destruction of the wall of the stomach, while the bottom of the ulcer becomes a nearby organ. Usually it is the pancreas. Hydrochloric acid and pepsin destroy its structure, causing acute destructive pancreatitis. The first symptoms of penetration are a sharp girdle pain in the abdomen, fever and an increase in alpha-amylase in the blood.
Perforation is the destruction of the wall of an organ and the entry of its contents into the abdominal cavity or retroperitoneal space. Occurs in 7-8% of cases. Violation of the integrity of the wall can provoke weight lifting, hard physical labor, eating fatty and spicy foods, drinking. The clinical picture is characterized by all the signs of diffuse peritonitis (general weakness, abdominal pain throughout, intoxication, and others).
Plain radiography of the abdominal cavity in an upright position helps to diagnose gastric perforation! On it you can see disc-shaped enlightenment (gas) under the dome of the diaphragm.
Malignancy is the degeneration of an ulcer into stomach cancer. This complication occurs infrequently, in about 2-3% of patients. It is noteworthy that duodenal ulcers never transform into a malignant tumor. With the development of cancer, patients begin to lose weight, they have an aversion to meat food, and their appetite is reduced. Over time, symptoms of cancer intoxication appear (fever, nausea, vomiting), pallor of the skin. A person can lose weight up to cachexia (complete exhaustion of the body).
Pyloric stenosis occurs if the ulcerative defect is localized in the pyloric region. The pylorus is the narrowest part of the stomach. Frequent relapses lead to scarring of the mucosa and narrowing of the pyloric region. This leads to disruption of the passage of food into the intestines and its stagnation in the stomach.
There are 3 stages of pyloric stenosis:
Compensated - the patient has a feeling of heaviness and fullness in the epigastric region, frequent belching of sour, but the general condition remains satisfactory;
Subcompensated - patients complain that even a small meal causes a feeling of fullness and heaviness in the abdomen. Vomiting is frequent and brings temporary relief. Patients lose weight, afraid to eat;
Decompensated - the general condition is severe or extremely severe. The food eaten no longer passes into the intestine due to the complete constriction of the pylorus. Vomiting is profuse, repeated, happens immediately after eating food. Patients are dehydrated, they have a loss of body weight, electrolyte imbalance and pH, muscle cramps.
Bleeding.
Gastrointestinal bleeding occurs due to the destruction of the vessel wall at the bottom of the ulcer (the cause of bleeding from the anus). This complication is quite common (about 15% of patients). Clinically, it is manifested by vomiting "coffee grounds", chalky and general signs of blood loss.
Vomiting "coffee grounds" got its name due to the fact that the blood, entering the lumen of the stomach, enters into a chemical reaction with hydrochloric acid. And in appearance it becomes brown-black with small grains.
Melena is tarry or black stools (causes of black stools). The color of feces is also due to the interaction of blood with gastric juice. However, it should be remembered that some medications (iron preparations, activated charcoal) and berries (blackberries, blueberries, black currants) can stain the stool black.
Common signs of blood loss include general pallor, decreased blood pressure, tachycardia, and shortness of breath. The skin is covered with sticky sweat. If the bleeding is not controlled, the person may lose too much blood and die.
Perforated (perforated) ulcer is the most severe complication of peptic ulcer of the stomach and duodenum, leading, as a rule, to the development of peritonitis. Perforation of an acute or chronic ulcer is understood as the occurrence of a through defect in the wall of an organ, usually opening into the free abdominal cavity.
ICD-10 CODES
K25. Gastric ulcer. K25.1. Acute with perforation. K25.2. Acute with bleeding and perforation. K25.3. Acute without bleeding or perforation. K25.5. Chronic or unspecified with perforation. K25.6. Chronic or unspecified with bleeding and perforation. K25.7. Chronic without bleeding or perforation. K26. Duodenal ulcer. K26.1. Acute with perforation. K26.2. Acute with bleeding and perforation. K25.3. Acute without bleeding or perforation. K26.5. Chronic or unspecified with perforation. K26.6. Chronic or unspecified with bleeding and perforation. K26.7. Chronic without bleeding or perforation. Gastroduodenal ulcers are more likely to perforate in men with a short history of ulcers (up to 3 years), usually in the autumn or spring, which is apparently associated with a seasonal exacerbation of peptic ulcer. During wars and economic crises, the frequency of perforation increases by 2 times (due to poor nutrition and a negative psycho-emotional background). The number of patients with perforated ulcers of the stomach and duodenum is currently 13 per 100,000 population (Pantsyrev Yu.M. et al., 2003). Ulcer perforation can occur at any age: both in childhood (up to 10 years) and senile (after 80 years). However, it mostly occurs in patients 20-40 years old. Young people are characterized by perforation of duodenal ulcers (85%), for the elderly - gastric ulcers. It is possible to prevent the occurrence of a perforated ulcer with the help of persistent, adequate conservative treatment of patients with peptic ulcer. Preventive anti-relapse seasonal treatment is of great importance. By etiology:
- perforation of a chronic ulcer;
- perforation of an acute ulcer (hormonal, stress, etc.).
- gastric ulcer (small or large curvature, anterior or posterior wall in the antral, prepyloric, pyloric, cardial section or in the body of the stomach);
- duodenal ulcer (bulbar, postbulbar).
- perforation into the free abdominal cavity (typical or covered);
- atypical perforation (into the omental sac, lesser or greater omentum, retroperitoneal tissue, cavity isolated by adhesions);
- combination with bleeding in the gastrointestinal tract.
- chemical peritonitis (period of primary shock);
- bacterial peritonitis with systemic inflammatory response syndrome (a period of imaginary well-being);
- diffuse purulent peritonitis (a period of severe abdominal sepsis).
A.I. Kirienko, A.A. Matyushenko
Perforated ulcer. Treatment
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medbe.ru
Ulcer according to the international classification of diseases
Stomach ulcer code for microbial code 10 - K 25. What do these numbers mean? We are talking about the international classification of diseases. This is a document that is considered one of the main ones in healthcare.
About ICD
The International Classification of Diseases was created to make it easier to systematize and analyze data on diseases and mortality in different countries. In addition, all diseases are recorded in the form of codes, which makes it easier to store patient data, and if necessary, they can be quickly decrypted.
The science of health does not stand still, new discoveries are made, besides, some errors may appear in the compiled document, or the researchers were able to come up with an interesting new classification that should be used instead of the old one. Therefore, from time to time, the International Classification of Diseases is revised. This happens once every 10 years.
Now the ICD of the Tenth Revision is relevant, which is designated as ICD-10. The last revision conference was held in the autumn of 1989 and approved in 1990. Since about 1994, various states began to use it, Russia switched to ICD-10 only in 1999. The basis of this classification is the use of a special code, which consists of one letter and a group of numbers. Since 2012, work has been underway to revise this classification, which will be referred to as ICD-11. Already in 2018, they plan to start using the new classification, but so far the ICD-10 version remains relevant.
Gastric ulcer in the classification
Once in Russia, patients were diagnosed with one diagnosis: "gastric ulcer and duodenal ulcer." But, according to ICD-10, gastric ulcer is a separate disease, code K25 is used for it. If the patient has a duodenal ulcer, then it is designated by another code - K26. But if it is peptic, then K27, and with gastrojejunal - K 28.
It is also important to know that if erosion has formed on the walls of the stomach, that is, the patient has acute erosive gastritis with bleeding, it is recorded using the K29 code. Erosive gastritis is very similar to a stomach ulcer, but the difference is that when healing, erosion does not leave scars, while with an ulcer, scars always form.
Designation of complications
Doctors who treat this condition know that gastric ulcers (PU) can progress differently in different patients. The doctor, having learned by code that the patient has an ICD-10 stomach ulcer - this is 25, will not be able to prescribe treatment, therefore an additional classification was introduced:
| K25.0 | The patient has an acute form, complicated by bleeding. |
| K25.1 | Also an acute form, but with perforation. A through defect is formed through which the contents of the stomach enter the abdominal cavity, causing peritonitis. |
| K25.2 | This is an acute perforated ulcer, accompanied by bleeding. |
| K25.3 | Acute, but without perforation or bleeding. |
| K25.4 | The patient has a chronic form, or it is not yet clear which one, accompanied by bleeding. |
| K25.5 | Also a chronic form or unspecified, there is also a perforation. |
| K25.6 | This refers to a chronic or unspecified disease in which there is both perforation and bleeding. |
| K25.7 | The patient has a chronic form or an unspecified diagnosis, but it proceeds without complications, that is, there is no perforation or bleeding. |
| K25.9 | It may be acute or chronic, but the patient did not have bleeding or perforation, the diagnosis is not specified. |
Are all complications noted in the ICD
In ICD-10, some complications of the disease are noted, but not all. For example, there is no mention of penetration. This is the spread of an ulcer to other organs that are nearby. Also, nothing is said about malignancy, that is, its gradual degeneration into a malignant tumor.
The stomach ulcer takes its place in the ICD-10, under the code K25. Here you can also learn about the complications that the patient had, understand what kind of disease the patient had: acute or chronic. But some complications are not displayed here, so it makes sense to soon switch to ICD-11, where, perhaps, the information will be more complete.
zhivot.info
Gastric and duodenal ulcer without bleeding and perforation
Treatment tactics
Treatment goals: eradication of Helicobacter pylori, healing of a peptic ulcer, "suppression" of active inflammation in the mucous membrane of the stomach and duodenum. Disappearance of pain and dyspeptic syndromes, prevention of complications and recurrence of the disease.
Non-drug treatment: diet No. 1 (1a, 5) with the exception of dishes that cause or increase the clinical manifestations of the disease (for example, spicy seasonings, pickled and smoked foods). Food is fractional, 5~6 times a day.
Drug treatment of Helicobacter-associated peptic ulcer of the stomach and/or duodenum
In accordance with the Maastricht Consensus (2000) for the treatment of HP infection, priority is given to regimens based on proton pump inhibitors (PPIs), as the most powerful of the antisecretory drugs. It is known that they are able to maintain a pH greater than 3 in the stomach for at least 18 hours a day, which ensures the healing of duodenal ulcers in 100% of cases.
PPIs, lowering the acidity of gastric juice, increase the activity of antibacterial drugs, worsen the environment for the life of H. pylori. In addition, PPIs themselves have antibacterial activity. In terms of anti-Helicobacter pylori activity, rabeprazole is superior to other PPIs and, unlike other PPIs, is metabolized non-enzymatically and excreted mainly through the kidneys. This metabolic pathway is less dangerous in terms of possible adverse reactions when PPIs are combined with other drugs that are competitively metabolized by the cytochrome P450 system.
The first line therapy is a three-component therapy.
Proton pump inhibitor (rabeprazole 20 mg, omeprazole or lansoprazole 30 mg, or esomeprazole 20 mg) + clarithromycin 7.5 mg/kg (max-500 mg) + amoxicillin 20-30 mg/kg (max 1000 mg) or metronidazole 40 mg /kg (max 500 mg); All medicines are taken 2 times a day for 7 days. The combination of clarithromycin with amoxicillin is preferred over clarithromycin with metronidazole, as it may result in a better outcome in second-line therapy.
In case of ineffectiveness of first-line drugs, unsuccessful eradication, a second course of combination therapy (quadrotherapy) is prescribed with the additional inclusion of colloidal bismuth subcitrate (de-nol and other analogues) at 4 mg / kg (max 120 mg) 3 times a day, for 30 min. before meals and the 4th time 2 hours after eating, at bedtime. The inclusion of this drug potentiates the anti-Helicobacter effect of other antibiotics.
Rules for the use of anti-Helicobacter therapy:
1. If the use of the treatment regimen does not lead to the onset of eradication, it should not be repeated.
2. If the scheme 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 spectrum of antibiotics used should be determined.
4. If a bacterium appears 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, a more effective treatment regimen should be used.
After the end of combined eradication therapy, it is necessary to continue treatment for another 1-2 weeks with duodenal ulcers and for 2-3 weeks with gastric localization of ulcers using one of the antisecretory drugs. Preference is given to the IPP, because. after the abolition of the latter (unlike histamine H2-receptor blockers), the so-called secretory “rebound” syndrome is not observed.
In the case of peptic ulcer, not associated with H. pylori, the goal of treatment is the relief of the clinical symptoms of the disease and scarring of the ulcer. The appointment of antisecretory drugs - proton pump inhibitors (rabeprazole or omeprazole 20 mg 1-2 times a day, lansoprazole 30 mg 2 times a day, esomeprazole 20 mg 2 times a day) is shown.
To normalize the motor function of the duodenum, biliary tract, the use of prokinetics is indicated - domperidone at 0.25-1.0 mg / kg 3-4 times a day, for 20-30 minutes. before meals, the duration of treatment is at least 2 weeks.
In order to reduce the tone and contractile activity of the smooth muscles of the internal organs, reduce the secretion of exocrine glands, hyoscine butylbromide (Buscopan) is prescribed 10 mg 2-3 times a day. If necessary - antacids (maalox, almagel, phosphalugel), cytoprotectors (sucralfate, de-nol, ventrisol, bismofalk), synthetic E1 prostaglandins (misoprostol), mucosal protectors (solcoseryl, actovegin) vegetotropic drugs (Pavlov's mixture, valerian root infusion) . The duration of treatment is at least 4 weeks. In case of excretory insufficiency of the pancreas, after the severity of the process subsides, pancreatin * is prescribed at 10,000 lipase (or creon 10,000, 25,000) x 3 times with meals, for 2 weeks.
The effectiveness of treatment for gastric ulcers is controlled by the endoscopic method after 8 weeks, with duodenal ulcers - after 4 weeks.
Preventive actions:
Prevention of bleeding;
Penetration prevention;
Perforation prevention;
Stenosis prevention;
Malignancy warning.
Further management
Within 1 year after discharge from the hospital, the child is examined by the local pediatrician every 3 months, then 2 times a year (in spring, autumn). EFGDS is desirable to do after 6 months. after the onset of exacerbation to assess the effectiveness of the therapy.
Anti-relapse treatment is carried out in the spring and autumn periods. The principle of anti-relapse therapy is the same as the treatment of exacerbation (mental and physical rest, clinical nutrition, drug therapy). Course duration 3-4 weeks. Physical education is carried out in a special group of exercise therapy. According to indications, the student is organized 1 additional day per week. Sanatorium treatment is carried out no earlier than 3-6 months after the disappearance of the pain syndrome and the healing of ulcers in local sanatoriums.
List of essential medicines:
1. Rabeprazole 20 mg, 40 mg tab.
2. Omeprazole 20 mg, tab.
3. Clarithromycin, 250 mg, 500 mg, tab.
4. Metronidazole, tb. 250 mg
5. Amoxicillin, 500 mg, 1000 mg tab., 250 mg, 500 mg capsule; 250 mg/5 ml oral suspension
6. Domperidone, 10 mg, tab.
7. Famotidine, 40 mg, tab., 20 mg/ml solution for injection
8. Actovegin, 5.0 ml, amp.
9. Bismuth tripotassium dicitrate, 120 mg, tab.
10. Metronidazole, 250 mg tab.; 0.5% in vial, 100 ml solution for infusion
List of additional medicines:
1. Hyoscinbutyl bromide, 10 mg dragee, 1 ml amp.; 10 mg suppositories
2. Pavlova mixture, 200 ml
3. Pancreatin 4500 units, caps.
4. Aevit, capsules
5. Pyridoxine hydrochloride, 1 amp. 1 ml 5%
6. Thiamine bromide, 1 amp. 1 ml 5%
7. No-shpa, amp. 2 ml 2% tablets 0.04
8. Folic acid, tab. 0.001
9. Almagel suspension, bottle 170 ml
10. Maalox, tablets, suspension, bottle 250 ml, suspension in sachets (1 pack - 15 ml)
11. Valerian extract, tab.
12. Adaptol, tab.
Treatment effectiveness indicators:
1. Eradication of Helicobacter Pylori.
2. The beginning of the healing of the ulcer.
3. "Kupirovanie" (suppression) of active inflammation in the mucous membrane of the stomach and duodenum.
4. Disappearance of pain and dyspeptic syndromes.
5. Prevention of complications (perforation, penetration, malignancy, bleeding) and the occurrence of relapses of the disease.
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Probodnaya(perforated) ulcer - the most severe complication of peptic ulcer of the stomach and duodenum, leading, as a rule, to the development of peritonitis. Perforation of an acute or chronic ulcer is understood as the occurrence of a through defect in the wall of an organ, usually opening into the free abdominal cavity.
ICD-10 CODES
K25. Gastric ulcer.
K25.1. Acute with perforation.
K25.2. Acute with bleeding and perforation.
K25.5. Chronic or unspecified with perforation.
K25.6. Chronic or unspecified with bleeding and perforation.
K25.7. Chronic without bleeding or perforation.
K26. Duodenal ulcer.
K26.1. Acute with perforation.
K26.2. Acute with bleeding and perforation.
K25.3. Acute without bleeding or perforation.
K26.5. Chronic or unspecified with perforation.
K26.6. Chronic or unspecified with bleeding and perforation.
K26.7. Chronic without bleeding or perforation.
Epidemiology
Gastroduodenal ulcers are more likely to perforate in men with a short history of ulcers (up to 3 years), usually in the autumn or spring, which is apparently associated with a seasonal exacerbation of peptic ulcer. During wars and economic crises, the frequency of perforation increases by 2 times (due to poor nutrition and a negative psycho-emotional background). The number of patients with perforated ulcers of the stomach and duodenum is currently 13 per 100,000 population (Pantsyrev Yu.M. et al., 2003). Ulcer perforation can occur at any age: both in childhood (up to 10 years) and senile (after 80 years). However, it mostly occurs in patients 20-40 years old. Young people are characterized by perforation of duodenal ulcers (85%), for the elderly - gastric ulcers.Prevention
It is possible to prevent the occurrence of a perforated ulcer with the help of persistent, adequate conservative treatment of patients with peptic ulcer. Preventive anti-relapse seasonal treatment is of great importance.Classification
By etiology:- perforation of a chronic ulcer;
- perforation of an acute ulcer(hormonal, stress, etc.).
- stomach ulcer(small or large curvature, anterior or posterior wall in the antral, prepyloric, pyloric, cardiac section or in the body of the stomach);
- duodenal ulcer(bulbar, postbulbar).
- perforation into the free abdominal cavity(typical or covered);
- atypical perforation(into the omental sac, lesser or greater omentum, retroperitoneal tissue, cavity isolated by adhesions);
- combination with bleeding into the gastrointestinal tract.
- chemical peritonitis(period of primary shock);
- bacterial peritonitis with systemic inflammatory response syndrome(period of imaginary well-being);
- diffuse purulent peritonitis(period of severe abdominal sepsis).
Etiology
Of the factors provoking perforation of ulcers, one can name the overflow of the stomach with food, errors in diet and alcohol intake, physical stress, accompanied by an increase in intragastric pressure.Pathogenesis
Perforation of the ulcer typically leads to the entry into the abdominal cavity from the stomach and duodenum of contents that act on the peritoneum as a chemical, physical, and then bacterial irritant. The initial reaction of the body to perforation is very similar to the pathogenesis of shock (which gives reason to call this phase the stage of primary shock). This is due to a burn of the peritoneum by acidic gastric juice that poured into the abdominal cavity. Subsequently, serous-fibrinous, and then purulent peritonitis occurs. The rate of development of peritonitis is the higher, the lower the acidity of gastric juice. That is why the phenomena of widespread (diffuse) purulent peritonitis may not be 6 or even 12 hours after perforation of a duodenal ulcer (it is characterized by a high level of acidity of gastric juice). At the same time, during these periods, they are usually expressed with perforation of gastric ulcers (very quickly, within 2-3 hours, diffuse purulent peritonitis occurs during destruction and perforation of the stomach tumor).Pathomorphology
There are very few morphological differences between perforated gastric and duodenal ulcers. A through defect in the organ wall is visually determined. In most cases, perforation is localized on the anterior wall of the duodenum (in the region of the bulb), in the pyloric antral zone and on the lesser curvature of the stomach. On the part of the visceral peritoneum, hyperemia, tissue edema and fibrin overlays around the perforation are noted, with a long history of ulcerative disease - pronounced chronic perigastritis, periduodenitis with deformation and cicatricial changes in organs and surrounding tissues.From the side of the mucous membrane, a round or oval defect is visible in the center of the ulcer. The edges of a chronic ulcer are dense to the touch, unlike an acute one, which looks like a “stamped” hole without cicatricial changes in its edges. The microscopic picture is characterized by the destruction of the layers of the gastric or intestinal walls, the abundant development of scar tissue, degenerative and obliterating lesions of the arteries around the ulcer with abundant leukocyte infiltration.
A.I. Kirienko, A.A. Matyushenko
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