Diseases of the esophagus recommendations. Prevention of the esophagus - symptoms, methods and recommendations

Moscow 2014

Academician of the Russian Academy of Sciences V.T. Ivashkin*, Corresponding Member of the Russian Academy of Sciences I.V. Maev**, Professor A.S. Trukhmanov*, Professor E.K. Baranskaya*, Professor O.B. Dronova***, Professor O.V. Zayratyants", Professor V.D. Pasechnikov", Professor R.G. Saifutdinov"", Professor A.A. Sheptulin*, associate professor Yu.A. Curly**, Associate Professor T.L. Lapina*, Ph.D. O.A. Storonova*, V.O. Kaibyshev*

*Department and clinic of propaedeutics of internal diseases, gastroenterology and hepatology. V.Kh. Vasilenko First Moscow State Medical University. THEM. Sechenov;

**Department of propaedeutics of internal diseases and gastroenterology, Moscow State University of Medicine and Dentistry. A.I. Evdokimova;

*** Department of Surgery, Faculty of Postgraduate Training, Orenburg State Medical Academy,

"Department of Pathological Anatomy of the Moscow State University of Medicine and Dentistry named after A.I. Evdokimov,

"Department of Therapy with a Dietetics Course of the Stavropol State Medical University,

"" Department of Therapy of the Kazan State Medical Academy.

• Introduction
• Definition
• Epidemiology
• The main factors of pathogenesis
• Clinical picture
• Extraesophageal manifestations of the disease
• Complications
• Staged diagnosis of gastroesophageal reflux disease
• In a clinic setting
• In a hospital setting
• Treatment
• Management of patients with Barrett's esophagus
• Conclusion

List of abbreviations

Introduction

The Russian Gastroenterological Association (RGA) continues to prepare draft national clinical guidelines containing standards for the diagnosis and treatment of major diseases of the digestive system. Recommendations on peptic ulcer, chronic gastritis, functional dyspepsia, Crohn's disease and ulcerative colitis, chronic pancreatitis, autoimmune hepatitis were discussed and published. Work continues on the release of other recommendations on a wide range of diseases of the digestive system.

These recommendations for the diagnosis and treatment of gastroesophageal reflux disease are presented due to the fact that despite the undoubted success, there is still a need to introduce modern standards for managing patients with this disease. The urgency of the problem of GERD is determined by a number of circumstances. Epidemiological studies of recent years have shown that in terms of its prevalence, GERD takes a leading position among other gastroenterological diseases. Heartburn - the leading symptom of GERD - is detected in 20-40% of the population of developed countries.

In Russia, the prevalence of GERD is 18-46% [Ivashkin V.T., Maev I.V., Trukhmanov A.S., 2011]. The relevance of GERD is also due to the fact that it leads to a significant decrease in the quality of life of the patient, especially with nocturnal symptoms, the appearance of extraesophageal symptoms (chest pain, persistent cough) and the risk of complications such as bleeding from ulcers and erosions, the development of peptic strictures and, what causes the greatest suspicion, adenocarcinoma of the esophagus against the background of Barrett's esophagus. Certain difficulties arise in the treatment of patients with GERD. If the average healing time for duodenal ulcers is 3-4 weeks, for gastric ulcers - 4-6 weeks, then the healing time for esophageal erosions in many patients can reach 8-12 weeks. At the same time, in some patients, refractoriness to taking antisecretory agents is observed. Discontinuation of medications is accompanied in 60-70% of patients by a rapid (during the first 3 months) development of a relapse of the disease. Recurrence of erosive esophagitis is the main risk factor for developing Barrett's esophagus, so it is extremely important to identify risk factors for recurrence.

The purpose of these recommendations was to present unified strategic and tactical guidelines regarding adequate diagnosis, management tactics and schemes for rational pharmacotherapy based on the principles of evidence-based medicine.

Clinical guidelines “Gastroesophageal reflux disease. Recommendations for Diagnosis and Treatment" contains the most up-to-date information on pathological physiology, clinical picture and principles of GERD diagnostics. They present the latest data on approaches to the treatment of patients with GERD, taking into account modern advances in pharmacology. Designed for general practitioners, gastroenterologists, endoscopists, specialists in related specialties, heads of health authorities.

Definition

Gastroesophageal reflux disease is a chronic relapsing disease caused by a violation of the motor-evacuation function of the organs of the gastroesophageal zone and characterized by spontaneous or regularly repeated throwing of gastric or duodenal contents into the esophagus, which leads to damage to the distal esophagus with the development of functional disorders and / or dystrophic changes in it non-keratinizing stratified squamous epithelium, simple (catarrhal), erosive or ulcerative esophagitis (reflux esophagitis), and in some patients over time - cylindric (glandular) metaplasia (Barrett's esophagus).

Erosive esophagitis and non-erosive reflux disease (NERD) should be considered two forms of gastroesophageal reflux disease. The Vevey NERD Expert Consensus Meeting (Switzerland, 2007) adopted the following definition of NERD: “NERD is a subcategory of GERD characterized by the presence of symptoms caused by [gastroesophageal] reflux and reducing quality of life, without erosions/damages of the esophageal mucosa detected during routine endoscopic examination, and in the absence of antisecretory therapy at the moment. The diagnosis of NERD can be confirmed by drug testing with antisecretory treatment, the detection of pathological [gastroesophageal] reflux, or the identification of specific symptoms during new [high-tech] endoscopy.” In some patients with NERD, using the latest endoscopic technologies (high-resolution magnification, narrow-spectrum endoscopy), signs of esophagitis are found. These patients deserve examination and treatment in full, as well as patients with erosive esophagitis.

NERD should be differentiated from functional heartburn, which is the absence of pathological gastroesophageal reflux. Patients with functional heartburn represent a very small heterogeneous group with different mechanisms of symptom development. Drug tests using antisecretory drugs cannot be considered specific, but their negative result demonstrates a high probability of the absence of gastroesophageal reflux disease. Barrett's esophagus - the appearance of a cylindrical (glandular) metaplastic epithelium in the mucosa of the distal esophagus, in some cases increasing the risk of developing esophageal adenocarcinoma (AKA).

Epidemiology

The prevalence of GERD among the adult population is up to 40%. Extensive epidemiological studies indicate that 40% of individuals constantly (with varying frequency) experience heartburn, the main symptom of GERD. In general, the prevalence of GERD in Russia among the adult population is 40-60%, and esophagitis is found in 45-80% of people with GERD. In the general population, the prevalence of esophagitis is estimated at 5-6%; while 65-90% of patients have mild and moderate esophagitis, 10-35% have severe esophagitis.

The incidence of severe esophagitis in the general population is 5 cases per 100,000 population per year. The prevalence of Barrett's esophagus among individuals with esophagitis approaches 8% with fluctuations ranging from 5 to 30%. In recent decades, there has been an increase in the incidence of AKP, which develops against the background of the progression of dysplastic changes in the intestinal-type metaplastic epithelium of the mucous membrane of the distal esophagus. AKP and high-grade dysplasia develop in 0.4-0.6% of patients with Barrett's esophagus with intestinal metaplasia per year. AKP develops in 0.5% of patients with low-grade epithelial dysplasia, in 6% per year with high-grade dysplasia, and in less than 0.1% without dysplasia.

Formation of structures of the esophagus was noted in 7-23% of patients with erosive-ulcerative esophagitis, the occurrence of bleeding - in 2% of patients. Among persons over 80 years of age with gastrointestinal bleeding, erosion and ulcers of the esophagus were their cause in 21% of cases, among patients in intensive care units who underwent surgery - in 25% of cases.

The main factors of pathogenesis

Gastroesophageal reflux disease is considered as an integral part of the group of acid-dependent diseases, since gastric hydrochloric acid is the main damaging factor in the development of clinical symptoms and morphological manifestations of GERD. It should be remembered, however, that pathological reflux is a reflection of insufficiency of the lower esophageal sphincter, that is, GERD is a disease with an initial violation of the motor function of the digestive system.

A key factor in the pathogenesis of GERD is a pathologically high frequency and / or duration of episodes of reflux of stomach contents into the esophagus. This dysfunction in a large proportion of patients is accompanied by a significant delay in the recovery of the pH of the distal esophagus after each episode of reflux. Esophageal clearance disorder develops as a result of a combination of two factors: a weakening of the peristalsis of the thoracic esophagus and a decrease in saliva secretion. A significant increase in gastric acid secretion (as, for example, in Zollinger-Ellison syndrome) significantly increases the risk of GERD.

Reflux episodes develop due to a significantly weakened tone of the lower esophageal sphincter (LES), unable to perform a barrier function in relation to the retrograde flow of gastric contents. GERD patients with severe erosive esophagitis or large hiatal hernia (HH) have prolonged periods of low LES pressure (below 5 mmHg).

In the vast majority of patients with GERD, reflux episodes occur predominantly during the so-called transient relaxation of the lower esophageal sphincter (PRNES). During transient relaxation of the lower esophageal sphincter, the antireflux barrier between the stomach and esophagus usually disappears for 10-15 seconds. PRNPS occur outside of the act of swallowing. In patients with non-erosive reflux disease, as well as mild erosive esophagitis, which together constitute the vast majority of patients with GERD, transient relaxation of the LES can cause episodes of reflux in almost 85% of cases.

PRNPS, the principal mechanism of reflux, is thought to be mediated through the same pathways from the dorsal vagus nucleus (nucleus dorsalis and nucleus ambiguus) that mediate esophageal motility and LES relaxation in a healthy individual. Mechanoreceptors located in the upper part of the stomach respond to stretching of the organ wall and send signals to the hindbrain along the afferent fibers of the vagus nerve. In those centers of the hindbrain that perceive these signals, the formation of structured motor programs of PRNPS occurs, reaching the lower esophageal sphincter along the descending pathways. Efferent pathways are carried through the vagus nerve, where nitric oxide (NO) is a postganglionic neurotransmitter. This process is significantly influenced by higher centers, as a result of which, for example, PRNPS are blocked during deep sleep or general anesthesia. Contraction of the crura of the diaphragm is controlled by the respiratory center in the brainstem and the nucleus of the phrenic nerve. The legs of the diaphragm receive innervation from the right and left phrenic nerves through N-cholinergic receptors. An increase in intra-abdominal pressure caused by a person's normal motor activity during the day, when coinciding in time with a transient relaxation of the LES, significantly increases the likelihood of acid reflux.

Currently, in understanding the mechanism of gastroesophageal reflux, one should be guided by the paradigm of the mutual influence of transient relaxation of the lower esophageal sphincter and the consequences of destructuring of the esophageal junction. Weakness of the crura of the diaphragm leads either to a delay in the onset of action, or to a significant degradation of the actual compression effect of the diaphragm contraction on the lower esophageal sphincter. A hernia of the esophageal opening of the diaphragm, depending on its size and structure, has a mechanical effect on the LES: it impairs the antireflux function during PRNPS and / or reduces the actual tonic component of the sphincter. The most important consequence of the destructurization of the gastroesophageal junction zone is the reflux of relatively large volumes of fluid from the stomach into the esophagus during the period of PRNPS. The processes leading to the destructuring of the esophagogastric junction zone have not been definitively deciphered, although it is obvious that they must be associated with the weakness of the connective tissue structures.

In a significant number of patients, episodes of GER develop with normal LES pressure. The GER mechanism is associated with a high pressure gradient between the stomach and the esophagus, due to various reasons: in some patients, a violation of the evacuation of the contents, in the other part, a high residual pressure due to the spread of the pressure gradient from the duodenum. In these cases, GER develop due to the inability of the locking mechanisms to counteract the high pressure gradient in the stomach. In addition, in some patients, due to violations of the motor function of the stomach, food does not mix well with its contents and a "lake" of acid is formed near the cardia. This mechanism plays a role in the occurrence of postprandial refluxes.

Thus, from a pathophysiological point of view, GERD is an acid-dependent disease that develops against the background of a primary violation of the motor function of the upper digestive tract. In the pathogenesis of NERD, the features of the esophageal mucosa play a special role.

Clinical picture

Esophageal manifestations

A typical reflux symptom complex - heartburn, belching, regurgitation, painful and difficult passage of food - are painful for patients, significantly worsen their quality of life, and adversely affect their performance. The quality of life of patients with GERD, in whom the clinical symptoms of the disease are observed at night, is especially significantly reduced.

Heartburn is the most characteristic symptom, occurs in 83% of patients and occurs due to prolonged contact with acidic (pH< 4) желудочного содержимого со слизистой пищевода. Типичным для данного симптома считается усиление при погрешностях в диете, приеме алкоголя, газированных напитков, физическом напряжении, наклонах и в горизонтальном положении. Интенсивность и частота изжоги (как дневной, так и ночной) прямо зависит от показателей индекса массы тела, что соответствует предрасположенности людей с избыточным весом к гастроэзофагеальному рефлюксу.

Belching, as one of the leading symptoms of GERD, occurs quite often and is found in 52% of patients. Belching, as a rule, intensifies after eating, taking carbonated drinks.

Regurgitation of food, observed in some patients with GERD, increases with physical exertion and with a position that promotes regurgitation. Dysphagia and odynophagia are observed in 19% of patients with GERD. A characteristic feature of these symptoms is their intermittent character. Their occurrence is based on hypermotor dyskinesia of the esophagus, which disrupts its peristaltic function, and the cause of odynophagia can also be an erosive and ulcerative lesion of the mucous membrane. The appearance of more persistent dysphagia and a simultaneous decrease in heartburn may indicate the formation of a stricture of the esophagus.

For patients with HH, one of the characteristic symptoms is pain in the epigastric region, which appears in the projection of the xiphoid process shortly after eating and is aggravated by bending over, lifting weights, after which heartburn occurs.

Other symptoms of GERD include a sensation of a lump in the throat when swallowing, pain in the lower jaw, burning of the tongue.

Chest pain occurs in patients with GERD due to hypermotor esophageal dyskinesia (secondary esophagus spasm), which may be caused by a defect in the inhibitory transmitter system - nitric oxide. The starting point for the occurrence of esophagospasm and, accordingly, pain, however, always turns out to be pathological (i.e., prolonged) gastroesophageal reflux.

Extraesophageal manifestations of the disease

Extraesophageal manifestations of the disease include:

• bronchopulmonary syndrome;
• otorhinolaryngological syndrome;
• dental syndrome;
• cardiac syndrome;
• anemic syndrome;

The variety of symptoms and syndromes leads in practice to numerous diagnostic errors when GERD is mistaken for angina pectoris, pneumonia, anemia. The clinical picture of this chronic disease is polymorphic, with many "masks" of other diseases.

Bronchopulmonary manifestations include cough, frequent bronchitis, pneumonia, bronchial asthma, pulmonary fibrosis. Numerous foreign and domestic studies have shown an increase in the risk of bronchial asthma, as well as the severity of its course in patients with GERD. Gastroesophageal reflux is detected in 30-90% of patients with bronchial asthma, predisposing to its more severe course. The reasons for the development of bronchial obstruction in GERD are: 1) vago-vagal reflex, 2) microaspiration.

Bronchopulmonary manifestations may be the only clinical sign of gastroesophageal reflux and cause insufficient effectiveness of the treatment of bronchial asthma. On the contrary, the inclusion in such cases of drugs prescribed for GERD in the complex therapy increases the effectiveness of the treatment of bronchial asthma.

A sore throat, hoarseness or even loss of voice, a rough barking cough may be the result of the reflux of gastric contents into the larynx and patients develop an “otolaryngological mask of GERD”. The formation of ulcers, granulomas of the vocal cords, stenosis of the departments located distal to the glottis is described. Laryngitis is common (78% of patients with chronic hoarseness have symptoms of GERD). The cause of chronic rhinitis, recurrent otitis, otalgia, may be pathological GER.

Dental syndrome is manifested by damage to the teeth due to damage to tooth enamel by aggressive gastric contents. In patients with GERD, caries, the development of halitosis, and dental erosions are possible. In rare cases, aphthous stomatitis develops. Pain behind the sternum, along the esophagus, can give the impression of coronary pain, the so-called “non-cardiac chestpain” symptom. These pains are caused by spasm of the esophagus, they are stopped by nitrates, but unlike angina pectoris, they are not associated with physical activity, walking. As a result of the esophagocardiac reflex, arrhythmia may occur.

Anemic syndrome occurs due to chronic bleeding from erosions or ulcers of the esophagus. The most common is hypochromic iron deficiency anemia.

The differential diagnosis for extraesophageal manifestations of GERD is based on a comprehensive clinical and instrumental assessment. It is necessary to carefully analyze the time and causes of the onset of clinical symptoms. In the case of GERD, they occur when bending over, in a horizontal position, combined with heartburn, belching, stop when taking antacids, a sip of water.

The most accurate way to verify the relationship of extraesophageal symptoms of GERD with episodes of pathological reflux is when conducting 24-hour intraesophageal pH-metry and pH-impedancemetry. This method (see below) allows you to establish the presence of a correlation between the onset of a symptom and episodes of reflux (symptom index > 50%).

Inflammatory changes in the mucous membrane of the esophagus.

Complications

Reflux esophagitis detected by endoscopic examination includes simple (catarrhal) esophagitis, erosions and ulcers of the esophagus. Erosive esophagitis can be of varying severity - from A to D stage according to the Los Angeles classification and from the 1st to the 3rd stage according to the Savary-Miller classification - depending on the area of ​​​​the lesion, while to the 4th stage according to Savary-Miller classifications include complications of GERD: strictures of the esophagus, ulcers (bleeding from ulcers), Barrett's esophagus.

GERD can be complicated by esophageal strictures in 7%-23%, esophageal ulcers in 5%, bleeding in 2%. Strictures require further expensive surgical and endoscopic (and often repeated) procedures (bougienage, surgical treatment, etc.). Each such case should be considered as the result of inadequate conservative therapy, which justifies the need to improve it to prevent the development of strictures. Bleeding caused by erosive and ulcerative lesions of the esophagus can complicate the course of liver cirrhosis, and is also observed in patients who have undergone surgery and in elderly patients. Among people over 80 years of age with gastrointestinal bleeding, erosion and ulcers of the esophagus become their cause in one case out of five, among patients in intensive care units who underwent surgery - in one case out of four.

The most formidable complication of GERD - Barrett's esophagus - is the development of a cylindrical (glandular) metaplastic epithelium in the mucosa of the esophagus, which subsequently increases the risk of developing AKP. The exposure of hydrochloric and bile acids in the esophagus, on the one hand, increases the activity of protein kinases that initiate the mitogenic activity of cells and, accordingly, their proliferation, and, on the other hand, inhibits apoptosis in the affected areas of the esophagus. Approximately 95% of cases of AKP are diagnosed in patients with Barrett's esophagus. Therefore, the main role in the prevention and early diagnosis of esophageal cancer is played by the diagnosis and effective treatment of Barrett's esophagus. After the use of proton pump inhibitors (PPIs) in patients with Barrett's esophagus, a decrease in the level of proliferation markers is noted, which is absent in those patients who have persistent pathological acid reflux (pH<4). Длительное применение ИПП может приводить к частичной регрессии ограниченного участка цилиндрической метаплазии.

Among the risk factors for the development of complications of GERD, the most important are the frequency of occurrence and duration of symptoms, in particular, heartburn, the severity of erosive esophagitis, the presence of hiatal hernia (HH), obesity, and the presence of nocturnal reflux. There is a direct relationship between body mass index and the main indicators of daily monitoring of pH in the esophagus. In particular, the degree of overweight correlates with the duration of the decrease in pH in the esophagus to 4 and below.

Consequently, overweight and obesity mucosa of the esophagus is longer exposed to the acidic contents of the stomach. One of the reasons can be called an increase in intra-abdominal pressure, contributing to gastroesophageal reflux. Rapidly progressive dysphagia and weight loss may indicate the development of AKP, but these symptoms occur only in the later stages of the disease, so the clinical diagnosis of esophageal cancer is usually delayed. As a result, prevention and early diagnosis of esophageal cancer requires timely detection and adequate treatment of Barrett's esophagus.

Staged diagnosis of gastroesophageal reflux disease

In a clinic setting

Diagnosis of the early stages of GERD is based on primary referral and analysis of the clinical picture of the disease. An important component that helps to identify patients with GERD and contributes to the prevention of its complications should be considered the introduction of questionnaires, including those that patients themselves can fill out at outpatient appointments.

Additional research methods

Endoscopy

Endoscopic examination is one of the main methods for diagnosing GERD, because. allows you to determine the level of the Z-line and the condition of the pancreatic mucosa, to conduct clarifying techniques (chromoscopy, fluorescence, ZOOM - endoscopy, NBI mode).

In patients complaining of heartburn, endoscopic examination may show signs of reflux esophagitis of varying severity. These include hyperemia and friability of the mucous membrane of the esophagus (catarrhal esophagitis), erosion and ulcers (erosive esophagitis of varying severity - from the 1st to the 4th stage - depending on the area of ​​​​the lesion), the presence of exudate, fibrin or signs of bleeding.

Many classifications have been proposed to determine changes in the mucosa of the esophagus in reflux esophagitis, but the most common are: the classification of M. Savary and G. Miller (1978) and the classification that was first proposed at the World Congress of Gastroenterology in Los Angeles in 1994 (Armstrong D. Endal., 1996), developed by the International Working Group of Experts. Classification M. Savary and G. Miller, no which distinguishes 4 stages of reflux esophagitis:

Stage 1 - diffuse or focal hyperemia of the mucosa of the distal esophagus, separate non-confluent erosions with a yellowish base and red edges, linear aphthous erosions extending upward from the cardia or the esophageal opening of the diaphragm;

stage 2 - merging, but not capturing the entire surface of the mucous erosion;

Stage 3 - inflammatory and erosive changes merge and capture the entire circumference of the esophagus;

Stage 4 - similar to the previous stage, but there are complications: narrowing of the lumen of the esophagus, which worsens or prevents the endoscope from passing into the underlying sections, ulcers, Barrett's esophagus.

The Los Angeles classification provides for a four-degree gradation of reflux esophagitis and also takes into account the prevalence of the process, but complications of GERD: strictures, ulcers, Barrett's esophagus - are considered separately and can be at any stage.

Stage A- one (or more) area of ​​the damaged mucosa up to 5 mm in size, which does not capture the mucosa between the folds (located at the top of the fold).

Stage B- one (or more) area of ​​the damaged mucosa larger than 5 mm, which does not capture the mucosa between the folds (located at the top of the fold).

Stage C One (or more) mucosal injury that extends into the mucosa between two or more folds, but involves less than 75% of the esophageal circumference.

Stage D One (or more) mucosal lesions that involve more than 75% of the esophageal circumference.

In addition, there may be prolapse of the gastric mucosa into the esophagus, especially with vomiting, a true shortening of the esophagus with the location of the esophageal-gastric junction significantly higher than the diaphragm, reflux of gastric or duodenal contents into the esophagus. It is rather difficult to assess the closing function of the cardia during esophagoscopy, since the cardia can be reflexively opened in response to the introduction of an endoscope and air insufflation.

In many cases, the clinical symptoms of the disease are not accompanied by endoscopic and morphological changes characteristic of erosive esophagitis (non-erosive form of the disease, NERD).

In a hospital setting

In case of a torpid course of the disease (lack of clinical and endoscopic remission within 4-8 weeks of standard adequate therapy), as well as the presence of complications of the disease (strictures, Barrett's esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterological clinic, including in outpatient units these institutions. If necessary, patients should be carried out:

• esophagogastroduodenoscopy with biopsy of the esophagus and histological examination of biopsy specimens to exclude Barrett's esophagus and adenocarcinoma, as well as eosinophilic esophagitis;
• intraesophageal daily pH-metry or pH impedancemetry ;
• x-ray examination of the esophagus and stomach;
• complex ultrasound examination of internal organs.
• registration of the electrocardiogram and other special methods (see below).

Before conducting probe methods (EGDS, pH-metry), it is necessary to examine blood tests for hepatitis, HIV, syphilis. According to the indications (differential diagnosis of extraesophageal manifestations of GERD), consultations of specialists should be held: otorhinolaryngologist, pulmonologist, cardiologist.

Histological examination

Histological examination of biopsy specimens of the mucosa of the esophagus reveals dystrophic, necrotic, acute and chronic inflammatory changes expressed to varying degrees. With simple (catarrhal) esophagitis, the layer of non-keratinizing stratified epithelium can maintain its usual thickness (this happens only when the duration of the disease is from several months to 1-2 years). More often, its atrophy is detected, but occasionally, along with atrophy, areas of hyperplasia are found, in particular, the basal layer, which occupies up to 10-15% of the thickness of the epithelial layer.

Intercellular edema, dystrophy and foci of necrosis, especially in the surface layers, of epitheliocytes (keratinocytes) expressed to varying degrees are characteristic. The basement membrane of the epithelium in most cases is not changed, but in some patients it can be thickened and sclerosed. As a result of necrosis of various areas of the stratified squamous epithelium, erosions (erosive esophagitis) are formed, and with deeper lesions, up to the muscular membrane and even deeper - ulcers (ulcerative esophagitis).

Along with dystrophic-necrotic changes in the epithelium in the mucous membrane, microcirculation disorders with vascular hyperemia are noted. An increase in the number and change in the length of vascular-stromal papillae is characteristic. In the thickness of the epithelium and in the subepithelial layer, focal (usually perivascular) and in some places diffuse lymphoplasmic cell infiltrates with an admixture of neutrophilic leukocytes and single eosinophils are detected. A significant increase in the number of eosinophilic leukocytes, especially intraepithelial eosinophilic cell microabscesses in combination with subepithelial sclerosis of the lamina propria, serve as criteria for the diagnosis of eosinophilic esophagitis. The smooth muscle cells of the lamina propria show signs of severe dystrophy or atrophy, and in rare cases, a state of coagulative necrosis.

Inflammatory, necrotic, or hyperplastic changes may also extend to the esophageal glands. In a small percentage of cases, signs of active ongoing inflammation are not detected histologically. At the same time, in the mucous membrane of the esophagus, there is an overgrowth of loose, and in some places dense fibrous connective tissue (sclerosis), as well as in the bottom of persistent erosions and ulcers. Histological examination may reveal metaplasia of the stratified squamous non-keratinized epithelium of the esophagus, which leads to the development of a cylindrical (glandular) epithelium with cardiac or fundal (gastric) glands. The mucosa of the cardiac type usually has a villous surface, often characterized by short pits without well-formed glands (foveolar type), although the latter may be fully formed (glandular type), but always represented only by mucous cells, does not contain parietal or goblet cells. The mucous membrane of the fundus (gastric) type is distinguished by the presence of acid-producing parietal and chief cells in the glands, and the integumentary epithelium sometimes forms typical ridges covered with an integumentary pit epithelium. At the same time, the glands are often few in number, “compressed” by growths of connective tissue and diffuse lymphoplasmocellular, with an admixture of neutrophilic leukocytes, infiltrate.

With metaplasia of the mucous membrane of the esophagus of the cardiac or fundal types, the risk of developing adenocarcinoma of the esophagus does not increase. However, if metaplasia leads to the appearance of the so-called. specialized epithelium, as the glandular epithelium of the intestinal type is called, the risk of malignancy becomes apparent. The specialized epithelium is an incomplete small intestinal metaplasia of the glandular epithelium, and the main criterion for its histological diagnosis is the appearance of goblet cells (at least one within the biopsy).

The study of the motor function of the esophagus allows you to study the indicators of the movement of the esophageal wall and the activity of its sphincters. In GERD, a manometric study reveals a decrease in the pressure of the lower esophageal sphincter, the presence of a hernia of the esophageal opening of the diaphragm, an increase in the number of transient relaxations of the sphincter, and a decrease in the amplitude of peristaltic contractions of the esophageal wall.

Manometry allows to identify esophagospasm, atypical cases of achalasia of the cardia. The study allows you to verify the position of the LES for pH-metry. It is an indispensable attribute of the examination of the patient to decide on the surgical treatment of GERD.

Traditional manometry is being replaced by high-resolution manometry, which has a higher sensitivity in diagnosing disorders of the motor function of the esophagus and demonstrates the ability to analyze many indicators that have not been available so far. This method allows, using a multi-channel probe (sensors are located at a distance of 1 cm from each other), to obtain quantitative indicators of the total peristaltic activity, pressure in the esophageal sphincters, tone of the organ wall, and also, using a multi-color volumetric image, to see the progress of the peristaltic wave through it.

High-resolution manometry has a number of advantages over manometry performed with a 4- or 8-way water perfusion catheter. The Chicago Classification of Esophageal Motility Disorders should be considered when analyzing high-resolution manometry results.

The main method for diagnosing GER is pH-metry. The study can be carried out both on an outpatient basis and in a hospital.

When diagnosing GER, the results of pH-metry are evaluated by the total time during which the pH takes values ​​less than 4 units, the total number of refluxes per day, the number of refluxes lasting more than 5 minutes, the duration of the longest reflux.

Esophageal impedancemetry (from Latin impedio - I prevent) is a method of registering liquid and gas refluxes, based on measuring the resistance (impedance) that the content entering the lumen of the esophagus provides to an alternating electric current.

Impedancemetry is a technique for diagnosing gastroesophageal reflux disease, which allows you to determine episodes of reflux into the esophagus, regardless of the pH value of the reflux, as well as the physical state (gas, liquid) and clearance of the bolus that entered the esophagus during reflux.

pH-impedancemetry is used to detect gastroesophageal reflux in GERD, and this method has the following advantages over traditional esophageal pH-metry:

• detection of all types of refluxes, regardless of the pH value of the refluxate (acidic, alkaline, slightly acidic refluxes and superrefluxes);
• diagnosis of GERD during therapy with antisecretory drugs and evaluation of its effectiveness, as well as in hypo / anacid conditions;
• identifying the relationship of existing symptoms with slightly acidic, slightly alkaline refluxes;
• determination of the physical state of the refluxate (gas, mixed and liquid);
• determination of the height of the proximal spread of refluxes;
  
• bolus clearance calculation.

The method of impedancemetry, which is able to identify episodes of GER, regardless of the pH value of the reflux, is of particular value for patients with symptoms that persist against the background of antisecretory therapy, as it makes it possible to identify the relationship between existing complaints and episodes of non-acidic refluxes. The ability of the method to fix high and gas refluxes is indispensable for the diagnosis of GERD that occurs with atypical symptoms (chronic cough, pharyngitis, regurgitation, etc.). The main indications for pH-impedancemetry are:

1. Characteristic symptoms of GERD while taking antisecretory drugs (that is, with refractory GERD), as well as in hypo / anacid conditions (gastric resection, atrophic gastritis);
2. Atypical forms and extraesophageal manifestations of GERD: chronic cough, bronchial asthma, chronic pharyngitis, severe belching;
3. Evaluation of the effectiveness of antisecretory therapy for GERD without discontinuation of the drug in patients with persistent symptoms of the disease;
4. Evaluation of the effectiveness of surgical treatment of GERD.

X-ray examination

X-ray examination of the esophagus can be used to diagnose GERD and can detect hiatal hernias, esophageal strictures, diffuse esophagospasm, and gastroesophageal reflux as such.

In the diagnosis of GERD, methods such as bilimetry, scintigraphy, and the Bernstein-Baker test can be used. Bilimetry allows to verify bile refluxes, scintigraphy reveals violations of the motor-evacuation function of the esophagus. These techniques are used in highly specialized institutions.

The introduction of high-resolution endoscopy, NBI endoscopy, ZOOM endoscopy (magnifying endoscopy), chromoendoscopy helps to detect metaplastic changes in the esophageal epithelium for the purpose of targeted biopsy for histological examination, which is discussed in more detail in the methodological manual for the management of patients with Barrett's esophagus.

Endoscopic ultrasound of the esophagus is the main technique for detecting endophytically growing tumors.

Gastroesophageal reflux disease should be included in the range of differential diagnostic search in the presence of pain in the chest, dysphagia, gastrointestinal bleeding, broncho-obstructive syndrome.

Treatment for GERD

Treatment should be aimed at reducing reflux, reducing the damaging properties of refluxate, improving esophageal clearance, and protecting the esophageal mucosa. Currently, the following can be considered the main principles of GERD treatment: the need to prescribe proton pump inhibitors and conduct long-term basic (at least 4-8 weeks) and maintenance (6-12 months) therapy.

If these conditions are not met, the likelihood of a recurrence of the disease is very high. Studies conducted in many countries around the world have shown that more than 80% of patients who do not receive adequate maintenance treatment developed a relapse within the next 26 weeks, and within a year the probability of relapse is 90-98%.

From this follows the mandatory need for maintenance treatment. Lifestyle modification should be considered a prerequisite for effective antireflux treatment in patients with GERD. First of all, it is necessary to reduce body weight, if it is excessive, and stop smoking.

It is necessary to avoid the use of tomatoes in any form, sour fruit juices, foods that increase gas formation, as well as fats, chocolate, coffee, garlic, onions, peppers. It is necessary to exclude the use of alcohol, very spicy, hot or cold food and carbonated drinks.

Patients should avoid overeating; they should stop eating two hours before bedtime. You should not increase the number of meals: you must observe 3-4 meals a day without snacks.

Conditions that increase intra-abdominal pressure should be prevented (exclusion of loads that increase intra-abdominal pressure, wearing corsets, bandages and tight belts, lifting weights of more than 8-10 kg on both hands, work associated with tilting the body forward, physical exercises associated with overstrain of the abdominal muscles press);

Patients should be warned about the side effects of drugs that reduce the tone of the lower esophageal sphincter (theophylline, progesterone, antidepressants, nitrates, calcium antagonists), and can also cause inflammation themselves (non-steroidal anti-inflammatory drugs, doxycycline, quinidine). Elevating the head of the bed is necessary for patients who suffer from heartburn or regurgitation when lying down.

Drug treatment includes well-known groups of drugs.

Antacids

Antacids - aluminum phosphate 2.08 g. 1 pack 2-3 r per day, combined preparation - aluminum hydroxide 3.5 g and magnesium hydroxide 4.0 g in the form of a suspension, as well as aluminum hydroxide 400 mg and magnesium hydroxide 400mg tablets are effective in the treatment of mild and infrequent symptoms, especially those associated with non-compliance with the recommended lifestyle.

Antacids can be used both as monotherapy for clinical manifestations (heartburn) and in complex therapy regimens for GERD, effectively suppressing acid reflux provoked by reflux food. Liquid and tablet forms of drugs are very effective in quickly relieving the symptoms of GERD. Antacids should be taken frequently (depending on the severity of symptoms), usually 1.5 to 2 hours after meals and at bedtime.

Adsorbents - dioctahedral smectite 3 g. 1 pack. 3 r per day - have a complex effect: firstly, they have a neutralizing effect on hydrochloric acid of gastric juice, and secondly, they have an adsorbing effect, binding the components of the duodenal contents (bile acids, lysolecithin) and pepsin. Adsorbents can be used both as monotherapy for clinical manifestations of non-erosive reflux disease, and as part of complex therapy for GERD, especially in the case of mixed (acid + bile) reflux.

Alginates bind acid, pepsin and bile, form a “raft” on the surface of the gastric contents that blocks reflux and form a protective film on the esophageal mucosa.

Prokinetics (stimulators of gastrointestinal motility) lead to the restoration of the normal physiological state of the esophagus, effectively influencing the pathogenetic mechanisms of GERD, reduce the number of transient relaxations of the lower esophageal sphincter, improve esophageal clearance, including by improving the motor function of the underlying parts of the digestive tract.

The prokinetic drug Itopride hydrochloride 50 mg 3 r per day belongs to the pathogenetic treatment of GERD, since it normalizes the motor function of the upper digestive tract.

In the presence of both esophageal and extraesophageal manifestations of GERD, the administration of proton pump inhibitors is effective. Proton pump inhibitors (PPIs) are drugs that inhibit the activity of the enzyme H +, K + - ATPase, located on the apical membrane of the parietal cell and carrying out the last step in the synthesis of hydrochloric acid. To date, PPIs are considered the most effective and safe drugs for the treatment of GERD. In clinical trials, PPIs consistently demonstrate the greatest efficacy in the treatment of erosive esophagitis and the relief of GERD-associated symptoms. PPIs effectively control the pH level in the lower third of the esophagus, so the severity of symptoms quickly decreases and they disappear with the appointment of rabeprazole at a dose of 20 mg 1 r per day, pantoprazole 40 mg 1 r a day, omeprazole 20 mg 1-2 r a day, esomeprazole 40 mg 1 r a day, lansoprazole 30 mg 1 r a day. A decrease in acid production is considered the main factor contributing to the healing of erosive and ulcerative lesions. The prescription of PPI is necessary for the treatment of erosive esophagitis for at least 8 weeks in the presence of (B) 2nd and greater stages of esophagitis and at least 4 weeks in the presence of esophagitis (A) of the 1st stage. Patients with typical reflux symptoms who do not respond adequately to standard once-daily PPI therapy may be advised to take a twice-daily PPI. It should be borne in mind that this dosage is not approved in the instructions for use of these drugs. When prescribing PPIs in high doses for a long period (more than a year), the possibility of side effects should also be taken into account. Long-term PPI treatment should be at the lowest effective dose, including on-demand and intermittent courses. It has not been proven that PPI treatment can lead to a decrease in the effectiveness of clopidogrel when used together with PPIs.

It is recommended to apply an individual approach to the appointment of antisecretory and prokinetic therapy in the treatment of patients with gastroesophageal reflux disease, based on a thorough analysis of the clinical picture, as well as esophagogastroduodenoscopy data.

First of all, the patient's complaints are analyzed, in particular, heartburn (in addition to heartburn, other proven symptoms of GERD can be taken into account). The criteria for evaluating complaints are: the frequency of their occurrence: rarely (1-2 r / week) and often (> 2 r / week), as well as the duration of existence: small (< 6 месяцев) и значительная (>6 months). When assessing the patient's status and history, male gender and age over 50 years are taken into account as risk factors for relapse, indications of the presence of erosive esophagitis during endoscopy in the past, and the stage of pre-existing esophagitis (according to the Los Angeles classification or Savary-Miller) is essential. ). When assessing the patient's status, one should also pay attention to the presence of overweight (BMI> 25) and obesity (BMI> 30) and hiatal hernia. The presence of anxiety symptoms should be excluded: dysphagia, weight loss, anemia, fever. It should be emphasized that symptomatic improvement with proton pump inhibitor therapy can also occur in other diseases, including malignant neoplasm of the stomach, therefore, it is necessary to exclude such diseases.

In the presence of single erosions of the esophagus (A / 1st stage), the likelihood of their healing within 4 weeks of treatment is high. Therefore, the main course in this case, as well as in the absence of esophageal erosions, can be only 4 weeks (rabeprazole at a dose of 20 mg per day, or pantoprazole 40 mg per day, or esomeprazole 40 mg per day, or omeprazole at a dose of 20 mg 2 times per day, as well as itopride hydrochloride at a dose of 50 mg and antacids / adsorbents 3 times a day after meals), preferably with a control endoscopic examination. If multiple esophageal erosions (B-C/2-4th stages of esophagitis), as well as complications of GERD, are detected, the course of treatment with any drug from the PPI group, as well as antacids / adsorbents and prokinetics, should be at least 8 weeks, since with such a duration of therapy can achieve 90-95% effectiveness. With a 4-week course of treatment, the frequency of healing of multiple erosions of the esophagus is significantly lower. In addition, such an unreasonable reduction in the duration of treatment for erosive forms of GERD can be the cause of rapid subsequent recurrence, as well as the development of complications.

Maintenance therapy after healing of erosions should be carried out within 16-24 weeks. In the presence of complications of GERD, maintenance therapy should be carried out with proton pump inhibitors, also at a full dose.

Patients with GERD are subject to active dispensary observation with a control examination conducted at least once a year. In the presence of complications, it is necessary to examine such patients 2 times a year, including using endoscopic and morphological studies.

The highest percentage of effective treatment of GERD exacerbations and maintenance of remission is achieved with the combined use of PPIs, prokinetics, antacids/adsorbents.

Treatment of GERD in pregnant women is not an easy task and requires individual selection of therapy, taking into account potential harm. Recommendations for lifestyle changes, taking "non-absorbable" antacids can be considered universal.

As noted above, GERD is usually characterized by a chronic relapsing course. Patients in whom the clinical symptoms of the disease are not accompanied by the development of esophagitis need to take drugs pro re nata - on demand. However, patients with erosive-ulcerative esophagitis with this regimen of maintenance therapy will remain at a high risk (80-90%) of developing a relapse of the disease within a year.

The likelihood of recurrence increases in cases of resistance of the initial stages of esophagitis to therapy with antisecretory drugs, as well as when low pressure is detected in the lower esophageal sphincter. Such patients require the use of high doses of antisecretory drugs.

In complicated forms of GERD, it is possible to use short courses of intravenous forms of PPI, the advantages of which are the rapid achievement of an antisecretory effect and a higher concentration of the drug in the blood.

The most common reason leading to the lack of effect of the therapy is the lack of adherence of patients to treatment, that is, patients' failure to comply with recommendations for lifestyle changes and the rules for taking medications. Resistance to PPI therapy is often observed when these drugs are not prescribed correctly.

Compliance (or non-compliance) with the recommendations prescribed by the doctor is influenced, first of all, by the presence of symptoms and their severity, knowledge of the basics of the pathogenesis of the disease, concomitant therapy, taste and consistency of the drug taken, side effects, age, socio-economic status, patient motivation. Of course, the implementation of the doctor's recommendations, including diet, normalization of body weight should be considered the foundation of successful treatment.

The timing of taking the drug is important for some proton pump inhibitors, as it significantly affects their effectiveness. For example, the administration of omeprazole and lansoprazole before breakfast allows much better control of the gastric pH level than their administration without subsequent consumption of food.

The reason for the ineffectiveness of hydrochloric acid secretion inhibitors may be the presence of weakly acidic reflux, as well as the predominance of duodenal contents in the refluxate with a predominantly alkaline environment, when heartburn and other symptoms of GERD occur as a result of the action of bile components and pancreatic enzymes on the mucosa of the esophagus. Reflux is predominantly acidic in 50% of patients with GERD, acidic in nature with a bile component occurs in 39.7% of cases, and 10.3% of patients have bile reflux. The components of the duodenal contents that damage the mucosa of the esophagus are represented by bile acids, lysolecithin and trypsin. Of these, the role of bile acids, which seem to play a major role in the pathogenesis of esophageal injury in duodenogastroesophageal reflux (DGER), has been best studied.

In mixed reflux (acidic with a bile component), PPIs have a clinical effect not only due to the suppression of acid production itself, but also due to a decrease in the total volume of gastric secretion, which leads to a decrease in the volume of refluxate. However, increasing PPI doses to relieve symptoms is not indicated in this case.

In the case of DGER, the following drugs can be prescribed in various combinations (including in combination with PPIs): adsorbents, antacids, prokinetics, ursodeoxycholic acid, alginic acid. In the presence of biliary reflux, the purpose of prescribing adsorbents and antacids is not only the neutralization of hydrochloric acid, but also the adsorption of bile acids and lysolecithin, as well as increasing the resistance of the mucous membrane to the action of damaging aggressive factors.

The basis for the use of ursodeoxycholic acid is its cytoprotective effect.

If treatment of patients with GERD is ineffective within 4 weeks, confirmation of the presence of gastroesophageal reflux should be carried out using an objective method of studying 24-hour pH impedancemetry.

Patients with persistent symptoms who do not show pathological refluxes on pH-impedancemetry and do not correlate refluxes with the onset of symptoms most likely do not have GERD, but so-called "functional heartburn".

The decision on the duration of maintenance therapy for GERD should be made taking into account the age of the patient, the presence of comorbidities, existing complications, as well as the cost and safety of treatment. There is no need to determine H. pylori infection and, moreover, its eradication for GERD.

Antireflux surgical treatment is considered indicated in the complicated course of the disease (repeated bleeding, peptic strictures of the esophagus, the development of Barrett's syndrome with high-grade epithelial dysplasia, frequent aspiration pneumonia). In some cases, when a patient cannot receive conservative therapy for GERD due to one or another objective or subjective reasons, surgical treatment should be considered even in an uncomplicated course.

Surgical treatment of GERD may be effective in those GERD patients who have typical GERD manifestations and are treated with PPIs as well. If PPIs are ineffective, as well as extraesophageal manifestations, surgical treatment will also be less effective.

It is necessary to consider the issue of surgical treatment only in conjunction with an experienced surgeon in this field, if all measures to normalize the lifestyle have been completed, the presence of pathological gastroesophageal reflux has been proven (using pH-impedancemetry), and with the help of esophageal manometry the absence of defects in esophageal peristalsis.

Management of patients with Barrett's esophagus

The need for active dispensary monitoring of patients with Barrett's esophagus is due to the possibility of preventing adenocarcinoma of the esophagus in cases of early diagnosis of epithelial dysplasia. Verification of the diagnosis of Barrett's esophagus and the establishment of the degree of dysplasia is carried out using a histological examination.

If this reveals low-grade dysplasia, it is necessary to prescribe PPI in a standard or double dose (depending on the data obtained during the pH measurement) with a repeat histological examination after 3 months. If low-grade dysplasia persists, patients are advised to continue continuous full-dose PPIs and conduct a histological examination at 3 and 6 months. Then a histological examination is carried out annually. If high-grade dysplasia is detected, it is necessary to prescribe a double dose of PPI with a parallel assessment of the results of histological examination and subsequent decision on the endoscopic or surgical treatment of the patient. More detailed algorithms for managing patients with Barrett's esophagus are set out in special clinical guidelines.

Conclusion

When creating this methodological manual, the authors set themselves, first of all, the task of developing a coherent system for managing patients with gastroesophageal reflux disease in order to improve the quality of life of patients and prevent the development of such formidable complications as strictures of the esophagus and Barrett's esophagus. This system can function only if the standard recommendations are followed, in particular, if the necessary terms of treatment are observed, and active outpatient monitoring of the relevant groups of patients is carried out.

We hope that this methodological manual will help practitioners and healthcare organizers in realizing these goals.

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Among the diseases requiring clinical recommendations, GERD occupies one of the first places, since only in Russia the prevalence of this pathology is 18-46%.

Gastroesophageal reflux disease (GERD) is a chronic relapsing disease, the main manifestation of which is the injection of stomach contents into the esophagus, resulting in clinical symptoms that significantly reduce the patient's quality of life. According to the degree of distribution, complex clinic and the possibility of life-threatening complications, this disease is considered one of the acute problems of gastroenterology.

Causes

Sphincter dysfunction is considered to be the main cause of GERD. This formation is designed to keep the passage between the stomach and esophagus closed and stop the backflow (reflux) of stomach contents. In case of weakening of the sphincter, the hole opens, and the stomach, contracting, throws the food clot into the esophagus. If the refluxant has damaging properties, then the walls of the organ are irritated up to pathological disorders of the mucosa.

In addition, the causes of gastroesophageal disease are:

1. Disturbances in the motor functions of the esophagus.
2. High intra-abdominal pressure.
3. Excessive acidity of the gastric juice.

The possibility of reflux disease is increased by:

• Stress.
• Smoking.
• Excess weight.
• Medications: nitrates, calcium channel blockers, beta-blockers.

Symptoms

Insufficiency of the lower alimentary sphincter (LES) causes painful symptoms of GERD, including:

1. Typical related to the digestive system:
   • heartburn;
   • belching;
   • ulceration of the walls of the esophagus.
2. Atypical, called pulmonary signs of GERD, manifested in impaired respiratory function.

A burning sensation behind the sternum, heartburn, refers to the hallmarks of pathology and is the result of persistent damage to the walls of the esophagus by acid.

Gastric juice injures the mucosa of the organ, causing a burn. Constant heartburn caused by prolonged irritation of the walls is an alarming sign of GERD.

The presence of other symptoms is characteristic of more complex cases of the disease. So, sour belching, combined with heartburn, causes a strong cough that makes it difficult to sleep at night. In addition, heartburn can manifest itself as an imitation of angina pectoris. Observed:

• drop in blood pressure;
• heart palpitations;
• cold sweat;
• fear of death.

Additional Information! One of the most common and serious exacerbations is the formation of Barrett's esophagus, when the usual squamous epithelium is replaced by a cylindrical gastric one.

Treatment

Therapy is carried out by medical, surgical methods, as well as by conducting a healthy lifestyle. The medicinal effect is carried out in order to normalize acidity and improve motor skills.

Apply:

1. prokinetics (Domperidone, Metoclopramide) - fixes the state of the sphincter, regulates the passage of food mass in the gastrointestinal tract;
2. antisecretory drugs (blockers of H2-histamine receptors) - reduce the harmful effect of gastric juice on the mucous membrane;
3. antacids (Almagel, Maalox) - level the acidity of the stomach;
4. reparants (misoprostol and sea buckthorn oil) - contribute to the healing of erosive lesions.

Surgical intervention is used in the presence of complications:

1. Barrett's esophagus;
2. strictures;
3. reflux esophagitis III - IY degree;
4. mucosal ulcers.

The main result of the treatment is the regeneration of the physiological septum separating the stomach and esophagus.

Despite the fact that food does not linger in the esophagus, and therefore does not cause harm, rather severe pathologies of this organ are known. Many of them require surgical intervention, which is difficult due to the deep location and delicate structure of the muscular tube, which is 25 centimeters long. Consider the signs indicating violations in its work and methods of their treatment.

Symptoms of diseases of the esophagus

Diseases of the esophagus are accompanied by the following symptoms:

• Difficulty swallowing, sensation of the presence of a foreign body.
• Severe, sudden, unexplained pain, similar to an angina attack.
• Metallic taste in the mouth, profuse salivation, belching, heartburn.
• Vomiting after eating from spasm of the lower sphincter.

Thermal and chemical burns are accompanied by purulent mucous secretions. When concentrated caustic substances enter the walls of the esophagus, scars form. With malignant pathogenesis, a person’s weight decreases and he weakens before our eyes.

Such symptoms should alert and become a reason to visit a doctor. Only he can make a final diagnosis and choose an adequate treatment.

Reasons for development

Pathologies of the esophagus are sometimes congenital in nature and are formed at the stage of embryogenesis. They also occur in the presence of benign neoplasms (polyps), after swallowing foreign bodies, poisons, eating extremely hot or cold dishes. They can appear during chronic inflammatory processes, as well as due to infection of the tissues of the digestive tube, including pathogenic fungi that cause, for example, candidiasis.

Video: Diseases of the esophagus

Accurate diagnosis

If a lesion of the esophagus is suspected, in order to exclude oncology, laboratory tests are prescribed by the doctor, as well as:

• radiography;
• fibrogastroduodenoscopy;
• determination of the pH level of the gastric environment.

In parallel with endoscopy, a biopsy is performed with the collection of the affected parts of the mucosa for their histological examination. If necessary, methods are used to measure the pressure inside the tube and register the contraction of the walls of the organ.

Video: Endoscopy of the esophagus and stomach

Diseases of the esophagus

Understanding the importance of a small part of the gastrointestinal tract often comes only after its pathological degeneration, when unpleasant sensations appear that can radically change a person's life.

Prolonged stagnation of food provokes inflammation of the mucosa, that is, it contributes to the development of esophagitis. Its chronic variety is considered as a form preceding a cancerous tumor, which captures even the upper parts of the stomach.

Throwing chyme into the respiratory organs leads to pneumosclerosis, abscesses of the lung tissue, to aspiration types of bronchopneumonia. Such complications often affect the youngest children.

Achalasia cardia is diagnosed using multichannel probes that record motility and pressure inside the digestive tube.

Medical treatment of achalasia is effective only at an early stage. Thermal and mechanical sparing of food is recommended. Dealing with pain:

• calcium antagonists;
• ganglioblockers;
• nitropreparations, for example, Corinfar.

The main therapeutic technique is cardiodilatation, which expands the narrowing places.

Barrett's esophagus

It is a complication of reflux disease (GERD), when aggressive gastric or duodenal juice, including enzymes, hydrochloric and bile acids, irritates the mucosa of the digestive tube. It leads to metaplasia, that is, the replacement of squamous epithelium by its other types. Barrett's syndrome increases the risk of developing cancerous tumors.

Endoscopy with a biopsy study allows you to confirm or refute the initial diagnosis. A control biopsy is performed after a course of anti-inflammatory therapy in order to exclude a morphological error. Further treatment tactics depend on the clinical picture. If epithelial dysplasia is absent, modern techniques are used, such as:

• laser destruction.
• Photodynamic therapy.
• Argon plasma coagulation.

In cases of dysplasia, endoscopic resection is used, as well as dissection in the submucosa. Proton pump inhibitors help in the repair of squamous epithelium.

Video: Harbingers of cancer. Barrett's esophagus

Esophagospasm

A condition in which the lower sphincter is working normally and the walls of the tube are contracting spasmodically. It occurs more often in men. Patients complain of pain when swallowing. Spasm causes deformation of the esophagus, which is visualized during an X-ray examination.

Treatment of the esophagus consists in observing a sparing diet, taking nitro group drugs, antispasmodics. If medical therapy and balloon dilatation are ineffective, an operation to cut the muscle tissue is indicated.

Reflux esophagitis

Pathology occurs due to frequent reflux of chyme from the stomach upwards, which occurs due to the weakness of the lower sphincter. Hydrochloric acid irritates the delicate mucous membrane, which becomes inflamed and ulcerated. In places of scarring, the tube narrows.

Symptoms of the disease are more common in infants. Manifested in the form of belching, heartburn, burning in the sternum, spasm. Vomiting at night can trigger aspiration pneumonia. After some time, the tube narrows, and problems are created during the passage of the food bolus. The disease can cause hidden bleeding, recurrent pneumonia, scarring of the mucosa.

Video: Reflux esophagitis

Diagnosis is carried out using esophagogastroscopy, radiography with contrast, pH-metry.

From medical means the patient accepts:

• Vitamins, antihistamines.
• Calming compounds.
• Prokinetics to increase the contractile activity of the lower sphincter.
• Means with enveloping properties.
• Antispasmodics.
• Antacids.

Hernia of the esophagus

Hereditary or acquired defect of the esophageal opening in the diaphragm, when the abdominal organs are in the chest. Common symptoms include occult bleeding and anemia. If the tube is narrowed, surgical intervention is indicated. Conservative therapy aims to reduce the possibility of reflux.

Damage

The esophagus can be injured when foreign bodies enter its lumen: parts of children's toys, buttons, nails. The cause of organ damage can even be the mechanical impact of instrumental methods of diagnosis and treatment. Spontaneous rupture of the tube is possible with vomiting. Attempts to push through fish bones with a crust of bread lead to serious consequences. Those wedged into the mucosa and cause a progressive complication.

With perforation of the esophagus, the patient's condition deteriorates sharply. Subcutaneous emphysema develops.

Treatment of the disease is usually surgical. Medically eliminated only the consequences of shallow damage to the wall. For its implementation requires systematic medical supervision, monitoring the dynamics of the process.

Video: Hernia of the esophagus and heartburn: radical treatment

burns

Mucosal damage can be chemical and thermal. Occur accidentally or intentionally (hot food, aggressive compounds, a list of which is presented below). It includes:

• acids;
• potassium permanganate;
• hydrogen peroxide;
• ammonia;
• ethanol;
• phenol.

In 7 out of 10 cases, children under the age of 10 suffer from burns.

Acids are less destructive than alkalis. The formation of a kind of film prevents further tissue damage.

In case of poisoning with caustic soda, saponification of fats, denaturation of proteins occurs, cells turn into a gelatinous substance, which ultimately ends in more deplorable consequences. A through hole is formed when even 20 ml of alkali enters the initial section of the gastrointestinal tract.

First aid for chemical burns is to wash the alimentary canal. To neutralize the poison, its identification is necessary.

The acid is neutralized with a 2% soda solution (0.5 tsp per 1 liter), after which the gag reflex is stimulated.

In case of alkali burns, the affected organ is washed with vegetable oil diluted with citric or acetic acid.

The patient receives complex treatment in a hospital setting. After severe damage to the tube, a hole in the anterior wall or a gastrostomy is used to feed it.

Esophageal carcinoma

About 70% of all pathologies of the initial gastrointestinal tract are malignant in nature. Within 1-2 years, a dangerous disease does not manifest itself in any way. When the tumor reaches a large size, it prevents the promotion of a dense food bolus, the work of the larynx. Over time, difficulties also arise with the use of liquid food. A person suffers from pain behind the sternum, increased salivation, loses weight.

Gastroesophageal reflux disease (GERD) is a disease caused by 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.

EPIDEMIOLOGY

The true prevalence is not known, which is associated with a large variability in clinical symptoms: from episodically occurring heartburn to clear signs of complicated reflux esophagitis. The true prevalence of GERD is much higher than official statistics due to the existing difficulties in the use of diagnostic methods. In addition, less than 1/3 of GERD patients see a doctor.

Symptoms of GERD are found in 20-50% of the adult population, and endoscopic signs in more than 7-10% of individuals in the population.

In the US, heartburn (the main symptom of GERD) is experienced by 10-20% of adults on a weekly basis.

There is no complete epidemiological picture in Russia. There are separate epidemiological studies conducted in different regions. So, in Moscow, 34% of women and 15% of men complain of frequent heartburn.

CLASSIFICATION

According to ICD-10, GERD is subdivided into GERD with esophagitis and GERD without esophagitis. In clinical practice, a different terminology has been adopted:

Endoscopy-negative reflux disease, or non-erosive reflux disease;

Endoscopically positive reflux disease, or reflux esophagitis.

Rice. 39-1. The severity of reflux esophagitis.

Table 39-1. Classification of reflux esophagitis

Degree gravity	Characteristic
	One (or more) mucosal lesions less than 5 mm in size and limited to the mucosal fold
	One (or more) mucosal lesion larger than 5 mm, limited to the mucosal fold (the lesion does not extend into the area between the two folds)
	One (or more) mucosal lesions extending into two or more mucosal folds but covering less than 75% of the circumference of the esophagus
	One (or more) mucosal injury involving 75% or more of the circumference of the esophagus

Complications of GERD include:

Peptic strictures;

Esophageal bleeding;

Barrett's esophagus.

Approximately 60% of patients are diagnosed with non-erosive reflux disease, 30% have reflux esophagitis, and 5% develop complications.

ETIOLOGY AND PATHOGENESIS

The reasons for the development of GERD include the following.

Weakening of the function of the antireflux barrier (the locking mechanism of the cardiac part of the stomach).

Decreased clearance of the esophagus.

Reducing the resistance of the mucosa of the esophagus to the effects of damaging factors.

An increase in the production of hydrochloric acid, pepsin in the stomach, the flow of bile into the stomach.

Since the pressure in the stomach is always higher than in the chest cavity, there is a special mechanism that prevents the reflux of gastric contents - the so-called locking mechanism of the cardia. Normally, reflux occurs rarely, for a short time (less than 5 minutes). This physiological process, observed after eating and characterized by the absence of clinical symptoms, short duration of episodes, may occur during sleep. Normal pH values ​​in the esophagus are 5.5-7.0.

Esophageal reflux is considered pathological if the time during which the pH in the esophagus reaches 4.0 and below is 1 hour / day or the total number of gastroesophageal refluxes during the day exceeds 50, they develop day and night.

The mechanisms that support the viability of the function of the esophageal-gastric junction (the locking mechanism of the cardia) include:

lower esophageal sphincter;

Diaphragmatic-esophageal ligament;

Mucous "socket";

Acute angle of His, forming Gubarev's fold;

Intra-abdominal location of the lower esophageal sphincter;

Circular muscle fibers of the cardia of the stomach.

LOWER ESophageal Sphincter

The main role in the locking mechanism belongs to the condition of the lower esophageal sphincter. At rest, in a healthy person, it is closed. Normally, transient relaxation lasts for 5-30 seconds and helps to free the stomach from excess air swallowed during meals. In patients with GERD, these spontaneous episodes of relaxation of the lower esophageal sphincter are frequent and prolonged. The reason for this is a violation of the peristalsis of the esophagus, fast and plentiful food, when a large amount of air is swallowed.

The tone of the lower esophageal sphincter is reduced by:

Foods containing caffeine (chocolate, coffee, tea, coca-cola), citrus fruits, tomatoes, alcohol, nicotine and fats;

Some drugs: anticholinergics, sedatives and hypnotics, -blockers, calcium channel blockers, nitrates, theophylline and other drugs;

Vagus nerve lesions (vagal neuropathy in diabetes mellitus, vagotomy).

Pressure in the lower esophageal sphincter decreases under the influence of a number of gastrointestinal hormones: glucagon, somatostatin, cholecystokinin, secretin, vasoactive intestinal peptide, enkephalins.

Decreased antireflux barrier function can occur in three ways:

Primary decrease in pressure in the lower esophageal sphincter;

An increase in the number of episodes of his transient relaxation;

Complete or partial destruction of the sphincter, for example, with a hernia of the esophageal opening of the diaphragm, scleroderma, after surgical interventions, pneumocardiodilation.

GIS ANGLE

This is the angle of transition of one side wall of the esophagus into the greater curvature of the stomach, while the other side wall smoothly into the lesser curvature. The air bubble of the stomach and intragastric pressure contribute to the fact that the folds of the gastric mucosa, forming the angle of His, fit snugly against the right wall (Gubarev's fold), preventing the contents of the stomach from refluxing into the esophagus.

CLEARANCE REDUCTION

The esophagus is equipped with an effective mechanism that eliminates pH shifts to the acid side - esophageal clearance. In 50% of patients with GERD, esophageal clearance is reduced. In this case, the following variants of esophageal clearance suffer:

Chemical - due to a decrease in the neutralizing effect of bicarbonates of saliva and esophageal mucus;

Volumetric - due to inhibition of secondary peristalsis and a decrease in the tone of the wall of the thoracic esophagus.

The immediate cause of reflux esophagitis is prolonged contact of gastric or duodenal contents with the mucosa of the esophagus.

RESISTANCE OF THE ESOPHAGUS MUCOSA

Provided by preepithelial, epithelial and postepithelial factors.

Epithelial damage begins when hydrogen ions and pepsin or bile acids overcome the preepithelial mucus protective layer and active bicarbonate secretion.

Epithelial factor: features of the structure and functions of cell membranes, intercellular connections, intra- and intercellular transport, creating an optimal pH (7.3-7.4).

Post-epithelial factor: blood supply to the mucous membrane of the esophagus, providing adequate trophic processes, optimal acid-base balance.

CLINICAL PICTURE

The peculiarity of GERD is 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.

All symptoms can be combined into two groups: esophageal (heartburn; belching with sour, bitter or food; regurgitation; dysphagia; odynophagia; pain behind the sternum) and extraesophageal (cough, asthma attacks, shortness of breath, hoarseness or hoarseness, dry throat, salivation, caries, signs of anemia).

In the clinical picture, the leading place is occupied by heartburn, eructation of acidic contents that occurs when bending forward and at night. The second most common manifestation of this disease is retrosternal pain. Less commonly, dysphagia, regurgitation, and odynophagia (pain when swallowing) are observed.

HEARTBURN

A peculiar burning sensation or heat of varying intensity that occurs behind the sternum (in the lower 1/3 of the esophagus) or in the subscapular region. It is noted in 83% of patients with GERD. It occurs as a result of prolonged contact of the acidic contents of the stomach (pH ‹4) with the mucous membrane of the esophagus. The severity of heartburn does not correlate with the severity of esophagitis. It is characterized by its strengthening with errors in diet, intake of carbonated drinks, alcohol, physical stress, forward bending and in a horizontal position.

BUCKING AND RETURNING FOOD

52% of patients complain of belching. As a rule, it intensifies after eating, taking carbonated drinks. Regurgitation of food, observed in some patients, occurs during exercise and a position that promotes regurgitation. Belching and regurgitation are characteristic of a disease with severe impairment of the motor function of the esophagus.

CHEST PAIN

It spreads to the interscapular region, neck, lower jaw, left side of the chest and can mimic angina pectoris. In the differential diagnosis of the origin of pain, it is important to establish what provokes and relieves pain. Esophageal pain is characterized by a connection with food intake, body position and their relief by taking alkaline mineral waters and antacids.

DYSPHAGIA

Dysphagia has an intermittent character, noted in 19% of patients. The appearance of persistent dysphagia and a simultaneous decrease in heartburn indicates the development of esophageal stricture. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma.

DIAGNOSTICS

The main methods used to detect gastroesophageal reflux are:

X-ray examination;

Endoscopy;

Daily monitoring of the pH of the esophagus;

Examination of the motor function of the esophagus;

Histological examination.

X-ray study. When fluoroscopy of the esophagus, the ingress of a contrast agent from the stomach into the esophagus is determined, a hernia of the esophageal opening of the diaphragm, strictures, signs of esophagitis (thickening of the folds, changes in motility, uneven contours of the esophagus), erosion and ulcers of the esophagus are detected.

Endoscopic study. Used to diagnose reflux esophagitis and assess its severity (see above for the classification of reflux esophagitis).

Chromoendoscopy detects metaplastic and dysplastic changes in the epithelium of the esophagus by applying to the mucous membrane of substances that stain healthy and affected tissues in different ways. In addition, you can see the prolapse of the gastric mucosa into the lumen of the esophagus, which is especially noticeable during vomiting; true shortening of the esophagus with the location of the esophageal-gastric junction above the diaphragm. Evaluation of the closing function of the cardia is difficult, since it can be opened in response to the introduction of an endoscope or air insufflation.

Daily pH-metry esophagus. The most informative method for diagnosing GERD, especially non-erosive reflux disease, which makes it possible to judge the frequency, duration and severity of reflux. Compared with other methods [fluoroscopy, fibroesophagogastroduodenoscopy (FEGDS), lower esophageal sphincter pressure study], 24-hour pH-metry has a high sensitivity in detecting gastroesophageal refluxes (88-95%). The information obtained makes it possible to accurately determine how long the esophageal mucosa was exposed to hydrochloric acid, evaluate the effectiveness of esophageal clearance, compare the occurrence of refluxes with clinical symptoms, and investigate the acid-producing function of the stomach during the day.

For the diagnosis of GERD, the results of pH-metry are evaluated by the total time during which the pH value is ‹4.0, by the total number of refluxes per day, by the number of refluxes lasting more than 5 minutes and the duration of the greatest reflux.

Scintigraphy esophagus. A radioactive isotope of technetium is used to assess esophageal clearance. A delay of the received isotope in the esophagus for more than 10 minutes indicates a slowdown in esophageal clearance. The study of daily pH and esophageal clearance allows you to identify reflux before the development of esophagitis.

Manometry. A decrease in the pressure of the lower esophageal sphincter, an increase in the number of its transient relaxations, a decrease in the amplitude of peristaltic contractions of the esophageal wall are revealed.

Histological study. Histological examination of a biopsy of the esophageal mucosa is used to exclude Barrett's esophagus and esophageal adenocarcinoma. Histological examination reveals thinning and atrophy of the epithelium, proliferation of connective tissue (sclerosis). Metaplasia of the squamous non-keratinizing epithelium of the esophagus is found, leading to the growth of the cylindrical epithelium of the cardiac or fundal type of the gastric mucosa. If metaplasia leads to the appearance of a specialized small intestine columnar epithelium, then there is a risk of malignancy. Specialized columnar epithelium is diagnosed as incomplete small intestinal metaplasia with the presence of goblet cells.

COMPLICATIONS

Risk factors for the development of complications are the frequent occurrence and prolonged existence of symptoms, a pronounced stage of erosive esophagitis, the presence of a hiatal hernia. Complications of GERD include esophageal ulcers, bleeding, strictures, and Barrett's esophagus.

Peptic ulcers The esophagus is observed in 2-7% of patients with GERD, in 15% of them peptic ulcers are complicated by perforation, most often in the mediastinum.

Acute and chronic bleeding varying degrees are observed in almost all patients with peptic ulcers of the esophagus, and severe bleeding is noted in half of them.

Strictures occur in about 10% of patients with GERD: stenosis of the esophagus makes the disease more resistant (dysphagia progresses, health worsens, body weight decreases). Clinical symptoms of stenosis (dysphagia) occur when the lumen of the esophagus narrows to 2 cm.

Esophagus Barrett(See Section 39.2 Barrett's Esophagus).

TREATMENT

The choice of treatment method is associated with the characteristics of the course and the cause that caused GERD. Treatment for GERD can be medical or surgical.

THERAPEUTIC TREATMENT

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 exertion associated with overexertion of the abdominal press.

Avoid large meals and do not eat at night (no later than 3 hours before bedtime); after eating, avoid bending forward and do not lie down. Limit the consumption of foods that reduce the pressure of the lower esophageal sphincter and have an irritating effect on the esophageal mucosa: foods rich in fats (whole milk, cream, cakes, pastries, goose, duck, pork, lamb, fatty beef), alcohol, drinks containing caffeine (coffee, cola, strong tea, chocolate), citrus fruits, tomatoes, onions, garlic, fried foods. Do not take drugs that cause reflux (sedatives and tranquilizers, calcium channel inhibitors, β-blockers, theophylline, prostaglandins, nitrates).

Sleep with the head of the bed raised.

Give up smoking.

Normalize body weight.

Medical treatment

Terms of treatment: 4-8 weeks for non-erosive reflux disease and at least 8-12 weeks for reflux esophagitis, followed by maintenance therapy for 6-12 months. Drug therapy includes the appointment of prokinetics, antacids and antisecretory agents.

Prokinetics. Increase the tone of the lower esophageal sphincter, increase esophageal peristalsis, improve esophageal clearance. Assign domperidone, metoclopramide 10 mg 3-4 times a day 30 minutes before meals. Domperidone has the advantage of not penetrating the blood-brain barrier and has fewer side effects compared to metoclopramide. In the form of monotherapy, prokinetics are used only in the treatment of mild forms of GERD.

Antacids and antisecretory drugs. The goal of antisecretory therapy is to reduce the damaging effect of acidic gastric contents on the esophageal mucosa in gastroesophageal reflux. Antacids are effective for moderate and infrequent symptoms. Antacids have a cytoprotective effect and neutralize the hydrochloric acid of gastric juice. The most convenient pharmaceutical form is gels. Usually drugs are prescribed 3 times a day 40-60 minutes after meals and at night. Each episode of pain and heartburn should be stopped, as these symptoms indicate progressive damage to the esophageal mucosa.

In the treatment of reflux esophagitis, preparations containing sodium alginate have proven themselves well. It forms a foamy antacid suspension floating on the surface of the gastric contents, and, getting into the esophagus in case of gastroesophageal reflux, gives a therapeutic effect.

Blockers H 2 -receptors histamine. With reflux esophagitis, ranitidine and famotidine are widely used, which significantly reduce the acidity of the gastric contents thrown, which contributes to the relief of the inflammatory and erosive-ulcerative process in the mucosa of the esophagus.

Inhibitors proton pump. Currently, H + , K + -ATPase blockers (omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole) are considered the drugs of choice, which, by inhibiting the proton pump, provide a pronounced and prolonged suppression of gastric secretion of hydrochloric acid. These drugs are the most powerful antisecretory agents, they are particularly effective in peptic erosive-ulcerative esophagitis, providing scarring of the affected areas in 90-96% of cases after 4-5 weeks of treatment.

SURGERY

The issue of surgical correction is decided in the case of prolonged and/or ineffective drug therapy, the occurrence of complications (esophageal stricture, repeated bleeding, Barrett's esophagus). Especially often, indications for surgery occur when GERD is combined with a hernia of the esophageal opening of the diaphragm.

FORECAST

With non-erosive reflux disease and a mild degree of reflux esophagitis, the prognosis is favorable in most cases. The prognosis worsens with a long duration of the disease, combined with frequent, prolonged relapses, with complicated forms of GERD, especially with the development of Barrett's esophagus due to an increased risk of developing adenocarcinoma of the esophagus.

39.2. Barrett's Esophagus

Barrett's esophagus is an acquired chronic metaplastic condition of the esophageal mucosa, in which the stratified squamous epithelium in some areas is replaced by a single-layer cylindrical epithelium.

Barrett's esophagus with intestinal metaplasia develops in approximately 10-20% of individuals with GERD. The chance of developing adenocarcinoma in Barrett's esophagus is 1 in 200-400 patients per year. Barrett's esophagus is 10 times more likely to develop in men (especially the elderly) than in women.

Etiology and pathogenesis. The etiology is not clear. Factors predisposing to the development of the disease are the high secretion of hydrochloric acid in the stomach and the presence of bile in the gastric contents thrown into the esophagus.

Clinical painting Barrett's esophagus does not differ from that of GERD. In this regard, it is necessary to exclude the presence of Barrett's esophagus in any patient with a long history of GERD (more than 5 years).

Diagnostics. On endoscopic examination, the columnar epithelium has a characteristic red color and velvety appearance, which distinguishes it from the adjacent thin, pale, glossy epithelium of the esophagus. To confirm the diagnosis and establish the degree of epithelial dysplasia, a biopsy is performed from four sections of the esophageal mucosa.

Treatment

If low-grade dysplasia is detected, high (doubled) doses of proton pump inhibitors are prescribed. After 3 months, a repeated histological examination is carried out. If low-grade dysplasia persists, continue treatment with proton pump inhibitors at the same doses, performing control histological studies after 3 and 6 months, and then annually.

If high-grade dysplasia is detected, proton pump inhibitors are prescribed and the issue of endoscopic treatment (laser destruction, multipolar electrocoagulation, photodynamic coagulation of metaplastic epithelial areas) or surgical intervention is decided.

39.3. esophagitis

Esophagitis is a group of diseases characterized by the development of inflammatory and destructive changes in the mucous membrane of the esophagus, and sometimes deeper layers of its wall. Depending on the morphological picture, catarrhal, erosive, hemorrhagic and necrotic esophagitis are distinguished. The clinical picture of all esophagitis is characterized by dysphagia.

INFECTIOUS ESOPHAGITS

Infectious esophagitis usually occurs in immunocompromised individuals. Esophagitis is divided into viral (more often they are caused by the herpes simplex virus and cytomegalovirus), bacterial (due to Mycobacterium tuberculosis and bacteria of the genus Lactobacillus) and fungal (often caused by fungi of the genus Candida).

Viral esophagitis. Esophagitis caused by the herpes simplex virus often accompanies rashes in the nasolabial triangle. Cytomegalovirus infection, in addition to damage to the esophagus, is characterized by the involvement of other internal organs. Endoscopically, in lesions of the herpes simplex virus, typical vesicles are found on the mucosa of the esophagus, in place of which limited ulcers are then formed with edges raised above the surface (crater-shaped ulcers). When affected by cytomegalovirus, erosions are detected in the early stages, then linear sickle-shaped ulcers are formed. The diagnosis is confirmed by virological and immunohistochemical methods, as well as by the method of hybridization. in situ. Acyclovir is considered the drug of choice for infection caused by the herpes simplex virus, and ganciclovir for cytomegalovirus infection.

Bacterial esophagitis. With bacterial esophagitis, hyperemia, edema of the mucous membrane, raids, pseudomembranes, erosions and ulcers are detected endoscopically. To confirm the diagnosis, it is necessary, firstly, to detect signs of bacterial invasion in Gram-stained histological preparations and, secondly, to exclude the presence of a viral, fungal, or neoplastic lesion of the esophagus. In bacterial esophagitis, antibacterial agents are used, as well as a complex of astringent, enveloping and antisecretory drugs in combination with local anesthetics.

Fungal esophagitis. With fungal esophagitis, white or yellowish overlays are found endoscopically on the hyperemic mucosa of the esophagus. During bacteriological and histological examination of biopsy specimens, mycelial forms of the fungus are determined. Patients suffering from fungal esophagitis and immunodeficiencies are recommended to take drugs containing imidazole derivatives (bifonazole, oxiconazole) orally. Patients with granulocytopenia due to a high risk of dissemination of a fungal infection are prescribed amphotericin B intravenously.

MEDICINAL ESOPHAGITS

Most often, drug-induced esophagitis is caused by antibiotics (doxycycline, tetracycline, etc.), NSAIDs, quinidine, potassium chloride, etc. These drugs account for approximately 90% of all cases of drug-induced injury to the esophagus.

A characteristic clinical symptom is dysphagia, which occurs several hours or days after ingestion of the drug. Endoscopically, medicinal lesions of the esophagus are characterized by the presence of one or more separately located ulcers on the unchanged mucosa. In the edges of ulcers, particles of the drug are often found.

In uncomplicated cases, drug-induced injuries of the esophagus do not require active intervention and heal within 3 days to several weeks after discontinuation of the drug. In the presence of symptoms of GERD, antisecretory, astringent, enveloping drugs, local anesthetics are prescribed.

39.4. achalasia cardia

Achalasia (gr. a- - absence, chalasis- relaxation) of the cardia - a disease of the esophagus, in which there is no reflex relaxation of the lower esophageal sphincter during swallowing, and the tone and peristalsis of the thoracic esophagus are impaired.

Epidemiology. Achalasia of the cardia is a rather rare disease, the prevalence of which is 0.001-0.002%. Most patients are people aged 30-50 years. Most often (95% of cases) observe idiopathic achalasia of the cardia. In 2-5% of patients, achalasia of the cardia is familial (inherited in an autosomal recessive manner).

Etiology and pathogenesis. The etiology of the disease is not clear. The pathogenesis consists in a violation of the activity of the intramural nervous apparatus of the esophagus, possibly due to a deficiency of relaxing mediators, primarily nitric oxide.

Clinical painting. A characteristic symptom of achalasia cardia is dysphagia. At the beginning of the disease, dysphagia occurs only when taking solid food, then dysphagia gradually joins when drinking liquids. In some cases, dysphagia is relapsing in nature. As a result, patients need much more time to eat. To speed up the emptying of the esophagus, patients often resort to certain methods, for example, drink a glass of water in one gulp.

Progressive dysphagia causes weight loss in most patients. As dysphagia progresses, regurgitation develops, so patients often wake up at night coughing or choking. Hypermotor dyskinesia of the esophagus, as well as its overflow, lead to the development of pain behind the sternum of a pressing or compressive nature with irradiation to the neck, lower jaw or back.

Diagnostics. An x-ray examination performed on an empty stomach reveals the following signs:

Large amount of esophageal contents;

Violation of the evacuation of the contrast agent into the stomach;

Moderate or significant (fusiform or S-shaped) expansion of the esophagus with narrowing in the distal section (symptom of "mouse tail", "carrot tip" or "bird's beak");

No gas bubble in the stomach.

Esophagoscopy reveals an expansion of the esophagus, congestive esophagitis, sometimes with areas of epithelial metaplasia (leukoplakia). To exclude malignancy, a biopsy is performed from suspicious areas of the mucous membrane.

Manometrically, with achalasia of the cardia, hypertonicity of the lower esophageal sphincter, the absence of its reflex opening, and a violation of the peristalsis of the thoracic esophagus are revealed.

Differential diagnosis of achalasia cardia is carried out with diseases accompanied by dysphagia, primarily cancer of the esophagus and cardia of the stomach. X-ray and endoscopic examination with biopsy are of great help in this.

Treatment. The main treatment for achalasia cardia is pneumocardiodilatation (expansion of the cardiac opening of the stomach with the help of an inflated rubber balloon, resulting in a partial rupture of the muscles of the lower esophageal sphincter). The frequency of good results of this treatment method is 86-100%. The effect persists for 2-8 years or more; with the resumption of dysphagia, repeated courses of cardiodilatation are carried out.

Long-acting nitrates and calcium channel blockers reduce lower esophageal sphincter pressure and improve esophageal emptying, but are not a complete substitute for cardiodilatation.

Patients with achalasia cardia should be registered with a gastroenterologist. They are shown to conduct x-ray and endoscopic examination of the esophagus at least 1 time per year.

Forecast. The prognosis if left untreated is serious: the disease progresses and can lead to death from exhaustion. The prognosis worsens the high probability of cancer of the esophagus (2-7% of cases) and aspiration pneumonia.

39.5. TUMORS OF THE ESOPHAGUS

MALIGNANT TUMORS OF THE ESOPHAGUS

The incidence of esophageal cancer has recently increased significantly, its share is 2% of all malignant tumors and 7% of all malignant tumors of the gastrointestinal tract.

Men get sick 3-5 times more often than women. The peak incidence occurs at the age of 50-70 years.

Classification. The International Classification of Esophageal Cancer meets the accepted criteria for the TNM classification of cancer ( tumor- primary tumor nodulus- defeat of regional lymph nodes, metastasis distant metastases).

Malignant tumors of the esophagus in more than 95% of cases are squamous cell carcinoma or adenocarcinoma. In rare cases, small cell cancer, melanomas, sarcomas, malignant lymphomas, etc. are found.

Etiology and pathogenesis. The causes of esophageal cancer are unknown. Risk factors for developing squamous cell carcinoma are:

Achalasia of the cardia;

alcohol abuse;

Smoking;

Familial tilosis (hereditary hyperkeratosis of the palms and soles with a high (95%) risk of developing esophageal cancer over the age of 65);

The risk of developing adenocarcinoma is increased in the presence of Barrett's esophagus.

Clinical painting. For a long time the disease is asymptomatic. In the later stages, characteristic signs develop.

progressive dysphagia.

Regurgitation of gastric contents.

Pain behind the sternum.

Horner's syndrome (ptosis, miosis, enophthalmos), which occurs when the tumor grows into the sympathetic trunk.

Hiccups and impaired excursion of the diaphragm as a result of tumor invasion of the phrenic nerve.

Painful cough, stridor breathing when the tumor grows into the trachea and large bronchi.

Esophageal-tracheal or esophageal-bronchial fistulas, causing coughing when eating, as well as aspiration pneumonia.

Bleeding from the esophagus (streaks of blood in the vomit, anemia, a positive reaction to occult blood in the feces); when the tumor destroys the wall of a large vessel - massive bleeding.

Common symptoms include weakness, increased fatigue, decreased performance, and progressive weight loss.

Diagnostics. X-rays play an important role in the diagnosis of esophageal cancer. With exophytic tumor growth with decay and ulceration, a filling defect with uneven, corroded contours is revealed. The most informative method for diagnosing esophageal cancer is FEGDS.

The diagnosis must be confirmed histologically. The highest accuracy (90-100%) is provided with multiple biopsies of tumor tissue.

Endosonography can detect tumors up to 3 mm in size and assess the condition of the tissues surrounding the esophagus. To determine the spread of the tumor process, CT and MRI are used.

differential diagnostics. It is carried out with the following diseases characterized by symptoms of dysphagia:

Peptic and burn cicatricial strictures of the esophagus;

Esophagospasm;

Achalasia of the cardia;

Benign tumors and diverticula of the esophagus;

Lymphogranulomatosis, lymphosarcoma (characterized by an increase in the cervical and mediastinal lymph nodes);

Mediastinal pathology: mediastinal tumors, aortic aneurysm, retrosternal goiter, exudate in the pericardial cavity.

Treatment esophageal cancer in the early stages includes endoscopic resection of the mucous membrane with a tumor, laser and photodynamic destruction of a superficial tumor.

At later stages, in the absence of signs of metastasis, a radical surgical intervention is indicated - extirpation of the esophagus with lymphadenectomy and the creation of an artificial esophagus from the greater curvature of the stomach. If a radical operation is not possible, palliative surgical interventions are carried out aimed at providing nutrition to the patient: the imposition of bypass anastomoses, gastrostomy.

The most common type of palliative surgery for cancer of the middle and lower third of the esophagus is currently endoscopic dilatation of stenosis or recanalization of the tumor. Recanalization can be laser, thermal, chemical, or using stents.

Chemotherapy for esophageal cancer is ineffective. A combination of fluorouracil and cisplatin is usually used.

Forecast. Postoperative mortality averages 6-10%. The average five-year survival rate of patients after radical surgery at stage I is about 60%, at stage II - 30-40%, at stage III - 10-15%, at stage IV - 1-4%.

BENIGN TUMORS OF THE ESOPHAGUS

Benign tumors of the esophagus are detected approximately 80 times less often than malignant ones. Of these, the majority (60-70%) are leiomyomas, which are more often formed in the middle and especially the lower thirds of the esophagus and, as a rule, are asymptomatic.

Benign tumors are subject to surgical treatment in order to avoid malignant degeneration and the occurrence of complications (bleeding, inflammation, etc.).