ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
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The ICD-10 code for GERD stands for international classification diseases 10 revision and . For therapeutic purposes, diseases are divided into stages, which makes it possible to determine the choice of drugs and the duration of therapy.
If we talk about GERD, then it all depends on the degree of damage to the mucous membrane of the esophagus. Fibrogastroduodenoscopy is used to examine the lower part of the intestine, due to which the disease is classified, since the procedure clearly shows how deeply the organ is affected and what changes have occurred as a result of the disease.
The simplest description of the types of gastroesophageal reflux disease is given in a document called ICD-10. According to clinical signs, the disease in it is divided into the following types:
The endoscopic method for classifying GERD began to be used in the early 1990s and is still successfully used in modern medicine. How does GERD develop? On the border of the esophagus and stomach there is a muscle - the lower esophageal sphincter, which prevents the reverse reflux of digested foods into the esophagus. When it weakens, there is a violation of the functionality of the muscle, as a result of which the gastric contents, together with hydrochloric acid, are thrown back.
In the esophagus, due to such a violation, a number of changes occur, in which the mucous membrane is affected.
These changes formed the basis for the classification of the disease.
This classification is otherwise called Los Angeles. It appeared in the late 90s and includes the following degrees of GERD:
According to this classification, erosive changes can be at any of the stages. All of these species have been classified into stages in order to make it easier for practitioners to understand the progression of the disease and to correctly select the appropriate treatment. It is impossible to independently classify the disease only by symptoms, therefore, if unpleasant symptoms appear, you should consult a doctor. Delaying a visit to the doctor will cost more money and take longer.
K21.0 Gastroesophageal reflux with esophagitis.
Gastroesophageal reflux disease (GERD) is a chronic relapsing disease characterized by esophageal and extraesophageal clinical symptoms and various morphological changes in the mucosa of the esophagus due to retrograde reflux of the gastric or gastrointestinal content,
The incidence of GERD in children with lesions of the gastroduodenal zone in Russia ranges from 8.7 to 49%.
Etiology and pathogenesis
GERD is a multifactorial disease directly caused by gastroesophageal reflux (acid reflux is a decrease in pH in the esophagus to 4.0 or less due to acidic gastric contents entering the organ cavity; alkaline reflux is an increase in pH in the esophagus to 7.5 or more when it enters the organ cavity duodenal contents, more often bile and pancreatic juice).
There are the following forms of reflux.
Physiological gastroesophageal reflux,
not causing the development of reflux esophagitis:
occurs in completely healthy people of any age;
observed more often after meals;
characterized by low intensity (no more than 20-30 episodes per day) and short duration (no more than 20 s);
has no clinical equivalents;
does not lead to the formation of reflux esophagitis.
Pathological gastroesophageal reflux (provokes damage to the mucous membrane of the esophagus with the development of reflux esophagitis and related complications):
occurs at any time of the day;
often independent of food intake;
characterized by a high frequency (more than 50 episodes per day, the duration is at least 4.2% of the recording time according to daily pH monitoring);
leads to damage to the mucous membrane of the esophagus of varying severity, the formation of esophageal and extraesophageal symptoms is possible.
Leading factor in the occurrence of gastroesophageal reflux
violation of the "locking" mechanism of the cardia due to the following causes.
Immaturity of the lower esophageal sphincter in children under 12-18 months.
Disproportion of increase in body length and esophagus (heterodynamics of organ development and growth).
Relative insufficiency of the cardia.
Absolute insufficiency of the cardia due to:
malformations of the esophagus;
surgical interventions on the cardia and esophagus;
connective tissue dysplasia;
morphofunctional immaturity of the vegetative nervous system(VNS), CNS lesions;
taking certain medications, etc.
Violation of the regimen and quality of nutrition, conditions accompanied by an increase in intra-abdominal pressure (constipation, inadequate physical activity, prolonged inclined position of the body, etc.); respiratory pathology (bronchial asthma, cystic fibrosis, recurrent bronchitis, etc.); some medications(anticholinergics, sedatives and hypnotics, β-blockers, nitrates, etc.); smoking, alcohol; sliding hernia of the esophageal opening of the diaphragm; herpesvirus or cytomegalovirus infection, fungal infections.
The pathogenesis of GERD is associated with an imbalance of aggression and defense factors.
Factors of aggression: gastroesophageal reflux (acid, alkaline); hypersecretion of hydrochloric acid; aggressive effects of lysolecithin and bile acids; medications; some food.
Protective factors: antireflux function of the lower esophageal sphincter; mucosal resistance; effective clearance (chemical and volume); timely evacuation of gastric contents.
The severity of gastroesophageal reflux:
with esophagitis (I-IV degree).
Severity clinical symptoms: light, medium degree, heavy.
Extraesophageal symptoms of GERD:
Diagnosis example
The main diagnosis: gastroesophageal reflux disease (reflux esophagitis II degree), moderate form.
Complication: posthemorrhagic anemia.
Concomitant diagnosis; bronchial asthma, non-atopic, moderate form, interictal period. Chronic gastroduodenitis with increased acid-forming function of the stomach, Helicobacter pylori, in the stage of clinical subremission.
Esophageal symptoms: heartburn, regurgitation, "wet spot" symptom, belching of air, sour, bitter, periodic pain behind the sternum, pain or discomfort when food passes through the esophagus (odynophagia), dysphagia, halitosis.
Bronchopulmonary - bronchial asthma, chronic pneumonia, recurrent and Chronical bronchitis, protracted bronchitis, cystic fibrosis.
Otorhinolaryngological - constant coughing, a feeling of "stuck" food or a "lump" in the throat, developing as a result of increased pressure in the upper esophagus, a feeling of itching and hoarseness, ear pain.
Cardiovascular signs - arrhythmias due to the initiation of the esophagocardiac reflex.
Dental - erosion of tooth enamel and the development of caries. In children younger age frequent vomiting, weight loss
body, regurgitation, anemia, respiratory disorders up to apnea and sudden death syndrome are possible.
In older children, complaints are predominantly esophageal, respiratory disorders and posthemorrhagic anemia are possible.
Conduct research? ^ '^ oitekogtya and zhelugsk ^ with bapium in direct and lateral projection? 'small compression abdominal cavity. Passability of the esophagus, diameter, relief of the mucous membrane, elasticity of the walls, the presence of pathological narrowing, ampulla-shaped extensions, the nature of the peristalsis of the esophagus are assessed. With obvious reflux, the esophagus and stomach radiologically form an “elephant with a raised trunk” figure, and on delayed radiographs, a contrast agent is again found in the esophagus, which confirms the presence of reflux.
Below is a system of endoscopic signs of gastroesophageal reflux in children (according to J. Tytgat, modified by V.F. Privorotsky and others).
I degree - moderate focal erythema and / or friability of the mucous membrane of the abdominal esophagus.
II degree - total hyperemia of the abdominal esophagus with focal fibrinous plaque, single superficial erosions may occur, more often of a linear form, located on the tops of the mucosal folds.
III degree - the spread of inflammation to the thoracic esophagus. Multiple (sometimes merging) erosions located non-circularly. Increased contact vulnerability of the mucous membrane is possible.
IV degree - ulcer of the esophagus. Barrett's syndrome. Esophageal stenosis.
Moderate motor disturbances in the region of the lower esophageal sphincter (rise of the 2nd line up to 1 cm), short-term provoked subtotal (along one of the walls) prolapse to a height of 1-2 cm, decreased tone of the lower esophageal sphincter.
Distinct endoscopic signs of cardial insufficiency, total or subtotal provoked prolapse to a height of more than 3 cm with possible partial fixation in the esophagus.
Severe spontaneous or provoked prolapse above the crura of the diaphragm with possible partial fixation.
An example of an endoscopic report: reflux esophagitis P-B degree.
A targeted biopsy of the mucous membrane of the esophagus in children with subsequent histological examination of the material is carried out according to the following indications:
discrepancy between radiological and endoscopic data in unclear cases;
atypical course of erosive and ulcerative esophagitis;
suspicion of a metaplastic process in the esophagus (Barrett's transformation);
suspicion of malignant tumor of the esophagus.
To reliably determine the condition of the esophagus, it is necessary to take at least two biopsies 2 cm proximal to the 2nd line.
"gold standard" definition of pathological gastroesophageal reflux.
According to T.R. DeMeester (1993) normal daily pH monitoring values are:
maximum gastroesophageal reflux (time) - 00:19:48.
For young children, a separate normative
scale (J. Bua-Oshoa et al., 1980). The indicators of daily pH monitoring in children under one year of age differ from those in adults (fluctuations of ±10%, Table 1).
The method of intraesophageal impedancemetry is based on registering changes in intraesophageal resistance as a result of reflux, restoring the initial level as the esophagus clears. A decrease in the impedance in the esophagus below 100 ohms indicates the fact of gastroesophageal reflux.
Esophageal manometry is one of the most accurate methods for studying the function of the lower esophageal sphincter, allowing
Table 1. Normal performance daily pH monitoring
in children according to J. Bua-Oshoa et al. (1980) Indicators Mean value Upper limit of normal Total pH time
Before you know how GERD is classified according to the ICD 10 code, you need to consider what kind of disease it is.
It is a lesion of the mucous membrane of the esophagus. The abbreviation can be deciphered as follows: gastroesophageal reflux disease.
It is characterized by periodic reflux of stomach contents back into the esophagus. In this case, the sphincter is affected, inflammation develops.
Reflux esophagitis is a complex disease characterized by unpleasant symptoms, painful sensations. A person cannot eat what he wants, because after that there is severe discomfort.
Pathology is manifested by heartburn, regurgitation, bad smell from mouth. In some cases, there is an increase in temperature, the urge to vomit, the inability to swallow food.
Classification of esophagitis will help determine the direction of treatment. The international disease code is K21.
However, this pathology may various forms which also need to be considered:
Clinical manifestations of the disease are present in both cases, but they are different. In the second case, there is no threat to life.
Important! The cause of GERD can be both a physiological factor and a psychosomatic one. The cause of the development of pathology must be clarified before treatment is carried out.
If the pathology is not treated, it will progress. It has several stages in its development. The classification of GERD in this case is as follows:
Note! This classification is the most common and understandable. On its basis, therapeutic measures are prescribed to help eliminate damage to the mucous membrane and symptoms.
This classification was proposed in the last century in Los Angeles. It has its own characteristics. The Los Angeles classification proposes to define the disease by the parameter of how extensive the lesion is.
With any type of lesion according to this classification, various complications are possible.
Any classification of GERD according to the ICD code or other parameters provides for easier diagnosis for doctors. They have the opportunity to quickly begin treatment and eliminate the cause of the development of pathology.
Home > What is GERD
In therapy, much depends on the stages of the course of the disease. Such information affects the duration of treatment and the choice of certain drugs. In the case of GERD, the first thing that matters is how deeply the mucosa of the esophagus is affected. In medicine, the classification of gastroesophageal reflux disease is more often used, which is detected by such a research method as FGDS (fibrogastroduodenoscopy).
What symptoms will bother a person at each stage of the disease? Today we have to answer not only this question. There are several options for classifying GERD, consider the most common of them.
The simplest classification is written in one of the classic medical books called ICD-10 (this is the tenth revision of the international classification of the disease). Here clinical variant dividing GERD next.
Endoscopic classification was proposed in the late 80s by Savary and Miller, and is quite widely used in our time.
It has long been known that the mechanism for the development of GERD is a dysfunction of the lower esophageal sphincter (a muscle located on the border between the esophagus and stomach, which limits the reverse movement of food). When this muscle is weakened, gastric contents, including hydrochloric acid, are thrown into the esophagus. And over time, almost all of its shells undergo changes. So they served as the basis for this classification.
It can be presented in detail as follows.
In their practice, gastroenterologists often use this endoscopic classification to determine the stages of GERD development. Therapists also resort to it more often, considering it easier to understand and more exhaustive. But this is not the only division of GERD.
At the end of the 20th century, European Gastroenterology Week proposed the use of lesion extent. This is how the Los Angeles classification of GERD was born. Here's what it includes.
According to the Los Angeles classification, complications in the form of ulcers and narrowing may be present at any of the above stages.
The disease progression units were created to make the work of physicians easier. Thanks to classifications, it becomes easier to understand the manifestations of the process and better select methods for its treatment. Only a doctor can determine at what stage of the development of the disease each person suffering from GERD is. Therefore, at the first signs of illness, to speed up recovery, contact a specialist.
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Gastroesophageal reflux disease (GERD) is the development of inflammatory changes in the distal esophagus and / or characteristic symptoms due to regularly repeated reflux of gastric and / or duodenal contents into the esophagus.
ICD-10 K21.0 Gastroesophageal reflux with esophagitis K21.9 Gastroesophageal reflux without esophagitis.
EXAMPLE FORMULATION OF THE DIAGNOSIS
EXAMPLE FORMULATION OF THE DIAGNOSIS
EPIDEMIOLOGY The true prevalence of the disease is not known due to the large variability in clinical symptoms. Symptoms of GERD upon careful questioning are found in 20–50% of the adult population, and endoscopic signs in more than 7–10% of the population. In the US, heartburn, the main symptom of GERD, is experienced by 10–20% of adults weekly. There is no complete epidemiological picture in Russia. The true prevalence of GERD is much higher than the statistics, including because only less than 1/3 of GERD patients go to the doctor. Women and men get sick equally often.
CLASSIFICATION There are currently two forms of GERD. ■ Endoscopically negative reflux disease, or non-erosive reflux disease, in 60-65% of cases. ■ Reflux esophagitis - 30-35% of patients. ■ Complications of GERD: peptic stricture, esophageal bleeding, Berrett's esophagus, adenocarcinoma of the esophagus. For reflux esophagitis, it is recommended to use the classification adopted at the X World Congress of Gastroenterologists (Los Angeles, 1994) (Table 4-2).
Table 4-2. Los Angeles classification of reflux esophagitis
DIAGNOSIS Diagnosis of GERD should be suspected if the patient has characteristic symptoms B: heartburn, belching, regurgitation; in some cases, extraesophageal symptoms are observed B.
HISTORY AND PHYSICAL EXAMINATION
GERD is characterized by the absence of dependence of the severity of clinical symptoms (heartburn, pain, regurgitation) on the severity of changes in the mucosa of the esophagus. Symptoms of the disease do not allow differentiating non-erosive reflux disease from reflux esophagitis. The intensity of the clinical manifestations of GERD depends on the concentration of hydrochloric acid in the refluxate, the frequency and duration of its contact with the esophageal mucosa, and hypersensitivity of the esophagus.
ESOPHAGEAL GERD SYMPTOMS
ESOPHAGEAL GERD SYMPTOMS ■ Heartburn is a burning sensation of varying intensity that occurs behind the sternum (in the lower third of the esophagus) and/or in the epigastric region. Heartburn occurs in at least 75% of patients, occurs due to prolonged contact of the acidic contents of the stomach (pH less than 4) with the mucosa of the esophagus. The severity of heartburn does not correlate with the severity of esophagitis. It is characterized by its increase after eating, taking carbonated drinks, alcohol, with physical exertion, bending over and in a horizontal position. ■ Sour eructation, as a rule, increases after eating, taking carbonated drinks. Regurgitation of food, observed in some patients, is aggravated by exercise and a position that promotes regurgitation. ■ Dysphagia and odynophagia (pain when swallowing) are less common. The appearance of persistent dysphagia indicates the development of esophageal stricture. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma. ■ Pain behind the sternum can radiate to the interscapular region, neck, lower jaw, the left half of the chest; often mimic angina pectoris. Esophageal pain is characterized by a connection with food intake, body position and their relief by taking alkaline mineral waters and antacids.
EXTRAESophAGEAL GERD SYMPTOMS
EXTRA-ESophageal GERD SYMPTOMS: ■ bronchopulmonary - cough, asthma attacks; ■ otolaryngological - hoarseness, dry throat, sinusitis; ■ dental - caries, erosion of tooth enamel.
LABORATORY EXAMINATION Pathognomonic for GERD laboratory symptoms no. Recommended examination methods: complete blood count, blood type, Rh factor.
INSTRUMENTAL STUDIES OBLIGATORY EXAMINATION METHODS SINGLE STUDIES ■ FEGDS: allows to differentiate between non-erosive reflux disease and reflux esophagitis, to identify the presence of complicationsA. ■ Biopsy of the mucous membrane of the esophagus in complicated GERD: ulcers, strictures, Berrett's esophagusC. ■ X-ray examination of the esophagus and stomach: if a hernia of the esophageal opening of the diaphragm, stricture, adenocarcinoma of the esophagus is suspected.
RESEARCH IN DYNAMICS
■ FEGDS: it is possible not to carry out again with non-erosive reflux disease. ■ Biopsy of the mucous membrane of the esophagus in complicated GERD: ulcers, strictures, Berrett's esophagus.
ADDITIONAL EXAMINATION METHODS
SINGLE STUDIES ■ 24-hour intraesophageal pH monitoring: increased total reflux time (pH less than 4.0 more than 5% per day) and duration of reflux episode (greater than 5 minutes). The method allows you to evaluate the pH in the esophagus and stomach, the effectiveness of drugs; the value of the method is especially high in the presence of extraesophageal manifestations and the absence of the effect of therapy. ■ Intraesophageal manometry: carried out to assess the functioning of the lower esophageal sphincter, the motor function of the esophagus. ■ Ultrasound of the abdominal organs: with GERD without changes, it is carried out to identify concomitant pathology of the abdominal organs. ■ ECG, bicycle ergometry: used for differential diagnosis with IBSA, with GERD, no changes are found. ■ Proton pump inhibitor test B: relief of clinical symptoms (heartburn) while taking proton pump inhibitors.
DIFFERENTIAL DIAGNOSIS With a typical clinical picture of the disease, differential diagnosis is usually not difficult. In the presence of extraesophageal symptoms, it should be differentiated from ischemic heart disease, bronchopulmonary pathology (bronchial asthma, etc.). For differential diagnosis of GERD with esophagitis of a different etiology, a histological examination of biopsy specimens is performed.
INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS
INDICATIONS FOR OTHER SPECIALIST CONSULTATION The patient should be referred for specialist advice if the diagnosis is uncertain, atypical or extraesophageal symptoms are present, or complications are suspected. You may need to consult a cardiologist, pulmonologist, otorhinolaryngologist (for example, a cardiologist - in the presence of retrosternal pain that does not stop while taking proton pump inhibitors).
TREATMENT OBJECTIVES OF THERAPY ■ Relief of clinical symptoms. ■ Healing of erosions. ■ Better quality of life. ■ Prevention or elimination of complications. ■ Prevention of recurrence.
INDICATIONS FOR HOSPITALIZATION
INDICATIONS FOR HOSPITALIZATION ■ Carrying out antireflux treatment in case of complicated course of the disease, as well as in case of ineffectiveness of adequate drug therapy. ■ Conducting surgery (fundoplication A) in case of ineffectiveness of drug therapy and endoscopic or surgical interventions in the presence of complications of esophagitis: stricture, Berrett's esophagus, bleeding.
NON-DRUG TREATMENT ■ Lifestyle and dietary recommendations that have limited effect in the treatment of GERD. ✧ Avoid large meals. ✧Limit consumption of foods that reduce the pressure of the lower esophageal sphincter and have an irritating effect on the mucous membrane of the esophagus: foods rich in fats ( whole milk, cream, cakes, pastries), fatty fish and meat (goose, duck, as well as pork, lamb, fatty beef), alcohol, drinks containing caffeine (coffee, cola, strong tea, chocolate), citrus fruits, tomatoes, onions, garlic, fried foods, give up carbonated drinks. ✧After eating, avoid bending forward and horizontal position; the last meal - no later than 3 hours before bedtime. ✧Sleep with the head end of the bed elevated. ✧Exclude loads that increase intra-abdominal pressure: do not wear tight clothes and tight belts, corsets, do not lift weights of more than 8-10 kg on both hands, avoid physical activity associated with overexertion of the abdominal press. ✧ Quit smoking. ✧Maintain normal body weight. ■ Do not take drugs that cause reflux B (sedatives and tranquilizers, calcium channel inhibitors, β-blockers, theophylline, prostaglandins, nitrates).
DRUG THERAPY Terms of treatment for GERD: 4-6 weeks for non-erosive reflux disease and at least 8-12 weeks for reflux esophagitis, followed by maintenance therapy for 26-52 weeks. Drug therapy includes the appointment of prokinetics, antacids and antisecretory agents. ■ Prokinetics: domperidone 10 mg 4 times a day. ■ The goal of antisecretory therapy for GERD is to reduce the damaging effect of acidic gastric contents on the esophageal mucosa in gastroesophageal reflux. The drugs of choice are proton pump A inhibitors (omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole). ✧GERD with esophagitis (8-12 weeks): -omeprazole 20 mg 2 times a day, or -lansoprazole 30 mg 2 times a day, or -esomeprazole 40 mg / day, or - rabeprazole 20 mg / day. The criterion for the effectiveness of treatment is the relief of symptoms and the healing of erosions. If the standard dose of proton pump inhibitors is ineffective, the dose should be doubled. ✧ Non-erosive reflux disease (4-6 weeks): -omeprazole 20 mg/day, or -lansoprazole 30 mg/day, or -esomeprazole 20 mg/day, or -rabeprazole 10-20 mg/day. The criterion for the effectiveness of treatment is the persistent elimination of symptoms. ■ The use of histamine H2 receptor blockers as antisecretory drugs is possible, but their effect is lower than that of proton pump inhibitors. ■ Antacids can be used as a symptomatic treatment for infrequent heartburn B, but in this case, preference should be given to taking proton pump inhibitors on demand. Antacids are usually prescribed 3 times a day 40-60 minutes after a meal, when heartburn and chest pain most often occur, as well as at night. ■ With reflux esophagitis caused by the reflux of duodenal contents (primarily bile acids) into the esophagus, which is usually observed in cholelithiasis, a good effect is achieved by taking ursodeoxycholic acid at a dose of 250-350 mg / day. In this case, it is advisable to combine ursodeoxycholic acid with prokinetics at the usual dose. Maintenance therapy A is usually carried out with proton pump inhibitors in accordance with one of the following regimens. ■ Continuous use of proton pump inhibitors in a standard or half dose (omeprazole, esomeprazole - 10 or 20 mg / day, rabeprazole - 10 mg / day). ■ On-demand therapy - taking proton pump inhibitors when symptoms appear (on average once every 3 days) for endoscopically negative reflux disease.
SURGICAL TREATMENT The purpose of operations aimed at eliminating reflux (fundoplications, including endoscopic ones) is to restore the normal function of the cardia. Indications for surgical treatment: ■ ineffectiveness of adequate drug therapy; ■ complications of GERD (stricture of the esophagus, repeated bleeding); ■ Berrett's esophagus with epithelial dysplasia high degree because of the danger of malignancy.
APPROXIMATE TERMS OF TEMPORARY INABILITY TO WORK
APPROXIMATE TERMS OF TEMPORARY DISABILITY Are determined by the relief of clinical symptoms and the healing of erosions during the control FEGDS.
FURTHER MANAGEMENT
FURTHER MANAGEMENT OF THE PATIENT In the case of non-erosive reflux disease with complete relief of clinical symptoms, a control FEGDS is not necessary. Remission of reflux esophagitis should be confirmed endoscopically. When it changes clinical picture in some cases, FEGDS is performed. Maintenance therapy is mandatory, since without it the disease recurs in 90% of patients within 6 months (see the section "Drug therapy"). Dynamic monitoring of the patient is carried out to monitor complications, identify Berrett's esophagus and drug control of the symptoms of the disease. Monitor for symptoms suggestive of complications: ■ dysphagia and odynophagia; ■ bleeding; ■ weight loss; ■ early satiety; ■ pain in chest; ■ frequent vomiting. In the presence of all these signs, consultations of specialists and further diagnostic examination are indicated. Intestinal epithelial metaplasia serves as the morphological substrate of asymptomatic Berrett's esophagus. Risk factors for Berrett's esophagus: ■ heartburn more than twice a week; ■ male gender; ■ duration of symptoms for more than 5 years. Once the diagnosis of Berrett's esophagus is established, endoscopic studies with biopsy should be performed annually on the background of continuous maintenance therapy with a full dose of proton pump inhibitors. If low-grade dysplasia is detected, repeated FEGDS with biopsy and histological examination of the biopsy is performed after 6 months. If low-grade dysplasia persists, a repeat histological examination is recommended after 6 months. If low-grade dysplasia persists, repeated histological examinations are carried out annually. In the case of high-grade dysplasia, the result of the histological examination is evaluated independently by two morphologists. When the diagnosis is confirmed, the issue of endoscopic or surgical treatment of Berrett's esophagus is decided.
EDUCATION OF THE PATIENT The patient should be explained that GERD is a chronic condition, usually requiring long-term maintenance therapy with proton pump inhibitors to prevent complications. The patient must follow the recommendations for lifestyle changes (see section " Non-drug treatment"). The patient should be informed about possible complications GERD and advise him to consult a doctor if symptoms of complications occur (see the section "Further management of the patient"). Patients with prolonged uncontrolled symptoms of reflux should be explained the need for endoscopic examination to detect complications (such as Berrett's esophagus), and in the presence of complications, the need for periodic FEGDS with biopsy.
PROGNOSIS With non-erosive reflux disease and mild reflux esophagitis, the prognosis is generally favorable. Patients retain their ability to work for a long time. The disease does not affect life expectancy, but significantly reduces its quality during the period of exacerbation. Early diagnosis and timely treatment prevent the development of complications and maintain working capacity. The prognosis worsens with a long duration of the disease, combined with frequent long-term relapses, with complicated forms of GERD, especially with the development of Berrett's esophagus, due to an increased risk of developing adenocarcinoma of the esophagus.
EGDS is necessary for the diagnosis of GERD with reflux esophagitis. With endoscopy, the severity of reflux esophagitis is determined. Esophagogastroduodenoscopy is performed to identify Barrett's esophagus, perform a biopsy, and determine the severity of esophageal stricture.
About 50-60% of patients with GERD have no endoscopic signs of the disease. This is the so-called EGDS-negative form of GERD (GERD without reflux esophagitis).
Rice. During esophagogastrodenoscopy, an eroded, hyperemic mucosa of the esophagus (esophagitis) is visualized. To confirm the diagnosis, a histological examination of the biopsy is performed, since endoscopic data do not always correlate with the results of histology.
Oh degree. Mild focal or diffuse hyperemia and friability of the mucous membrane of the esophagus at the level of the gastroesophageal junction (cardia), slight flattening of the cardia, disappearance of the luster of the mucous membrane of the distal parts, hyperemia and swelling of the mucous membrane of the distal part of the esophagus, individual erosions.
Rice. Histological picture (in the study using transmission electron photomicroscopy) of the biopsy of the esophagus is normal
Rice. Histological picture (in the study using transmission electron photomicroscopy) of the biopsy of the esophagus with non-erosive esophagitis. Expansion of intercellular spaces is visualized.
I degree. The presence of one or more superficial erosions with or without exudate, often linear in shape, located on the tops of the folds of the esophageal mucosa. They occupy less than 10% of the mucosal surface of the distal esophagus.
II degree - confluent erosive lesions, occupying 10-50% of the circumference of the distal esophagus.
III degree. Confluent erosions covered with exudate or shedding necrotic masses that do not spread by circulation. The volume of damage to the mucosa of the distal esophagus is less than 50%.
Rice. Histological picture of the biopsy (in the study using transmission electron photomicroscopy) of the esophagus with erosive esophagitis.
IV degree. Circulatory confluent erosions or exudative-necrotic lesions occupying a five-centimeter zone of the esophagus above the cardia with spread to the distal esophagus.
V degree. Deep ulceration and erosion of various parts of the esophagus, stricture and fibrosis of its walls, short esophagus. Deep ulcers, stenosis of the esophagus, cylindrical metaplasia of the epithelium of the mucosa of its distal section indicate the occurrence of Barrett's esophagus. Barrett's esophagus is diagnosed in 8-15% of patients with GERD and may malignize into adenocarcinoma.
Rice. Histopathological picture of the mucosal biopsy in Barrett's esophagus.
Based on the endoscopic picture, 4 degrees of severity of narrowing of the esophagus are distinguished. When determining the degree, the extent of cicatricial stenosis of the esophagus is taken into account, since the success of non-operative expansion of the stricture and adequate restoration of oral nutrition and clinical manifestations dysphagia:
The inflammatory process that covers the mucous membrane of the esophagus with the formation of erosions and ulcers on it is called erosive esophagitis. This disease is equally common in men and women. According to the international classification of diseases, the ICD-10 pathology is code K 22.1, and when GERD is added, it is K 22.0.
The erosive form requires immediate treatment, since it can cause serious complications, up to malignant neoplasms. Therefore, when heartburn and burning sensation behind the sternum appear, you need to contact a gastroenterologist to receive special treatment.
We found out which erosive esophagitis has ICD code 10, we follow further. Esophagitis causes inflammation of the mucous membrane of the esophagus and develops in acute and chronic types. An acute course occurs when:
Also, discomfort in the form of heartburn causes overeating, physical work immediately after eating. In addition, esophagitis can be caused by reflux, that is, the reflux of stomach contents back into the esophagus. The hydrochloric acid contained in the gastric secretion irritates the epithelium of the esophageal tube. When affected by these factors, the mucous membrane of the esophagus becomes inflamed, reddens and swells. So what are the typical symptoms? Erosive esophagitis causes the patient:
This condition is treated with a sparing diet, and if the disease is caused by an infectious factor, then antibiotic therapy is added.
If treatment is not started in time, then erosion will appear on the mucous membrane in addition to hyperemia, hence the name erosive esophagitis. It develops with chronic course illness.
This is a form of the acute course of the disease, which is not very common and occurs in people with reduced immunity against the background of infectious diseases(scarlet fever, sepsis, measles, mycosis). The disease is characterized by a sharp inflammation of the esophageal mucosa, forming necrotic (dead) areas, which, when rejected, form deep ulcers. During the healing of ulcers, the epithelium of the esophagus becomes covered with purulent or bloody exudate.
Against the background of symptoms corresponding to the underlying disease, there are:
This form of the disease often causes complications in the form of bleeding, acute purulent inflammation of the mediastinum, retrosternal abscess.
Treatment of necrotizing esophagitis takes a long time and requires the patient to be patient and strictly follow all the doctor's instructions. After healing of ulcers in the esophagus, scarring is formed, which brings the patient discomfort.
The chronic course of the disease occurs due to the following reasons:
Gastroesophageal reflux disease results in chronic inflammation of the esophageal epithelium. Due to insufficient closure of the muscular ring of the sphincter that separates the esophagus and stomach, food can fall back into the esophageal tube, irritating the mucous membrane. Hyperemia and edema of the epithelium of the walls of this internal organ determined first stage diseases. Symptoms during this period are not pronounced, mainly heartburn. If GERD is not treated, then the membrane will not only turn red, but erosions will form on it. This second stage illness.
It is she who is diagnosed by doctors when patients come to them with complaints of heartburn and burning sensation along the esophagus. In endoscopic examination of the walls of the internal organ on the epithelium of the walls, the presence of single or multiple erosions is noted, which do not merge and form defects on the mucosa in the region of one fold. The walls of the esophagus are covered with fibrous plaque.
Third stage characterized by the degeneration of erosion into ulcers. This is erosive ulcerative esophagitis. At this stage, not only the surface layer of the epithelium is affected, but also the underlying tissues. Defects extend beyond one fold and may be observed around the mucosa of the esophagus. With further progression, the muscle tissue of the esophageal tube is damaged. The condition worsens as persistent symptoms are added to the above symptoms. cough, vomit mixed with blood pain along the esophagus occurring regardless of food intake.
This stage is dangerous for the development of complications:
In addition, when an infectious factor is attached against the background of erosive esophagitis, purulent inflammation of the esophagus may develop. These conditions lead to worsening general condition patient, and in case of bleeding require urgent hospitalization. Erosive fibrinous esophagitis should not be allowed to develop.
Therapy for the erosive form of the disease is similar in principles of treatment to other types of esophagitis and GERD. It consists of:
If complications arise or drug therapy is ineffective, then surgical intervention is performed. This can be a traditional technique (an incision in the chest or abdomen) or a laparoscopy method, which is less traumatic.
Diet plays a big role. The diet for erosive esophagitis is aimed at reducing the irritating effect of foods on the esophageal mucosa. The following dishes are excluded from the diet:
As well as products:
Alcohol and smoking are strictly prohibited.
Patients should eat small meals at least 5-6 times a day so as not to overload the stomach and cause reflux. After eating, you can’t lie down to rest, but you need to walk around a bit, but not do physical work, especially requiring the torso to bend forward. After the last meal and before sleep should go at least 3 hours.
Patients can use steamed food, baked or boiled. Also, do not take very hot or cold food. During the meal, you need to chew food well, do not eat rough food, so as not to injure the esophageal mucosa.
When GERD with erosive esophagitis is diagnosed, the diet must be followed.
Some more useful information You can learn how to properly treat and eat in this video.
After the treatment, patients need to monitor not only nutrition, but also change their lifestyle. Such people should not play sports associated with abdominal tension. You also need to reduce physical and emotional stress. If the work is related to the position - tilting the body forward, then this type of activity must be changed. Do not wear tight clothing, tight belts and corsets.
A good result is given by walking before bedtime, as well as taking tea ( mint, melissa, calendula,chamomile), which has a sedative and anti-inflammatory effect.
It must be remembered that when the first signs of the disease appear, you need to consult a doctor, since self-medication or use folk methods cannot completely cure the disease, and in some cases leads to exacerbations. Once a year, such patients need to visit a gastroenterologist with mandatory endoscopic examination. If the patient's condition worsens, then consultation is needed immediately.
Standards for the diagnosis and treatment of acid-dependent and HELICOBACTER PYLORI-associated diseases (fourth Moscow agreement)
LIST OF ABBREVIATIONS
GERD- gastroesophageal reflux disease. IPP - proton pump inhibitor. HP - Helicobacter pylori. NSAIDs - non-steroidal anti-inflammatory drugs. EGDS- esophagogastroduodenoscopy.
GASTROESOPHAGEAL REFLUX DISEASE
ICD-10 code:
K 21(Gastroesophageal reflux - GER), GER with esophagitis - K 21.0, GER without esophagitis - K 21.9
Definition
Gastroesophageal reflux disease (GERD) is a chronic relapsing disease characterized by reflux of gastric or duodenal contents into the esophagus, resulting from impaired motor-evacuation function of the esophagogastroduodenal zone, which are manifested by symptoms that disturb the patient and / or the development of complications. The most characteristic symptoms of GERD are heartburn and regurgitation, and the most common complication is reflux esophagitis.
CLASSIFICATION OF GERD
Esophageal syndromes |
Extraesophageal syndromes |
||
Syndromes that are exclusively symptomatic (in the absence of structural damage to the esophagus) |
Syndromes with damage to the esophagus (complications of GERD) |
Syndromes associated with GERD |
Syndromes suspected of being associated with GERD |
1. Classic reflux syndrome 2. Chest pain syndrome |
1. Reflux esophagitis 2. Esophageal strictures 3. Barrett's Esophagus 4. Adenocarcinoma |
1. Reflux cough 2. Laryngitis of reflux nature 3. Bronchial asthma reflux nature 4. Erosion of tooth enamel of reflux nature |
1. Pharyngitis 2. Sinusitis 3. Idiopathic pulmonary fibrosis 4. Recurrent otitis media |
According to the international scientifically based agreement (Montreal, 2005).
DIAGNOSTICS METHODS FOR GERD
Clinical. The most common is the classic reflux syndrome (endoscopically negative form of GERD), which is manifested exclusively by symptoms (the presence of heartburn and / or regurgitation that disturbs the patient). The diagnosis is made clinically and is based on the verification and evaluation of the patient's complaints, therefore, the same interpretation of the symptoms by the doctor and the patient is important. Heartburn is a burning sensation behind the sternum and / or “in the pit of the stomach”, spreading from the bottom up, individually occurring in a sitting position, standing, lying down or when bending the torso forward, sometimes accompanied by a feeling of acid and / or bitterness in the throat and mouth, often associated with a feeling of fullness in the epigastrium that occurs on an empty stomach or after the consumption of any type of solid or liquid food, alcoholic or non-alcoholic beverages, or the act of smoking (national definition of heartburn, approved by the VII Congress of NOHR, 2007). Regurgitation should be understood as the entry of stomach contents due to reflux into the oral cavity or lower part of the pharynx (Montreal definition, 2005).
Therapeutic test with one of proton pump inhibitors in standard dosages for 5-10 days.
Endoscopic examination allows to identify and evaluate changes in the distal esophagus, primarily reflux esophagitis. If metaplasia of the esophagus (Barrett's esophagus) and a malignant lesion are suspected, multiple biopsy and morphological examination are performed.
Daily reflux monitoring of the esophagus (pH monitoring, combined multichannel impedance-pH-monitoring ) to detect and quantify pathological gastroesophageal reflux, to determine its relationship with the symptoms of the disease, as well as to evaluate the effectiveness of therapy. Daily pH monitoring reveals pathological acid reflux ( pH < 4,0). Импеданс-рН-мониторинг наряду с кислыми дает возможность выявлять слабокислые, щелочные и газовые рефлюксы.
Esophageal manometry - to assess the motility of the esophagus (peristalsis of the body, resting pressure and relaxation of the lower and upper esophageal sphincters), differential diagnosis with primary (achalasia) and secondary (scleroderma) lesions of the esophagus. Manometry helps to correctly position the probe for pH monitoring of the esophagus (5 cm above the proximal edge of the lower esophageal sphincter).
According to the indications, an x-ray examination of the upper gastrointestinal tract is performed: for the diagnosis and differential diagnosis of peptic ulcers and / or peptic stricture of the esophagus.
According to indications - assessment of violations of the evacuation function of the stomach ( electrogastrography and other methods).
When identifying extraesophageal syndromes and when determining indications for surgical treatment of GERD - consultations of specialists (cardiologist, pulmonologist, ENT, dentist, psychiatrist, etc.).
MEDICAL THERAPY FOR GERD
Proton pump inhibitors are most effective in controlling symptoms and treating complications of GERD (reflux esophagitis, Barrett's esophagus) ( omeprazole 20 mg lansoprazole 30 mg pantoprazole 40 mg rabeprazole 20 mg or esomeprazole 20 mg), administered 1-2 times a day 20-30 minutes before meals. The duration of the main course of therapy is at least 6-8 weeks. In elderly patients with erosive reflux esophagitis, as well as in the presence of extraesophageal syndromes, its duration increases to 12 weeks. The effectiveness of all PPIs in the long-term treatment of GERD is similar. Features of metabolism in the system cytochromes P450 provide the smallest profile drug interactions pantoprazole, which makes it the safest if it is necessary to take drugs for the treatment of synchronously occurring diseases (clopidogrel, digoxin, nifedipine, phenytoin, theophylline, R-warfarin, etc.).
PPIs are characterized by a long latency period, which does not allow them to be used for rapid relief of symptoms. For quick relief of heartburn, use antacids and preparations of alginic acid (alginates). At the beginning of GERD therapy, a combination of PPIs with alginates or antacids is recommended until stable control of symptoms (heartburn and regurgitation) is achieved.
With the classic reflux syndrome (endoscopically negative GERD), as well as with the ineffectiveness of PPIs, monotherapy with alginates for at least 6 weeks is possible.
If violations of the evacuation function of the stomach and severe duodenogastroesophageal reflux are detected, the appointment is indicated prokinetics (metoclopramide, domperidone, itopride hydrochloride).
According to the indications (intolerance, lack of efficacy, refractoriness to PPIs), it is possible to use histamine H2 receptor antagonists (famotidine).
The criteria for the effectiveness of therapy is the achievement of clinical and endoscopic remission (the absence of symptoms and / or signs of reflux esophagitis during endoscopy).
It should be noted that the course of GERD, as a rule, is continuously relapsing, and in most patients, when antisecretory therapy is discontinued, symptoms and/or reflux esophagitis quickly return.
Management options for patients with GERD after persistent resolution of symptoms and reflux esophagitis:
With recurrent erosive and ulcerative reflux esophagitis, Barrett's esophagus - continuous maintenance therapy with PPI (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg, rabeprazole 20 mg or esomeprazole 20 mg) 1-2 times a day;
With often recurrent endoscopically negative GERD, GERD with reflux esophagitis, GERD in elderly patients - continuous maintenance PPI therapy in a minimal but effective dose (selected individually);
With the classic reflux syndrome (endoscopically negative form of GERD) - therapy with alginates, complex agents with antacid properties or PPI "on demand", under the control of symptoms.
GERD AND HELICOBACTER PYLORI:
Prevalence HP in patients with GERD is lower than in the population, but the nature of this negative relationship is unclear.
currently accepted point of view Hp infection is not the cause of GERD, Hp eradication does not worsen GERD.
Against the background of a significant and prolonged suppression of acid production, Hp spreads from the antrum to the body of the stomach (Hp translocation). This can accelerate the loss of specialized gastric glands, leading to the development of atrophic gastritis and, possibly, gastric cancer. Therefore, patients with GERD who need long-term antisecretory therapy should be diagnosed with Helicobacter pylori, if detected, eradicated (see the section "Drug therapy for gastric ulcer and duodenum associated with H. pylori”).
SURGICAL TREATMENT OF GERD
A differentiated selection of patients with GERD is recommended for surgical treatment - laparoscopic fundoplication. Accurate readings for surgical treatment GERD remains controversial, and long-term results do not guarantee complete elimination of PPIs.
Preoperative examination should include endoscopy (if Barrett's esophagus is suspected - with multiple biopsy and morphological examination), X-ray examination of the esophagus, stomach and duodenum, esophageal manometry and 24 hour pH monitoring . It is optimal to make a decision on the operation by a council, including a gastroenterologist, surgeon, if necessary, a cardiologist, pulmonologist, ENT, psychiatrist and other specialists.
Indications for surgery:
Persistent or persistent symptoms despite optimal therapy.
Negative impact on quality of life due to dependence on medications or due to their side effects.
The presence of complications of GERD (Barrett's esophagus, grade III or IV reflux esophagitis, stricture, esophageal ulcer).
Limitations in the quality of life or the presence of complications associated with hiatal hernia.
ULCER ASSOCIATED WITH HELICOBACTER PYLORI
ICD-10 code: stomach ulcer - K 25, Duodenal ulcer - K 27
Definition
Peptic ulcer is a chronic relapsing disease, the main morphological manifestation of which is a gastric or duodenal ulcer, usually developing against the background of chronic gastritis associated with HP.
METHODS OF DIAGNOSTICS OF ULCER DISEASE:
Clinical.
Endoscopic, with a stomach ulcer, it is mandatory to exclude malignancy - targeted biopsy (5-7 fragments) of the bottom and edges of the ulcer.
X-ray to detect complications (penetration, malignancy). Determination of the acid-forming function of the stomach ( pH meter ).
Diagnostic methods for Helicobacter pylori
1. Biochemical methods:
1.1. rapid urease test;
1.2. urease breath test with 13C-urea;
1.3. ammonium breath test;
2. Morphological methods:
2.1. histological method - detection of Hp in biopsy specimens of the mucous membrane of the antrum and body of the stomach;
2.2. cytological method - detection of Hp in the layer of parietal mucus of the stomach.
3. Bacteriological method with isolation of pure culture and determination of sensitivity to antibiotics.
4. Immunological methods:
4.1. detection of H. pylori antigen in feces (saliva, plaque, urine);
4.2. detection of antibodies to H. pylori in the blood using enzyme immunoassay.
5. Molecular genetic methods:
5.1. polymerase chain reaction (PCR) for the study of biopsies of the gastric mucosa. PCR is carried out not so much to detect H. pylori, but to verify strains of H. pylori (genotyping), including molecular genetic features that determine the degree of their virulence and sensitivity to clarithromycin.
DRUG THERAPY OF GASTRIC AND DUODENAL ULCER ASSOCIATED WITH H. PYLORI
The choice of treatment option depends on the presence of individual intolerance to certain drugs by patients, as well as the sensitivity of Helicobacter pylori strains to drugs. Application clarithromycin in eradication schemes is possible only in regions where resistance to it is less than 15-20%. In regions with resistance above 20%, its use is advisable only after determining the sensitivity of Hp to clarithromycin by bacteriological or PCR methods.
Antacids can be used in complex therapy as a symptomatic agent and in monotherapy - before carrying out pH-metry and diagnosing Hp.
First line anti-helicobacter therapy
First option. One of proton pump inhibitors at the standard dosage (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg, esomeprazole 20 mg, rabeprazole 20 mg 2 times a day) and amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day) in combination with clarithromycin ( 500 mg 2 times a day), or josamycin(1000 mg 2 times a day), or nifurator(400 mg 2 times a day) for 10 - 14 days.
The second option (four-component therapy). The drugs used in the first option (one of the PPIs in the standard dosage, amoxicillin in combination with clarithromycin, or josamycin, or nifuratel) with the addition of the fourth component - bismuth tripotassium dicitrate 120 mg 4 times a day or 240 mg 2 times a day for 10-14 days.
The third option (in the presence of atrophy of the gastric mucosa with achlorhydria, confirmed by pH-metry ). Amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day) in combination with clarithromycin (500 mg 2 times a day) or josamycin (1000 mg 2 times a day), or nifuratel (400 mg 2 times a day), and bismuth tripotassium dicitrate (120 mg 4 times a day or 240 mg 2 times a day) for 10-14 days.
Note. If the ulcer persists according to the results of the control EGDS on the 10th-14th day from the start of treatment, it is recommended to continue cytoprotective therapy of bismuth tripotassium dicitrate (120 mg 4 times a day or 240 mg 2 times a day) and / or CAT at a half dose for 2 -3 weeks. Prolonged therapy of bismuth tripotassium dicitrate is also indicated in order to improve the quality of the post-ulcer scar and speedy reduction of the inflammatory infiltrate.
A) One of the standard dose PPIs in combination with amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day) and bismuth tripotassium dicitrate (120 mg 4 times a day or 240 mg 2 times a day) for 14 days .
B) Bismuth tripotassium dicitrate 120 mg 4 times a day for 28 days. In the presence of pain syndrome - a short course of PPI.
Fifth option (if there is a polyvalent allergy to antibiotics or the patient refuses antibiotic therapy). One of the proton pump inhibitors in a standard dosage in combination with a 30% aqueous solution propolis (100 ml twice a day on an empty stomach) for 14 days.
Second line anti-helicobacter therapy
It is carried out in the absence of eradication of Helicobacter pylori after treatment of patients with one of the first-line therapy options.
The first option (classical quadruple therapy). One of the standard dose PPIs, bismuth tripotassium dicitrate 120 mg 4 times a day, metronidazole 500 mg 3 times a day, tetracycline 500 mg 4 times a day for 10-14 days.
Second option. One of the standard dose PPIs, amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day) in combination with a nitrofuran drug: nifurator(400 mg 2 times a day) or furazolidone (100 mg 4 times a day) and bismuth tripotassium dicitrate (120 mg 4 times a day or 240 mg 2 times a day) for 10-14 days.
Third option. One of the standard dose PPIs, amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day), rifaximin(400 mg 2 times a day), bismuth tripotassium dicitrate (120 mg 4 times a day) for 14 days.
Third line anti-helicobacter therapy
In the absence of eradication of Helicobacter pylori after treatment with second-line drugs, it is recommended that therapy be selected only after determining the sensitivity of Helicobacter pylori to antibiotics.
DRUG THERAPY OF GASTRIC AND DUODENAL ULCER NOT ASSOCIATED WITH H. PYLORI
Antisecretory drugs: one of proton pump inhibitors (omeprazole 20 mg 2 times a day, lansoprazole 30 mg 1-2 times a day, pantoprazole 40 mg 1-2 times a day, esomeprazole 20-40 mg 1-2 times a day, rabeprazole 20 mg 1-2 times a day) or H2 receptor blockers (famotidine 20 mg twice a day) for 2-3 weeks.
Gastroprotectors: bismuth tripotassium dicitrate (120 mg 4 times a day), sucralfate 0.5-1.0 g 4 times a day for 14-28 days.
Antacids can be used in complex therapy as a symptomatic agent and in monotherapy - before conducting pH-metry and diagnosing HP.
CHRONIC GASTRITIS
ICD-10 code: chronic gastritis K 29.6 Definition
Chronic gastritis is a group of chronic diseases that are morphologically characterized by the presence of inflammatory and degenerative processes in the gastric mucosa, progressive atrophy, functional and structural changes with a variety of clinical signs.
most common cause chronic gastritis is Hp, which is associated with a high prevalence of this infection.
DIAGNOSIS METHODS:
Clinical;
Endoscopic with morphological evaluation of biopsy specimens;
Diagnosis of Hp (see above)
Determination of the acid-forming function of the stomach ( pH meter );
X-ray.
PRINCIPLES OF TREATMENT OF CHRONIC GASTRITIS
Therapy of chronic gastritis is differentiated, depending on the clinic, etiopathogenetic and morphological form of the disease.
CHRONIC ANTRAL GASTRITIS, HP-ASSOCIATED (TYPE B)
The main principle of treatment of this type of chronic gastritis is the eradication of Hp (see the section "Drug therapy of gastric and duodenal ulcer associated with H. pylori").
CHRONIC CHEMICAL (REACTIVE) GASTRITIS (REFLUX-GASTRITIS, TYPE C)
The cause of gastritis C is the reflux of duodenal contents into the stomach. At duodenogastric reflux damaging effects on the gastric mucosa bile acids and lysolecithin. The damaging properties of bile acids depend on the pH of the stomach: at pH< 4 наибольшее воздействие на слизистую оболочку желудка оказывают тауриновые конъюгаты, а при рН >4 - non-conjugated bile acids, have a significantly greater damaging effect.
In the treatment of reflux gastritis use:
bismuth tripotassium dicitrate(120 mg 4 times or 240 mg 2 times a day);
Sucralfate (500-1000 mg 4 times a day) most effectively binds conjugated bile acids at pH = 2, with an increase in pH this effect decreases, so its simultaneous administration with antisecretory drugs is impractical;
Preparations ursodeoxycholic acid(250 mg 1 time per day for 2-3 weeks to 6 months);
To normalize motor function - prokinetics(metoclopramide, domperidone, itoprid hydrochloride) and motility regulators (trimedat, mebeverine).
NSAID-GASTROPATHY
Definition
NSAID gastropathy is a pathology of the upper digestive tract that occurs in a chronological relationship with the use of non-steroidal anti-inflammatory drugs (NSAIDs) and is characterized by damage to the mucous membrane (the development of erosions, ulcers and their complications - bleeding, perforation).
DIAGNOSIS METHODS:
Clinical (study of complaints, collection of anamnesis of the disease, identification of the fact and duration of taking NSAIDs, aspirin, assessment of risk factors for the development of NSAID-gastropathy);
Complete blood count (hemoglobin concentration, red blood cell count, hematocrit), biochemical analysis blood (indicators of iron metabolism), fecal occult blood test to detect bleeding;
Endoscopic and / or radiological.
MEDICAL TREATMENT OF NSAID-GASTROPATHY
For the medical treatment of NSAID-associated gastric and duodenal injury, it is advisable to stop taking NSAIDs and use H2 blocker(famotidine) or PPI in standard dosages, a combination of PPI and bismuth tripotassium dicitrate for 4 weeks is also possible.
If NSAIDs cannot be discontinued, concomitant PPI therapy may be appropriate for the entire duration of NSAIDs.
If a patient with NSAID gastropathy is shown to continue taking NSAIDs, it is advisable to prescribe selective inhibitors COX-2. However, such treatment does not exclude the development of complications of NSAID gastropathy and does not eliminate the need to take antisecretory drugs or gastroprotectors as indicated.
As an alternative to NSAIDs as anti-inflammatory therapy in patients with osteoarthritis, it is possible to prescribe a drug based on ginger extract, 1 capsule 2 times a day for 30 days.
It is mandatory to diagnose Hp, upon detection of which eradication therapy should be carried out using the schemes presented in the section "Drug therapy for gastric and duodenal ulcer associated with H. pylori"
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When it comes to inflammation of the duodenal mucosa and the pyloric part of the stomach, gastroduodenitis is diagnosed. its types are classified according to the endoscopic picture. Until recently, this pathology was not distinguished into a separate group. The International Classification of Diseases (ICD-10) lists the diagnosis of "gastritis" (K29.3) and the diagnosis of "duodenitis" (K29). Now gastroduodenitis also has an ICD-10 code. A possible combination of gastritis and duodenitis is distinguished in the ICD-10 by paragraph K29.9 and is indicated by the phrase "gastroduodenitis unspecified", what it is, we will tell in the article.
In ICD-10, unspecified gastroduodenitis has been recently identified. Doctors are still arguing about whether the combination of two pathologies (inflammation of the gastric mucosa and duodenum) is justified. Those who vote "yes" pay attention to common pathogenetic mechanisms:
Domestic medicine, given that pathological processes in the stomach cause and support pathological processes in the duodenum, considers the disease as a whole. A disease such as gastroduodenitis is classified according to various factors, so it makes sense to list them all.
Detailed classification of gastroduodenitis:
For example , superficial gastroduodenitis is diagnosed if the inflammation affects only the walls of the gastric mucosa, while the walls of the intestine simply thicken, its vessels overflow with blood, and this causes swelling. In this case, the pastel mode will be effective and therapeutic diet.
The erosive type is accompanied by the appearance of painful scars, erosions and ulcers throughout the gastrointestinal tract. They can form for various reasons: due to insufficient secretion of mucus, the presence of reflux, the penetration of infections. Treatment should help eliminate the root cause of the disease. It is this stage that is distinguished by ICD 10, gastroduodenitis in this case is capable of provoking the development of peptic ulcer.
Catarrhal gastroduodenitis is diagnosed in the process of exacerbation, when the inflammatory process affects the walls of the stomach and the initial part of the duodenum. It can be caused by improper diet or overuse of medications. And here the therapeutic diet becomes the right lifeline.
The erythematous variety is diagnosed when inflammation of the mucosa of the gastrointestinal tract is in the nature of a focal formation. In this case, a large amount of mucus is formed, it causes swelling of the walls. Such a clinical picture signals that the disease is turning into chronic stage. Treatment in this case will be complex.
Source: http://zhkt.guru/gastroduodenit-2/mkb-10-vidy
Physiological duodenogastric
Duodenogastric reflux (DGR) - throwing the contents of the duodenum into the stomach. Valid spelling: duodeno-gastric reflux. Incorrect names: duodeno gastric reflux, duodenal reflux, gastric reflux, gastroduodenal reflux.
Duodenogastric reflux occurs in 15% of healthy people. At the same time, duodenogastric reflux is often a syndrome that accompanies many diseases of the upper gastrointestinal tract: chronic gastritis. peptic ulcer of the stomach and duodenum, gastroesophageal reflux disease.
If the contents of the duodenum are thrown not only into the stomach, but also into the esophagus, then such a reflux is called duodenogastroesophageal.
Existing for a long time duodenogastric reflux leads to reflux gastritis. stomach ulcers and gastroesophageal reflux disease.
In the clinical picture, with pronounced duodenogastric refluxes, there is a high frequency and severity of pain and dyspeptic syndromes, tongue coating with a yellow coating, diffuse abdominal pain on palpation. Duodenogastric refluxes are very often combined with pathological gastroesophageal refluxes (Pakhomovskaya NL and others).
pH-gram of the body of the patient's stomach, duodenogastric refluxes at night and in the morning (Storonova O.A. Trukhmanov A.S.)
The table shows the average quantitative estimates of acidity and duodenogastric reflux in "healthy" (without complaints of gastroenterological problems and without any subjective sensations) people (Kolesnikova I.Yu. 2009):
Source: http://www.gastroscan.ru/handbook/117/361
There are similar signs in gastritis and duodenitis. Only fibrogastroduodenoscopy helps to identify gastroduodenitis reflux. If the described phenomenon proceeds independently, its treatment is reduced to observing a strict sparing diet. It is based on several rules, which should be discussed separately.
The menu for DGR and GERD will have to include only easily digestible dishes. The main amount of food should be divided into three parts, it is important to organize snacks between them. They will prevent starvation - the main provocateur. For snacks, it is better to choose foods that promote the excretion of bile. These are crackers rye croutons, bran and oat liver.
So, for example, both there and here you can eat only low-fat varieties of meat and fish, they must be steamed. Forbidden dairy products and sour juices. From dairy products are allowed: milk, low-fat cottage cheese and yogurt. You can form a menu by studying the diet "Table No. 1" and "Table No. 2", and coordinate all incomprehensible points with a gastroenterologist.
It is important to understand that the diet will not be able to help if the causes of the disease have not been eliminated. Almost all symptoms will return immediately after it ends. Therefore, it is so important not to self-medicate. You should always remember that the first mild stages of pathology, such as superficial reflux gastroduodenitis, are easily treated. If no steps are taken towards recovery, the superficial form of the disease quickly develops into a chronic one, which is characterized by a protracted course.
Dealing with them will be much more difficult. Help will have to call for drug therapy. It is complex. The doctor will advise taking prokinetics, antacids, histamine receptor blockers. Physiotherapy, traditional medicine helps well. But they must be paired with medications.
Functional dyspepsia is a symptomatic complex of disorders in the digestive process that are functional in nature. Dyspeptic syndrome of a functional type is manifested by discomfort, heaviness in the epigastric region of the abdomen and other symptoms. Nausea, bouts of vomiting, heartburn, belching, excessive gas formation, and bloating may occur. Dyspepsia of this type is considered one of the most common pathologies of the gastrointestinal tract. provoke development functional dyspepsia may disrupt the motor function of the digestive organ.
According to the international classification of diseases ICD 10, functional dyspepsia has the code K30.
Dyspepsia according to the ICD implies a complex type of disorder of the gastrointestinal tract. Dyspeptic syndrome is a kind of indigestion, a general disorder digestive system. Pathology has a similar clinical picture with many other diseases of the gastrointestinal tract.
Of particular importance in the formation of functional dyspepsia are bad habits, as well as a set of alimentary errors. Often this is smoking, alcohol abuse and drugs.
A similar disorder of the gastrointestinal tract occurs against the background of a lack of digestive enzymes, as a result of which there is a violation of the absorption of nutrients, minerals and vitamins in the intestinal cavity. In some cases, the banal indigestion of the digestive system provokes the disease. Failures can be caused by the abuse of fatty and heavy products, as well as overeating. One of the main reasons for the development of pathology is an improper or unbalanced diet.
Functional dyspepsia is common in newborns. In this case, the inconsistency of food with the capabilities of the gastrointestinal tract acts as a provocateur. The reason may be early feeding or overfeeding.
There are several types of non-ulcer dyspepsia of a functional form. The fermentation type develops in case of abuse of carbohydrates, which provoke bouts of strong fermentation. These products include cabbage, fruits, sweets, yeast dough, and legumes. Putrefactive dyspeptic syndrome manifests itself against the background of the consumption of a large amount of protein (red meat). This type of food is hard to digest, which allows bacteria to actively multiply in the intestines. The cause of fatty dyspepsia is the consumption of indigestible fats.
A disorder of the gastrointestinal tract, which is directly related to a deficiency of food enzymes, may be the result of pathologies of the intestines, gallbladder, liver, and stomach.
Dyspeptic syndrome is based on a variety of disorders and failures in gastroduodenal motility, manifested as follows:
The clinical picture of dyspeptic functional syndrome depends on the disorders that provoked it. Common signs of gastrointestinal distress include nausea, vomiting, belching, pain syndrome and a feeling of heaviness in the stomach.
The cause of heartburn may be the penetration of the food bolus from the stomach cavity back into the esophagus. From the side of the intestine there are the following signs:
diarrhea is characteristic symptom any kind of dyspeptic syndrome. There are also pains in the abdomen, excessive formation of intestinal gases, taste in oral cavity, lack of appetite, nausea. In some cases, intolerance to fried and fatty foods occurs.
Before starting therapy, it is important to undergo a complete diagnosis. It is necessary to conduct a blood test for biochemistry to determine inflammation and malfunctions in the functioning of the kidneys, liver, stomach, and pancreas. Based on the analysis of fecal masses, diseases manifested by dyspepsia can be detected.
Corpogram can detect undigested food in feces as well as dietary fiber and fats. Measurement of acidity will help determine the pathological syndrome of functional dyspepsia. Esophagogastroduodenoscopy allows you to assess the condition of the mucosa of the organ. For this, an endoscope is used, and tissue is taken (biopsy).
Of particular importance is pH-metry, which helps to determine the level of acidity of gastric secretions. An important diagnostic indicator is a test for Helicobacter pylori, a peculiar microorganism that provokes the development of gastritis, duodenal ulcer and stomach ulcers. Thanks to ultrasound, there is a chance to detect malignant tumor in the gastrointestinal tract, occurring against the background of functional dyspepsia.
If the listed clinical picture is found, it is urgent to contact a gastroenterologist. Therapy with medications is selected based on the cause of the disease. Basically, doctors prescribe drugs that increase the motility of the digestive tract.
In the treatment of functional dyspepsia, it is important to adhere to a strict diet. Fractional and frequent meals are shown, at least five times a day. It is strictly forbidden to overeat, starve, and eat before bedtime. It is forbidden to drink alcohol and soda, as well as smoke cigarettes. If the cause of the pathology is considered to be a lack of enzymes, then special drugs are prescribed without fail that can make up for the lack of these substances in the human body.
If the disease is detected in a child, severe dehydration of the body may begin against the background of diarrhea. You need to see a doctor urgently. As a rule, various medications are prescribed that eliminate the cause of dyspepsia, as well as prevent dehydration. You can give your child Regidron, rice water or sweet tea. Vitamins B are well suited to enhance motility and peristalsis. In the case of pathogenic microflora, the use of Enterofuril, dill water is required.
Dyspeptic functional syndrome is a combination of pathogenic manifestations of the gastrointestinal tract. It is important to consult a doctor in time and not self-medicate.
Source: http://vashzhkt.com/bolezni/dispepsiya-kod-po-mkb-10.html
Duodenogastric reflux is functional disorder gastrointestinal tract. It occurs when the contents of the duodenum, along with bile salts, instead of passing into small intestine returns to the stomach. This content mixes with digestive acids and has a toxic effect on the stomach.
The causes of duodeno-gastric reflux are not entirely understood. This disease can be caused by a disorder in the nerve signals to the duodenum and bile ducts(hence, reflux occurs in patients after gallbladder removal). In addition, it occurs with excessive relaxation of the pylorus, changes in its motility or peristaltic strength.
Duodenogastric reflux can cause gastric hyperplasia or blood stasis. In addition, the composition of bile that enters the stomach affects the secretion of prostaglandins, which are responsible for the activity of the protective mechanisms of the gastric mucosa, which further exacerbates the problem and makes treatment more difficult.
Duodenogastric reflux causes:
It should be noted that these symptoms do not appear immediately, but as the disease progresses.
This ailment can be easily treated on its own, following a diet and using folk remedies. Duodenogastric reflux is not a complex disease - it is rather a violation of the gastrointestinal tract, which in the future can lead to diseases. Until that happens, take responsibility for your health into your own hands.
An important step in treatment is changing eating habits. A sensible diet minimizes the symptoms of duodenogastric reflux and helps to improve the functioning of the digestive system.
Treatment with medicinal herbs, roots, honey and other folk remedies gives an amazing effect, which in many respects exceeds the effect of medical procedures. After all, it is best to improve the functioning of the body in natural ways - this will help eliminate side effects.
These three herbs are the three "pillars" on which the health of our digestive system is built. They can treat many diseases - gastritis, heartburn, indigestion, nausea, dysbacteriosis and, of course, duodenogastric reflux. Mix yarrow, chamomile and St. John's wort in any proportions (that is, take the ingredients "by eye"), pour boiling water, and make delicious tea with honey. Drink this drink every morning and evening.
If the disease has become so aggravated that you have not only pain, but also vomiting with bile, treat with fume herb. You need to make infusions from it (2 tablespoons of the plant per half liter of boiling water, hold it under the lid for 1 hour). Take 50 ml of infusion every 2 hours until vomiting and pain subside. Then move on to treatment with chamomile, yarrow and St. John's wort (as described in the previous recipe).
The root of marshmallow is no less effective. From it you need to make cold infusions - that is, pour the plant cold water at the rate of 2 tablespoons of crushed roots per half liter of water. The mixture should be infused for 5-6 hours. Take it in small portions throughout the day until the bilious vomiting stops.
Flaxseed treatment is effective for heartburn, gastritis and all types of reflux (including duodenogastric reflux). It envelops the gastric mucosa, protecting it from the negative effects of bile salts. Pour a tablespoon of seeds with cool water (about 100 ml) and wait until they swell and mucus comes out of the seeds. This mixture should be drunk on an empty stomach before meals. In addition, treat with other plants that would support duodenal peristalsis.
Mix these herbs:
Warm infusions should be made from this mixture - 1 tsp. pour a glass of boiling water over the herbs, cover with a lid, strain and drink after 20 minutes. For taste, you can add honey to the drink. Drink the medicine 3 times a day, one hour after meals.
Rue also has a stimulating effect on duodenal motility. It can be brewed instead of tea. But the easiest way is to just chew 1-2 leaves of the plant each time after a meal.
In therapy, much depends on the stages of the course of the disease. Such information affects the duration of treatment and the choice of certain drugs. In the case of GERD, the first thing that matters is how deeply the mucosa of the esophagus is affected. In medicine, the classification of gastroesophageal reflux disease is more often used, which is detected by such a research method as FGDS (fibrogastroduodenoscopy).
What symptoms will bother a person at each stage of the disease? Today we have to answer not only this question. There are several options for classifying GERD, consider the most common of them.
The simplest classification is written in one of the classic medical books called ICD-10 (this is the tenth revision of the international classification of the disease). Here, the clinical variant of the division of GERD is as follows.
Endoscopic classification was proposed in the late 80s by Savary and Miller, and is quite widely used in our time.
It has long been known that the mechanism for the development of GERD is a dysfunction of the lower esophageal sphincter (a muscle located on the border between the esophagus and stomach, which limits the reverse movement of food). When this muscle is weakened, gastric contents, including hydrochloric acid, are thrown into the esophagus. And over time, almost all of its shells undergo changes. So they served as the basis for this classification.
esophageal lesions
It can be presented in detail as follows.
In their practice, gastroenterologists often use this endoscopic classification to determine the stages of GERD development. Therapists also resort to it more often, considering it easier to understand and more exhaustive. But this is not the only division of GERD.
At the end of the 20th century, European Gastroenterology Week proposed the use of lesion extent. This is how the Los Angeles classification of GERD was born. Here's what it includes.
According to the Los Angeles classification, complications in the form of ulcers and narrowing may be present at any of the above stages.
The disease progression units were created to make the work of physicians easier. Thanks to classifications, it becomes easier to understand the manifestations of the process and better select methods for its treatment. Only a doctor can determine at what stage of the development of the disease each person suffering from GERD is. Therefore, at the first signs of illness, to speed up recovery, contact a specialist.