Dysphagia syndrome in the practice of a general practitioner. Dysphagia: causes and effective treatment Dysphagia syndrome and surgical diseases of the esophagus

Dysphagia is a violation of a complex reflex swallowing act. This is not a separate nosology, but a syndrome that manifests itself in many diseases. Patients complain of difficulty in swallowing food, pain in the retrosternal region, salivation, belching, heartburn. In case of violation of the act of swallowing, symptoms associated with the ingress of food into the Airways which is manifested by coughing, hoarseness of voice. The tactics of the doctor is aimed primarily at identifying the causes.

To do this, pharyngoscopy, radiography of the esophagus with contrast, measurement of pH indicators and esophageal manometry are used. After differential diagnosis and detection of a disease that occurs with dysphagia syndrome, an etiotropic conservative or surgical treatment.

Esophageal dysphagia: symptoms

Esophageal dysphagia is most often caused by esophageal diseases, diseases of the gastrointestinal tract, pathology of the mediastinal organs.

Acute esophageal dysphagia occurs as a result of:

• allergic edema (Quincke's edema);
• obturation.

Causes of esophageal dysphagia:

• The narrowing of the lumen of the esophagus causes cancer of the esophagus (stomach cancer with localization in the cardia also manifests itself), GERD. Cicatricial narrowing occurs after chemical burns, radiotherapy in thoracic oncology.
• When squeezing the esophagus with tumors of the organs chest(cancer of the lung, bronchi), enlarged mediastinal lymph nodes, paraesophageal, cardiac pathology with severe myocardial hypertrophy.
• Violation of the coordinated contraction of the muscles of the esophagus can be a sign of achalasia, total spasm of the esophagus, diabetes mellitus, scleroderma.
• Esophageal peristalsis can be impaired infectious diseases(tuberculosis), uncontrolled intake of certain drugs (calcium antagonists, nitrates).

Symptoms of esophageal dysphagia:

• V initial stage diseases patients complain about;
• appear retrosternal pain, salivation, often heartburn, dry cough, hoarseness;
• as the symptoms progress, the symptoms increase, there is difficulty in swallowing soft food, and then liquids.

Types of dysphagia

All diseases that occur with dysphagia syndrome, depending on the anatomical level of swallowing disorders, are divided into:

1. Oropharyngeal (oropharyngeal) dysphagia is a violation of the formation of a food coma and its advancement into the pharynx, in this case, the initial swallowing movements are disturbed.

The causes may be neurological pathology, thyromegaly, lymphadenopathy, oncological diseases of the head and neck, degenerative processes of the spine. Main symptoms:

• cough;
• nasal regurgitation;
• bouts of suffocation.

Treatment depends on the causes of this syndrome.

1. Esophageal (esophageal) dysphagia is a violation of the movement of food from the pharynx into the stomach. The causes of the disease are narrowing or compression of the esophageal tube, as well as a violation of its motility.

In addition, all dysphagia is divided into:

• sharp;
• chronic

By the nature of the flow:

• intermittent;
• permanent;
• progressive, with increasing clinic.

Dysphagia - what is it

Dysphagia (Greek dys - denial, phagein - to eat) is the general name for a swallowing disorder.

Dysphagia is a syndrome (complex of symptoms), manifested by a violation of the act of swallowing.

Oropharyngeal dysphagia

Oropharyngeal dysphagia is also called "upper", with this form of dysfunction, the oral and oropharyngeal phases of swallowing are disturbed.

Oropharyngeal dysphagia syndrome includes the following symptoms:

• difficulty at the very beginning of swallowing;
• return of food through the nasal passages;
• cough;
• asthma attack;
• neurological diseases leading to oropharyngeal dysphagia often occur with dysarthria (impaired articulation and pronunciation) and diplopia (impaired function of the visual muscles);

Causes of oropharyngeal dysphagia:

1. Obstruction of the esophagus.

• various infectious processes(tonsillitis, pharyngitis, abscesses);
• increase thyroid gland(thyreomegaly);
• various lymphadenitis;
• Zenker's diverticulum;
• various types of myositis and fibrosis;
• cervical osteochondrosis;
• oropharyngeal malignancy;

1. Violation of the conduction of nerve impulses to muscle fibers:

• CNS diseases (brain tumors, stroke, Parkinson's disease);
• a disorder in the conduction of a nerve impulse to smooth muscles (VPS dysfunction).

1. Psychosomatic disorders (neurosis, various functional disorders).

Treatment of oropharyngeal dysphagia depends on the etiology of the disease.

• degenerative diseases of the central nervous system;
• previous diseases (strokes, head injuries, diseases of the gastrointestinal tract);
• oncological diseases;
• the presence of severe chronic diseases (diabetes mellitus, coronary artery disease, hypertension).

Dysphagia in children

Dysphagia in children has some peculiarities. First of all, this is due to the diseases that cause this syndrome.

The causes are the following pathologies:

1. Cerebral palsy is the general name for a large group of diseases that have in common damage to the structures of the brain responsible for voluntary movements.
2. Athetosis (hyperkinesis) - involuntary movements in individual muscle groups, occurs when subcortical structures are damaged. It appears immediately after birth, is the result of birth trauma, nuclear jaundice.
3. Various congenital pathologies oral cavity and nasopharynx.
4. Infectious lesions of the pharynx, larynx, esophagus.
5. Consequences of surgery.
6. Oncological pathology.

The efforts of doctors are aimed at treating the disease that caused dysphagia and at eliminating or reducing the severity of this syndrome.

Particular attention is paid to neurological pathology, since these diseases have not only medical, but also social significance. A whole program of rehabilitation of patients with cerebral palsy has been developed. Rehabilitation measures begin almost from the first days of life (drug therapy, massage, exercise therapy, physiotherapy procedures are carried out). From the age of three, a speech therapist joins the treatment.

Dysphagia after fundoplication

In severe forms of GERD, a fundoplication operation is performed - this is an antireflux operation, which consists in the fact that a special cuff is formed around the esophagus from the bottom of the stomach, preventing the refluxate from being thrown into the esophagus (). The operation has proven itself and gives good results. However, after fundoplication in the early postoperative period, dysphagia and moderate epigastric pain are often observed. This is due to the fact that a “new” valve of the esophagus is being formed and the body is adapting to it. These discomforts go away without any treatment.

Functional dysphagia

Functional dysphagia is a manifestation of various neuroses. This form of pathology can manifest itself at any age. People suffering have a special psychological characteristic - they:

• suspicious;
• anxious;
• subject to various kinds of phobias.

In children, functional dysphagia of the esophagus and pharynx may be present from the very early age. It is often accompanied by the following symptoms:

• poor appetite;
• frequent regurgitation, vomiting
• bad night sleep.

Without treatment, by the age of 7, children experience dystrophy, increased fatigue, poor tolerance of physical and mental stress.

Diagnosis of dysphagia

The dysphagia syndrome itself usually does not cause diagnostic difficulties. All the efforts of doctors are aimed at identifying the disease that caused dysphagia. In terms of diagnosis, the following examinations are carried out:

1. Pharyngoscopy - this method allows you to identify the causes of oropharyngeal dysphagia: glossitis, tonsillitis, neoplasms, foreign bodies. Pharyngoscopy is complemented by indirect laryngoscopy, the method allows you to identify the pathology of the epiglottis.
2. allows you to identify violations of the motility of the esophagus,.
3. EFGS reveals foci of inflammation, areas suspicious for. If necessary, a tissue biopsy is performed for morphological examination.
4. Long-term measurement of the pH of the medium inside the esophagus is the most reliable method for detecting GERD; esophageal manometry is performed (to determine abnormalities in the work of the ESP).
5. Laboratory research methods are non-specific:

• in the peripheral blood, a slight leukocytosis, anemia, increase in ESR;
• V venous blood most often there is a decrease in total protein, dysproteinemia;
• stool testing for occult blood.

In order to identify neurological pathology, an in-depth neurological examination is performed. If clinical diagnosis is in doubt, instrumental diagnosis is carried out:

• CT scan of the brain;

If cardiac and pulmonary pathology is suspected, the following is performed:

• chest x-ray;
• echocardiography.

Treatment of dysphagia is carried out after the final diagnosis.

Degrees of dysphagia

According to the severity of the clinical picture, the following degrees of dysphagia are distinguished:

1. The patient has difficulty swallowing hard, dry food.
2. The patient can only swallow liquid food.
3. Swallowing not only solid, but also liquid food is disturbed.
4. Unable to swallow any food.

Treatment

The doctor's tactics in the treatment of dysphagia is determined by the cause of the disease and the severity of the syndrome. The efforts of doctors are aimed at the speedy restoration of the act of swallowing and the prevention of aspiration complications.

Acute cases of dysphagia require urgent care:

• the foreign body is immediately removed.
• desensitizing therapy is urgently carried out.

With a long course of the disease, complicated by dysphagia, a full course of etiopathogenetic treatment is carried out. From medications apply:

1. Means for improving the neuroregulation of the act of swallowing. In degenerative diseases, dopamine agonists and precursors, central H-anticholinergics are prescribed. Membrane stabilizers, neuroreparants, and neuroprotectors are widely used in strokes.
2. calcium antagonists. The drug reduces the concentration of intracellular calcium, due to this, the spasm of muscle fibers (diffuse esophageal spasm, achalasia) is eliminated, thereby improving the passage of food.
3. Antisecretory drugs. These drugs are used for GERD and eosinophilic esophagitis with dysphagia. Antacids, PPIs, IGRs are used.
4. With an infectious etiology of the disease (tonsillitis, abscesses, pharyngitis), antibiotic therapy is indicated.
5. During treatment functional disorders swallowing are widely used traditional medicine.

In some cases, the elimination of dysphagia is possible only surgically. In case of neoplasia that closes the lumen of the esophagus or compresses it, resection or removal of the pathologically altered organ (removal of the stomach, lung) is performed, followed by radiation and chemotherapy.

Also, patients with Zenker's diverticulum can be treated only in surgery; timely cricopharingeal myotomy practically cures dysphagia.

Relevance of the topic: Differential diagnosis of dysphagia syndrome is one of the important and complex problems in gastroenterology. 2-5% of the industrial population developed countries complain of swallowing disorders. Dysphagia is the cause of 3-4% of visits to general practitioners and 10% of visits to a gastroenterologist. In 25% of patients presenting such complaints, the pains turn out to be functional, and in other cases - organic, and moreover, every 10th situation is considered as requiring surgical intervention.

Thus, the general practitioner will often have to deal with issues of tactics and strategy regarding dysphagia syndrome. A number of patients (with tumors, strictures, hernias) may need help in a surgical setting, hospitals. Another category of patients with a chronic variant of the dysphagia syndrome requires reasonable conservative treatment.

Purpose: To be able to make a preliminary diagnosis and outline management tactics in patients with dysphagia syndrome.

Dysphagia is terminologically defined as difficulty or discomfort when swallowing. This is perceived by the patient as a sensation of "sticking" of food when passing through the oral cavity, pharynx or esophagus.

The normal transport of the food bolus through the swallowing canal depends on the size of the bolus, the diameter of the canal, the peristaltic contraction and the state of the swallowing center, which ensures normal relaxation of the upper and lower esophageal sphincters during swallowing and inhibition of persistent contractions in the body of the esophagus. In an adult, the esophagus, due to the elasticity of its wall, can stretch to more than 4 cm in diameter. In cases where the esophagus is not able to stretch to a lumen diameter of more than 2.5 cm, dysphagia develops. In the same cases, when it cannot be stretched over 1.3 cm in diameter, a violation of swallowing will be mandatory. The discrepancy between the size of the food bolus and the diameter of the esophagus or external compression of the lumen of the swallowing canal leads to mechanical dysphagia, and swallowing disorders due to the pathology of the muscles of the swallowing apparatus, its regulation by the nervous system, the lack of coordinated peristaltic contractions of the esophagus and adequate suppression of the swallowing center - to motor dysphagia.

The causes of dysphagia are many and varied. From the main goals, namely, the timely establishment of a diagnosis and the appointment of adequate treatment, it follows that it is necessary to consider the semiotics of swallowing disorders. First of all, the localization of swallowing disorders requires clarification. In this regard, oropharyngeal and esophageal dysphagia are isolated (see table).

A pathological condition in which the act of swallowing is disturbed. It is manifested by difficulty in swallowing solid food, liquids, saliva, their entry into the respiratory system, increased formation of saliva, painful sensations behind the breastbone, hoarseness of voice, sore throat. Diagnosed by pharyngoscopy, x-ray of the esophagus, esophagogastroscopy, pH-metry, esophageal manometry. Treatment involves the appointment of etiopathogenetic therapy for a disease complicated by dysphagia. If a disorder occurs against the background of severe organic changes in the pharynx, esophagus, and adjacent organs, surgical interventions are performed.

Dysphagia is a secondary pathological process and develops against the background of other diseases. Swallowing disorders are found in all age groups, but the incidence increases with age. According to the results of observations, the prevalence of pathology is 11% in the whole population and reaches 13% in patients older than 65 years. At a young age, dysphagia often complicates the course of injuries, malignant neoplasia of the head and neck. In elderly patients, the leading causes of impaired swallowing are disorders cerebral circulation, neurodegenerative diseases. The relevance of timely diagnosis of dysphagic syndrome is due to a significant deterioration in the quality of life of patients and a high risk of mortality in the event of complications.

Causes of dysphagia

Specialists in the field of gastroenterology separately consider the etiological factors leading to the development of oropharyngeal (“high”) and esophageal (“lower”) swallowing disorders, although some of them are detected in both types of pathology. The passage of the food bolus through the pharynx and the proximal esophagus is disturbed under the influence of such causes as:

• Mechanical obstruction. Violation of the oropharyngeal phase of swallowing can be caused by inflammatory processes (retropharyngeal abscess, tonsillitis), thyroid hyperplasia, enlarged lymph nodes, hypopharyngeal diverticulum, cervical osteophytes, muscle fibrosis, cricopharyngeal adhesions. Narrowing of the upper sections digestive tract also observed in malignant neoplasia of the oral cavity, pharynx, larynx, the consequences of their surgical treatment and radiation therapy.
• Neuromuscular disorders. Oropharyngeal dysphagia develops in the acute phase of cerebral stroke in 42-67% of patients, its severity directly correlates with the severity of cerebral circulation disorders. In half of patients with parkinsonism, clinical symptoms of impaired oropharyngeal swallowing are observed, in another 45% of patients, latent signs of the disorder are detected instrumentally. Dysphagia is complicated by multiple sclerosis, amyotrophic lateral sclerosis, pseudoparalytic myasthenia gravis.

Esophageal swallowing disorders are often caused by esophageal pathology, chronic diseases organs of the gastrointestinal tract, mediastinum. Acute forms of dysphagia occur with allergic Quincke's edema, sudden obstruction of the body of the esophagus and gastroesophageal transition by foreign bodies. The normal passage of solid and liquid food through the esophagus to the stomach can be interfered with by:

• Narrowing of the esophagus. The lumen of the organ decreases with eosinophilic pharyngitis, malignant tumors of the esophagus, stomach cancer with lesions of the cardiac section, complicated course of gastroesophageal reflux disease. Cicatricial stenosis develops after radiotherapy of thoracic cancer, chemical burns with caustic compounds, potassium chloride, salicylates, and some other drugs. Signs of dysphagia are noted when the lumen of the organ is narrowed to less than 12 mm.
• Compression of the esophagus from the outside. The passage of food is hindered by volumetric formations that put pressure on the esophageal wall. Esophageal dysphagia is often found in tumors (cancer of the lung, bronchi, thymoma), enlarged mediastinal lymph nodes, retrosternal goiter, infectious diseases (tuberculosis, histoplasmosis), paraesophageal hernia. Difficulties in swallowing are detected in cardiopathology - mitral valve defects, vascular compression.
• Contractile disorders of the esophagus. Esophageal swallowing disorders complicate achalasia, diffuse spasm of the esophagus, corkscrew deformity of the organ. Pathological changes in motility are observed in patients with systemic scleroderma, Chagas disease, diabetes. Violations of the contractions of the esophageal muscles that prevent the process of swallowing occur when taking nitrates, estrogens, methylxanthines, calcium channel blockers.

Pathogenesis

There are two key mechanisms for the development of dysphagia - obstructive and dysregulatory, which can be combined in some pathological conditions. With obstructive swallowing disorders, the passage of food is disturbed due to the existence of a mechanical obstacle - inflammatory, granulomatous processes, cicatricial changes, volumetric formations protruding into the lumen of the digestive organs or compressing them from the outside. In some cases, the situation is aggravated by pain syndrome, especially pronounced during inflammation. The basis of the pathogenesis of dysregulatory dysphagia are disorders of innervation due to damage to the swallowing center of the medulla oblongata, enteric nervous system, pathological changes at the level of the esophageal muscle layer. As a result of contraction of the muscles of the soft palate, the pharynx becomes discoordinated, the esophageal peristaltic reflex is disturbed, which leads to a change in the process of the natural passage of food.

Classification

Existing systematization clinical forms dysphagia takes into account both the anatomical level of swallowing disorders and the degree of their severity. This approach facilitates the identification of the root cause of disorders, allows assessing the prognosis and developing the optimal tactics for managing the patient. Gastroenterologists distinguish the following types of disease:

• According to the anatomical level: oropharyngeal (oropharyngeal) and esophageal dysphagia. In the first case, the formation of a food bolus, its movement in the direction of the throat, and the initial swallowing movements are disturbed. In the second, the passage of products through the esophagus and their entry into the stomach is difficult.
• By severity: there are 4 degrees of dysphagia. In degree I, the patient has difficulty swallowing solid foods; in degree II, only liquid food is swallowed. In patients with grade III dysphagia, swallowing of not only solid food, but liquids, saliva is impaired. At IV degree it becomes impossible to swallow any food.

Symptoms of dysphagia

At the initial stage of the disease, patients usually complain of difficulty in swallowing solid food, accompanied by discomfort in the pharynx and esophagus. They may also appear pain along the esophagus, increased salivation, a feeling of fullness behind the sternum. Characteristic symptoms diseases - hoarseness of voice, feeling of lack of air, dry cough, sore throat. The progression of dysphagia leads to impaired swallowing of liquid food, its entry into the respiratory organs of the patient. Sometimes the disease is accompanied by heartburn. With a long course, there is a deterioration in the general condition of the patient, a significant loss of body weight due to lack of food.

Complications

With dysphagia, esophagitis is often observed, which in a chronic course increases the risk of metaplasia of the epithelium of the esophageal mucosa with the development of a tumor. The constant reflux of food particles into the respiratory tract causes aspiration pneumonia, which is characterized by a severe course and resistance to ongoing therapy. A constant nutritional deficiency causes a sharp weight loss of the patient up to cachexia, which is accompanied by dystrophic changes internal organs. When the trachea is compressed by tumors of the esophagus, acute disorder breathing (asphyxia), threatening the life of the patient and requiring emergency measures.

Diagnostics

Identification of swallowing disorders is usually not difficult due to the typical clinical picture of the pathological condition. However, the key task of a diagnostic search for dysphagia is the diagnosis of diseases that could cause the disorder. The examination of the patient is carried out comprehensively and includes the following methods:

• Pharyngoscopy. During the examination of the oral cavity and pharynx with the help of a reflector, the causes of oropharyngeal dysphagia are detected: tonsillitis, glossitis, neoplasms, foreign bodies. The method is supplemented with indirect laryngoscopy, which allows diagnosing the pathology of the epiglottis.
• X-ray of the esophagus. X-ray examination with oral administration of a contrast agent reveals violations of the involuntary phase of swallowing and changes in esophageal motility characteristic of dysphagia. X-ray can also determine the presence of diverticula.
• Esophagogastroscopy. In endoscopic examination, the mucous membrane of the esophagus, the cardia of the stomach is well visualized, which helps to detect macroscopic changes in the epithelium that cause dysphagia. At the same time, a tissue biopsy is performed for histological examination.
• Daily pH-metry. It is the most accurate study for the diagnosis of reflux esophagitis in order to confirm the organic nature of dysphagia. Additionally, esophageal manometry can be performed to detect disorders of the lower gastroesophageal sphincter.

Changes in clinical analysis blood in dysphagia are nonspecific and correspond to the underlying disease. Anemia, moderate leukocytosis, increased ESR can be determined. IN biochemical analysis blood revealed a decrease in the level of total protein, dysproteinemia, possibly an increase in the content of liver enzymes. To assess the state of the digestive tract, an ultrasound of the abdominal cavity is performed. In order to exclude the pathology of the nervous system, a comprehensive neurological examination is carried out, according to the indications, an MRI of the head, a CT scan of the brain, and an EEG are prescribed. To exclude possible pulmonary and cardiac pathology, chest x-ray, echocardiography, and ECG are recommended.

Differential diagnosis in dysphagia syndrome is made between diseases that can cause this pathological condition. The disease is differentiated with odynophagia, hysterical "lump in the throat" (globus pharyngeus), dyspnea, phagophobia. In addition to observation by a gastroenterologist, a patient may need to consult an otorhinolaryngologist, thoracic surgeon, pulmonologist, phthisiatrician, oncologist, infectious disease specialist, neuropathologist, rheumatologist, allergist, endocrinologist, psychiatrist.

Treatment of dysphagia

The etiology and course of the disorder has the greatest influence on the choice of medical tactics. The main therapeutic objectives are to restore swallowing, prevent possible complications, in the first place - aspiration in oropharyngeal dysphagia of neuromuscular origin. Patients with sharp forms swallowing disorders, usually associated with mechanical obstruction of the esophagus, is indicated urgent Care for removal foreign body. Correction of long-term disorders involves complex etiopathogenetic treatment of pathology complicated by dysphagia. Of the pharmaceutical preparations, taking into account the causes of the disease, the following are used:

• Means for improving neuroregulation. To restore swallowing, patients with parkinsonism are prescribed dopamine agonists and precursors, central N-anticholinergics. Manifestations of dysphagia in myasthenia are reduced by taking anticholinesterase drugs. With cerebral strokes, intensive complex therapy with neuroreparants, neuroprotectors, and membrane stabilizers is carried out.
• Calcium channel blockers. They reduce the concentration of calcium ions in muscle fibers, eliminating spastic conditions (diffuse esophageal spasm, achalasia) and improving the passage of food. If necessary, dysphagia therapy is supplemented with nitrates, which have a relaxing effect, anticholinergics, phosphodiesterase inhibitors that affect neuromuscular regulation.
• Antisecretory drugs. Recommended for combination of dysphagia with GERD, eosinophilic esophagitis. Most often, proton pump inhibitors are used, which reduce the secretion of hydrochloric acid and thus reduce irritation of the esophageal mucosa by gastric secretions. In the presence of eosinophilic esophagitis, aerosol forms of local steroid preparations are additionally used.

With a proven infectious genesis of the disease, accompanied by dysphagia, antibacterial and antiviral therapy is indicated. Most patients require dietary modification - replacing solid foods with soft foods, a restrictive diet in the presence of hypersecretory disorders. In all cases of neurological pathology, rehabilitation is prescribed using techniques to improve oral swallowing.

In a number of patients, persistent dysphagic disorder can only be eliminated surgically. With neoplasia that compresses the esophagus, resection or removal of the affected organs is performed. According to the indications, the operation is supplemented with chemotherapy and radiotherapy. With dysfunction of the upper esophageal sphincter, Zenker's diverticula, cricopharyngeal myotomy is effective. Bougienage, balloon dilatation, stenting of the esophagus, endoscopic dissection of strictures make it possible to restore the esophageal lumen in case of its cicatricial narrowing, compression by adjacent organs. For the treatment of therapeutically resistant achalasia, esophagocardiomyotomy is performed. In case of dysphagia associated with irreversible changes in the esophagus, esophagoplasty is performed.

Forecast and prevention

The likelihood of complete recovery depends on the cause that led to the development of dysphagia. The prognosis is considered relatively favorable if the symptoms are caused by increased acidity of the gastric juice and other conditions that respond well to drug therapy. Prevention of dysphagia includes timely treatment of diseases of the digestive tract ( peptic ulcer, GERD), refusal to eat very hot, fried foods, alcohol, smoking cessation, careful supervision of children, which excludes the child from swallowing small objects, toys.

In contact with

The main questions of the topic.

1. Etiology and pathogenesis of DM.

2. Classification.

3. SD clinic.

4. Diagnostic methods.

5. Emergency health care, including during the evacuation phases.

6. Correction of homeostasis disorders.

7. Indications and principles of surgical treatment.

Dysphagia syndrome (impaired swallowing) is characteristic of all stenosing diseases of the esophagus, such as cardiospasm, diverticula, cicatricial stenosis of the esophagus and benign tumors.

Features of physiology. The main function of the esophagus is to transport swallowed food. It is the disorders of motor function that are accompanied by clinical symptoms, while the absorption and secretory functions are not clinically manifested. At the proximal end of the esophagus there is a regulatory mechanism that performs the function of one-way passage of food, except in unusual situations. The esophageal stage of transporting food is a reflex act. The vagus nerve performs both motor and inhibitory functions.

The movement of food through the esophagus depends on the pressure gradient. The main factor causing this pressure is peristaltic contractions, which move the food bolus down the esophagus. As the contraction wave approaches, the esophageal-gastric angle opens and the contents of the esophagus enter the stomach.

The basal pressure that exists in the esophagus, in the absence of motor activity, is lower than atmospheric pressure and ranges from 4 to 6 cm of water column, due to the fact that the esophagus is located in the chest cavity. In all other departments, gastrointestinal tract basal pressure is positive and much higher than atmospheric pressure. Sphincters separate low pressure in the esophagus from pressure in the throat and stomach. Zones high pressure in the sphincters prevent air and saliva from the pharynx and gastric contents from entering the esophagus. As such, in the morphological sense of the word, sphincters do not exist, but there is only a motor-functional mechanism that has the character of a sphincter.

Violation of motor activity.

Upper sphincter. A number of diseases, including diseases of the central nervous system, can cause dysfunction of the phagingo-esophageal sphincter. Patients with bulbar poliomyelitis, as well as cerebrovascular disorders and multiple sclerosis, suffer from dysphagia. Abnormal relaxation of the sphincter is characteristic of these diseases and causes difficulty in swallowing.

The following diseases most often cause it: muscular dystrophy, myasthenia gravis, dermatomyositis. Violations of the act of swallowing also occur with pharyngo-esophageal diverticula. This disrupts the normal relationship between contraction of the pharynx, and contraction and relaxation of the pharyngoesophageal sphincter. In these patients, the contraction of the sphincter occurs before the contraction of the pharynx ends.

Pathology of the lower sphincter.

Achalasia of the esophagus (cardiospasm) is a disease of unknown etiology, characterized by the absence of esophageal peristalsis and impaired activity of the lower esophageal sphincter, which does not relax when swallowing. The frequency of achalasia is from 5 to 10% of all diseases of the esophagus. Although the cause of the disease is unclear, there is no doubt that it is based on neurogenic disorders. Pathological findings support this view.

Many patients with this disease have an absence of Auerbach's plexus ganglion cells in the wall of the esophagus. Changes are found at any level of the thoracic esophagus. Not only is the cause of ganglion cell damage unknown, but also at what level of the nervous system there are primary disorders.

Observations of cases of cardiospasm in childhood led to the creation of a theory of the congenital origin of cardiospasm. It is assumed that the cause in these cases is the underdevelopment of the intramural nerve plexus.

There is also a psychoneurotic theory that links the origin of cardiospasm with neuropsychic trauma that disrupts nervous coordination. Achalasia occurs equally often in both men and women, observed at any age, but most often from 30 to 60 years.

Pathological changes depend on the duration and stage of the disease. In the later stages, the esophagus is enlarged and elongated, the walls are thickened due to a sharp hypertrophy of the muscular layer of the esophagus. In the mucosa and submucosa, inflammatory changes are observed: first, hypertrophy of muscle fibers occurs, which are then replaced by connective tissue. In the intramural nerve plexus, dystrophy phenomena are found, in nerve cells - dissolution or wrinkling of the protoplasm.

Clinic. The earliest and most permanent symptom is a violation of the act of swallowing - dysphagia, which at the beginning of the disease is intermittent, then as the disease progresses it becomes more and more constant. Then there are pains behind the sternum, radiating to the back. Dysphagia first occurs when eating cold food, then warm food, often dense food is better than liquid. The appearance of pain is mainly associated with the appearance of concomitant esophagitis. When food is delayed, pressing pains behind the sternum occur. Regurgitation is observed with expansion and stagnation in the esophagus, especially at night when the patient relaxes, as a result, they eat in an elevated position of the body. Trying to help food pass into the stomach, patients drink a large amount of liquid (hydrophagia), swallow air (aerophagia), while eating while standing, walk, jump, take on frilly forms. Because, as a rule, they avoid canteens, eat alone.

B. V. Petrovsky distinguishes 4 stages of the disease:

1 stage. The patient's condition is satisfactory. Patients feel a delay in food, which passes with difficulty. Evacuation from the esophagus, although slow, but complete, regurgitation is not observed.

2 stage. Along with more pronounced dysphagia, there are pains behind the sternum of a pressing character. In the esophagus, increased peristalsis and antiperistalsis are noted, food masses are retained, and regurgitation is intermittent. The diameter of the esophagus and cardia narrows somewhat.

In stage 3, organic changes appear in the esophagus in the form of a fibrous-cicatricial process, its walls thicken. Food enters the stomach in small quantities. In the esophagus above the obstruction, a large amount of food accumulates, regurgitation with a disorder of peristalsis, with segmental spasms and antiperistalsis. There is weight loss of patients, disability.

In stage 4, there is a sharp narrowing of the cardiac canal, above the esophagus is sharply expanded, curved. The wall of the esophagus is thinned, atonic, does not peristaltize. Food is delayed for a day or more, decomposes in the lumen of the esophagus, causing the formation of cracks and ulcers, periesophagitis and mediastinitis often develop. Regurgitation occurs even when the torso is tilted, exhaustion develops.

Achalasia is characterized by a slow course with a gradual long transition from one stage to another.

The most common complications are pulmonary and inflammatory diseases, cancer development, bleeding in severe esophagitis and perforation.

Diagnostics. IN different stages achalasia of the esophagus, there is only obstruction of the cardia with a slight dilatation of the proximal section. As the disease progresses, characteristic radiological signs appear. The esophagus is dilated, in the lower section it is conically narrowed over a small extent with a coracoid expansion at the site of the narrowed segment. Although the radiological picture of cardiospasm is quite characteristic, it is still necessary to differentiate it from cancer in early stages disease, especially in people over 50 years of age.

The greatest benefit in this is esophagoscopy. Confirmation of the clinical manifestations of the disease is the study motor function esophagus. Low pressure is found in the esophagus with dilatation of its lumen and the absence of peristalsis in the esophagus after swallowing. When swallowing, there is a rise in pressure throughout the esophagus. With achalasia, the esophageal sphincter does not open during the act of swallowing. In some patients, the violation of peristalsis turns into a diffuse spasm of the esophagus or there are repeated severe spasms in response to the act of swallowing.

Treatment. The disorder of esophageal peristalsis that characterizes esophageal achalasia does not respond well to medical treatment. Relief of the symptoms of the disease can be achieved by using a sparing diet, antispastics, vitamins, sedatives. However, such therapy usually gives only a temporary effect. Forced expansion of the cardia can be performed using a hydrostatic, pneumatic or mechanical dilator. Pneumatic dilators are mainly used as the safest ones.

A probe with a balloon at the end is inserted into the stomach under X-ray control. In the lumen of the stomach, it is inflated with air, then pulled outward, thus expanding the lumen of the esophagus. According to B.V. Petrovsky, ruptures of the mucosa or wall of the esophagus are observed when using an elastic dilator in 1% of cases, when using a mechanical dilator in 6%. In 80% of cases, dilatation is successful and relieves the patient of the painful symptoms of the disease.

In the absence of the effect of dilation, surgical treatment is used. Many operations have been proposed, including vagotomy, vagolysis, sympathectomy, transgastric retrograde expansion of the cardia, esophagofundoanastomosis. Modern surgery is based on the proposal of Geller, who in 1913 performed the first bilateral cardiomyotomy. It consists of a longitudinal dissection of the muscular layers of the distal esophagus by transpleural access. The mucosa protruding through the incisions is covered with a flap of the omentum. Sometimes only an anterior cardiomyotomy is sufficient. About 90% of patients are cured after this operation. Unsatisfactory results are usually associated with scarring in the long term. This operation is the operation of choice in children and in advanced stages of the disease. It is necessary to spare the vagus nerve, if damaged, perform pyloroplasty. Dissection of the esophageal opening of the diaphragm can lead to the formation of a hernia. B.V. Petrovsky closes the defect formed after the excision of the muscular membrane of the esophagus with a pedunculated flap from the diaphragm, which also gives a good result. A.N. Berkutov sews the fundus of the stomach into the defect. Experience suggests that anterior myotomy can be performed by abdominal access.

Diffuse spasm of the esophagus and hypertension of the gastroesophageal sphincter.

While with achalasia there is a weakening of peristalsis, with diffuse spasm, on the contrary, there is hyperperistalsis. Fortunately, diffuse spasm of the esophagus is extremely rare.

Clinically, this disease differs from achalasia in that pains join earlier, while dysphagia is rare or does not happen at all. The intensity of pain varies from a slight feeling of discomfort behind the sternum to severe pain radiating to the back, neck, similar to pain in the heart. The pains may come on while eating, but also at night when the patients wake up from them. They are more pronounced in patients with unstable nervous system. During attacks, despite the intensity of pain, the disease does not seem severe.

X-ray signs are found in less than half of the cases. The esophagus looks twisted in the form of a corkscrew, it gives the impression of pseudodiverticulosis, there are signs of muscle hypertrophy. Often these phenomena are combined with diaphragmatic hernia or epiphrenic diverticulum. The diagnosis is confirmed by the study of the motor ability of the esophagus, its peristalsis. Perversion of peristalsis is usually found in the lower half or in the lower third of the esophagus, where several peristaltic waves are detected simultaneously, continuously repeating. In most patients, the activity of the sphincter is not disturbed, except for the gastroesophageal, where the pressure increases to 140 cm of the water column. In very severe variants of the course of this disease, it is sometimes necessary to use a modified Heller operation. Before the operation, it is necessary to examine the patient in order to exclude other diseases. Dissection of the muscles must be performed over a large distance from the cardia to the aortic arch. If there is a diverticulum, then a diverticulectomy is performed. The results of this operation are not as favorable as with achalasia, but about 70% of patients are completely cured. Careful selection of patients for surgery is required.

Hypotension of the lower esophageal sphincter.

The slogan "XX century - the century of peptic ulcer, XXI century - the century of gastroesophageal reflux disease" (GERD). Reflux esophagitis (RE) - first mentioned by Hunter (1786).

Definition: GERD is a clinical symptom complex resulting from the reflux of stomach contents into the esophagus.

Epidemiology: Occurs in 20-40% of the general population. In 46% of pregnant women. Reflux esophagitis - in 3-4% of the total population.

Etiology and pathogenesis: the leading place in the pathogenesis is occupied by a violation of the function of the antireflux barrier, which may occur as a result of a primary decrease in the tone of the lower esophageal sphincter (LES, normally 15-35 mm Hg. Art.). If the pressure in the lower esophageal sphincter is less than 12 cm of water column, then gastroesophageal reflux may occur. An increase in the number of spontaneous relaxations of the LES, structural changes in the LES (hernia of the esophageal opening of the diaphragm - HH); decrease in chemical, volumetric and esophageal clearance (decrease in the neutralizing effect of saliva and bicarbonates of esophageal mucus, inhibition and weakening of esophageal motility, the ability to remove contents back into the stomach). Very high intra-abdominal pressure is also important. The reasons are operations on the sphincter, collagen diseases such as scleroderma.

Other pathogenic factors are the damaging effect of refluctanate, a decrease in the resistance of the esophageal mucosa, a violation of gastric emptying, an increase in intra-abdominal pressure. Forced position of the body, smoking, alcohol.

Classification: There are 4 degrees of severity (Savari-Miller) RE: 1 - catarrhal esophagitis, less than 10% of erosions of the distal esophagus; 2 - 50% drain erosion; 3 - circular erosion of almost the entire surface of the esophagus; 4 - peptic ulcer and esophageal stricture, as well as the development of small intestinal metaplasia of the esophageal mucosa (Barrett's syndrome).

Clinical picture: heartburn (80% of patients); belching and regurgitation; dysphagia, sometimes accompanied by edinophania - 20%; pain in the epigastric region or the xiphoid process. External esophageal symptoms include pain, sometimes resembling angina pectoris, persistent cough, dysphonia.

Complications: peptic stricture, bleeding, Barret's syndrome (precancer).

Diagnosis: The "gold standard" remains endoscopic method research. Endoscopic ultrasonography, which allows assessing the condition of the submucosal layer; histological examination; manometry (a decrease in LES, HH, episodes of transient relaxation of the LES, a decrease in the amplitude of peristalsis of contractions of the esophageal wall; daily monitoring of pH in the esophagus (determination of the total number of refluxes, normally no more than 50 times a day); X-ray examination; bilemetry (identification of bile reflux) ; scintigraphy (clarification of the motor function of the esophagus); omeprazole test (significant decrease clinical symptoms RE with omeprazole 40 mg daily). There is no direct connection between HH and RE. True HH can cause a more severe course of RE.

Differential diagnosis: Cardiac syndrome of unknown origin, dysphagia, GI bleeding, broncho-obstructive syndrome. Treatment: preventing the occurrence of reflux, improving esophageal clearance, increasing the protective properties of the esophageal mucosa. Lifestyle changes (stopping smoking, alcoholic and carbonated drinks, avoiding spicy and hot foods, sour fruit nipples, onions, garlic, peppers, fats, chocolate; last meal at 18:00; raising the head end of the bed by 15-20 cm; abstinence from loads associated with torso bending.

Treatment. Antacids and alginates: antacids (maalox, phosphalugel, etc.) for symptomatic purposes. Prokenetics that normalize gastrointestinal motility (domoperidone -10 mg x 4 times a day; cisapride - stimulates the release of acetylcholine in the intermuscular neuronal plexuses of the gastrointestinal tract, cerucal, raglan). Healing of erosions occurs if pH> 4 in the esophagus for 20-22 hours a day. H2-blockers (ranitidine, fomatidine) have recently given way to proton pump blockers (the most powerful antisecretory drugs) - omeprazole, lansoprozol.

The method of surgical correction is fundoplication in combination with selective proximal vagotomy (SPV) (although there are more than 50 types of operations). In case of violation of the pulp function, the most pronounced valvular effect is given by the fundoplication developed by R. Nissen. IN last years developed laparoscopic Nissen fundoplication. Indications: stricture of the esophagus, deep peptic ulcer resistant to drug treatment.

Narrowing of the esophageal opening of the diaphragm (AH) is not mandatory. With a short esophagus, the stomach is not always able to be brought down into abdominal cavity, in such cases, "mediastinilization" of the cardia is recommended, i.e. leave the fundoplication cuff in the posterior mediastinum.

Mortality after primary surgery for RE usually does not exceed 2%. One of frequent complications after antireflux operations is postoperative dysphagia, which is more often temporary, and sometimes permanent. The next complication is pylorospasm.

Currently, it is noted that fundoplication in combination with SPV gives the best results.

Thus, surgical treatment of patients with RE remains a serious problem, many aspects of which are far from being resolved. Of the many proposed operations, as a result of a long journey of trial and error, a thorough study of the pathogenesis of the disease, immediate and long-term results of treatment, antireflux operations are currently coming to the fore, taking into account, in addition to anatomical disorders, the functional state of the esophagus, cardia, gastric secretion and motility, as well as condition of other organs digestive system. With all this, the question of the strict selection of patients for surgery, and hence the correct selection of patients for surgery, remains important. conservative treatment these patients.

Diverticula of the esophagus.

Esophageal diverticula are sac-like protrusions from the lumen of the esophagus. They can be classified according to localization, type of development, as well as the origin - whether they are true or false. Depending on the anatomical position, they are divided into pharyngoesophageal, midthoracic and epiphrenic. According to the mechanism of formation, they are divided into pulsion, traction and combined pulsion-traction. Diverticula are also divided into congenital and acquired. Congenital diverticula include those whose wall contains all layers of the esophageal wall, while acquired diverticula have only a small number muscle tissue or not included at all.

Pharyngoesophageal diverticula. Esophageal pulsation diverticula develop as a result of increased pressure in the lumen of the esophagus. Pulsion diverticula include Zenker's diverticulum, located near the pharyngoesophageal junction. This diverticulum is not truly esophageal as it is in the hypopharyngeal region. The weak point of the posterior wall of the pharyngoesophageal junction is a triangular defect between the oblique fibers of the inferior laryngeal constrictor and the transverse fibers of the crico-pharyngeal muscle. With normal neuromuscular coordination during the passage of food from the larynx to the esophagus and contraction of the constrictor, the crico-pharyngeal muscles relax. With violations of neuromuscular coordination, compression of the constrictor and non-relaxation of the crico-pharyngeal muscles, a protrusion of the posterior wall of the pharyngeal fossa appears. If this violation is not eliminated, then soon the protrusion turns into a sac-like defect, and only the mucous and submucous layers with very rare muscle fibers swell in the intermuscular space. There are several points of view on the occurrence of this diverticulum, however, the above is the most common.

Another cause may be chronic pharyngitis, which disrupts the normal relaxation of the sphincter and causes a bulge to form. A possible cause may also be a wider anteroposterior diameter of the pharynx in men than in women, which is the cause of higher pressure, which is indirectly confirmed by the frequent findings of a diverticulum in men. Reflux esophagitis in esophageal hernia can also play an etiological role. In the stage of formation of a diverticulum, its sac, consisting of mucous and submucosal membranes, is localized first on the back wall, then, as it increases, it shifts to the left. In the early stages, the hernial sac has a spherical shape, later it becomes pear-shaped. Its dimensions can be very large and shift into the mediastinum, but even with a large bag, the inlet remains small.

Men get sick three times more often than women. The overall frequency is 0.1%. In old age, weakening of the muscles of the pharynx can also play an etiological role.

Clinic. The development of clinical symptoms goes through three stages.

In the first stage, only inflammatory changes in the throat are observed. In the second stage, dysphagia joins. In the third, symptoms of compression of the esophagus appear.

In most cases, symptoms develop gradually. Initially, patients feel irritation in the throat, salivation and a feeling of a foreign body when swallowing. Interference with swallowing can occur even when taking liquids. Sometimes there is a dry cough. With an increase in the diverticulum, regurgitation appears, especially at night, after a heavy meal, eaten and undigested food. With the onset of regurgitation, pulmonary complications may follow as a result of aspiration of the contents of the diverticulum. Sooner or later, obstruction of the esophagus joins, which in rare cases is complete. There is exhaustion, weight loss. Sometimes you can see swelling and swelling on the left side of the neck, but this is very rare. Symptoms in some cases develop quickly, within a few months, sometimes within 10-15 years. The diagnosis is usually made by barium fluoroscopy, sometimes without barium, if the level of fluid in the retrotracheal space can be seen. With fluoroscopy, the diameter of the neck of the diverticulum can be determined. Stagnation of food is observed in large diverticula, which is sometimes taken as a filling defect. For a more accurate X-ray examination, it is necessary to empty the diverticulum before examination.

Treatment. Some relief can be obtained by taking semi-liquid food, and also by drinking water after eating, yet a cure can only be achieved with surgical treatment. Expansion of the lumen of the esophagus due to compression by the diverticulum is not recommended because of the risk of perforation of the diverticulum wall. Early surgery is necessary due to the risk of infection, mediastinitis, pneumonia.

There are several methods of operation. The most widely used single-stage resection of the diverticulum. Skin incision along the anterior edge of the sternocleidomastoid muscle. The diverticulum is exposed by retraction of the thyroid gland medially and the carotid artery laterally. The neck of the diverticulum, which is usually quite narrow, is divided and the diverticulum is removed. The mucous membrane of the larynx is sutured with separate interrupted sutures. The edges of the muscle layer are also carefully sutured. The operation does not pose a particular risk, relapses are rare. For small diverticula, a cricopharyngeal myotomy is suggested. Access is the same, an additional longitudinal incision is made through the crico-pharyngeal muscles 3-4 cm long. The rationale for this operation is the opinion about the origin of the diverticulum due to discoordination of the pharyngoesophageal sphincter mechanism. Sometimes esophagoscopy is used to facilitate the search for a diverticulum, to control the suturing of the wall to avoid narrowing of the lumen of the esophagus.

For large borderline pharyngeal-esophageal diverticula, [Korolev B. A., 1953] was proposed and successfully performed an anastomosis operation between the bottom of the diverticulum and the thoracic esophagus by transpleural left-sided access to the IV intercostal space.

Diverticula of the midthoracic esophagus are much less common than in other areas. They are commonly referred to as traction diverticula because they form due to tension in the esophageal wall. Diverticula usually develop against the bifurcation of the trachea or the left main bronchus. Due to inflammation of the lymph glands, adhesions are formed, which are stretched for three swallows, dragging the wall of the esophagus with them. Traction diverticula are small and fill quickly and empty quickly. Their diameter is rarely more than 2 cm, they are rarely accompanied by severe clinical symptoms. Very rarely, there are complications in the form of mediastinal abscesses and esophago-bronchial fistulas, as well as, extremely rarely, partial obstruction of the esophagus. The presence of esophagitis in a patient threatens the development of an ulcer in the diverticulum, followed by perforation and the development of mediastinitis.

Epiphrenal diverticula are localized in the distal esophagus. They are sometimes called supradiaphragmatic. According to the classification, they are classified as pulsation-traction, but the elements of traction are not always visible. Almost half of patients with this type of diverticulum suffer from cardiospasm or diffuse spasm of the esophagus. With diverticula, as a rule, hypertrophy of the muscles of the lower esophagus is found.

Clinic. Compared with diverticula of the upper esophagus, epiphrenic diverticula are less often accompanied by clinical symptoms, and sometimes they are completely absent. The diagnosis is usually made on the basis of an X-ray examination. On fluoroscopy, diverticula look like a rounded depot of barium, located 2-4 cm in diameter, its neck is wide and short. Small diverticula are sometimes difficult to differentiate from an ulcer, so the diagnosis must be confirmed by esophagoscopy. If the diverticulum is causing the dysphagia, or severe pain, or esophagitis, surgical treatment is indicated.

Tumors.

Benign tumors of the esophagus are much less common than malignant ones, accounting for 0.5-0.8% of their number. They occur at a younger age, grow for a long time and end with obstruction of the esophagus. Tumors can arise from any tissue of the esophageal wall - muscular, epithelial, and others.

According to the structure of the tumor are divided into two groups: 1) epithelial tumors: cysts, papillomas, polyps; 2) non-epithelial: leiomyomas, fibromas, lipomas, etc.

According to the type of growth, they are divided into intraluminal and intraparietal. Intraluminal tumors are more common in the upper esophagus, intramural in the lower esophagus. The most common leiomyoma, which in 90% of cases is localized in the lower third of the esophagus. Multiple leiomyomas are very rare. Symptoms are determined by the size of the tumor, its ability to compress the lumen of the esophagus and neighboring organs. Most common symptom is dysphagia. It appears with the use of solid food and progresses slowly over several years. Dysphagia is intermittent in nature, more often appears with circular tumors on the leg, hanging down into the lumen of the esophagus. With tumors of large sizes, pushing back other organs of the mediastinum, the main symptom is pain. The pain is localized behind the sternum or in the epigastric region, radiates to the back and shoulder blade, but is never pronounced. The symptoms of compression also include cough, shortness of breath, palpitations, arrhythmia. The main role in the diagnosis is played by X-ray examination. The esophagus in the area of ​​the tumor is expanded, there is a filling defect with even contours. The shadow of the tumor may shift when swallowing. The mucous membrane above the tumor is flattened, and on the opposite side it has a normal structure. Sometimes calcium inclusions can be seen in the tumor. With esophagoscopy, the mobility of the tumor is determined. If ulceration is found during examination of the mucosa, then a biopsy should be taken to clarify the nature of the disease. Treatment of leiomyomas is only surgical. Removal of the tumor is the prevention of complications such as asphyxia, bleeding, perforation of the wall. Access is determined by the location of the tumor. When the tumor is located in the upper or middle third of the esophagus, it is preferable to use right-sided access in the 5th or 6th intercostal space. When the tumor is localized in the lower third of the esophagus, it is better to use left-sided access in the 7th or 8th intercostal space. Some of the tumors located in the lower third of the esophagus can be removed by laparotomy, but this is technically more difficult to do. Malignant degeneration occurs rarely, so the tumor can be removed by evacuation after splitting the outer muscle layer over the tumor without damaging the mucous membrane. Exfoliation fails with large multinodular tumors closely associated with the muscular and mucous membranes of the esophagus. In these cases, one has to resort to partial excision of the esophageal wall with suturing or resection. The removed leiomyoma is a whitish tumor of a smooth consistency, covered on the outside with a capsule. Microscopically, it looks like smooth muscle cells with identical nuclei and the absence of mitotic division.

In second place in frequency are cysts. They are acquired (retention) and congenital (bronchogenic or enterogenic). Retentions are formed due to blockage of the glands of the esophagus and are located in the submucosal layer. They usually do not reach large sizes. Bronchogenic cysts are rounded and filled with light viscous. liquid, from the inside lined with ciliated epithelium.

Polyps of the esophagus occur with the same frequency as cysts. The tumor originates from the mucous or submucosal layer, covered with a normal mucous membrane. Polyps can be located at any level of the esophagus and are possible cause obstruction, regurgitation and even asphyxia. Esophagoscopy shows smooth masses in the lumen of the esophagus without ulceration of the mucosa. Some polyps can be removed during endoscopy.

Vascular tumors, hemangiomas, are also rare, their size can vary from a few millimeters to several centimeters. They are usually asymptomatic, but can sometimes cause bleeding. Lymphanginomas are also rarely observed and asymptomatic, the diagnosis of which can be made with esophagoscopy. There are very rare reports of fibromas, myxomas, myoblastomas, osteochondromatosis, papillomatosis of the esophagus. Diagnosis is usually made by histological examination.

Burn cicatricial stricture of the esophagus.

Acetic acid damage is second only to caustic soda. Especially dangerous is 70% vinegar essence. The scarring process occurs during the first 3-6 weeks (1.5 months). Periesophagitis and mediastinitis can join directly to the primary damage to the esophagus, but can also occur later when the esophagus is injured by bougies. Such complications may be latent at first. It is indicated by a moderate increase in temperature, an acceleration of ESR. Symptoms are aggravated by the formation of an abscess, its breakthrough into the pleural or abdominal cavity.

With 1 degree of burn - the mucous membrane is affected; 2 tbsp. - submucosal layer; 3 art. - all layers. Stenosis occurs only at grade 3. From the second week, acute inflammatory phenomena are replaced by ulceration. At 3 st. from the end of 2-3 weeks, the granulation stage begins.

Of primary importance in the diagnosis of cicatricial narrowing of the esophagus are X-ray examination and fibroesophagoscopy, which allow you to determine the degree of narrowing, localization, extent and nature of changes in the wall of the esophagus.

The diagnosis of a burn of the esophagus is established only after esophagoscopy (at admission or on days 3-5). If after three weeks epithelization appears, then a burn of 2 tbsp. may or may not be bogus.

Burn 3 tbsp. found only in 30% of children.

The method of early prophylactic bougienage is considered optimal in cases of moderate severity when carried out from 6 to 10 days. It is believed that bougienage should be performed no earlier than 7 weeks.

Complications with "blind bougienage" occur in 12% of patients.

It is generally accepted that bougienage should be performed by the same doctor in order to avoid perforation. Treatment should begin with bougienage along a metal guide wire with hollow bougie under local anesthesia. With forced bougienage under anesthesia, the esophagus should be intubated with a tube with a diameter of 11-13 mm and left for a period of 2-4 weeks.

There are the following dangers and complications during bougienage:

Aggravation inflammatory process after bougienage.

Obstruction of the narrowed esophagus

Damage to the esophagus (during bougienage, tears, cracks occur and the attached infection can penetrate the wall of the esophagus, sometimes it passes to the periesophageal tissue and causes mediastinitis with the subsequent development of a septic condition. This is the so-called spontaneous perforation after bougienage).

Perforation of the esophagus. It is facilitated by the presence of pockets in the cicatricial esophagus. Perforation during bougienage is one of the most common causes death after chemical burns of the esophagus.

With perforation above the diaphragm, the place of perforation is located on the right. Short annular strictures are prone to cure, while multiple strictures and total tubular strictures, on the contrary, often recur, when they have to use “by the string” bougienage through the gastrostomy.

According to our research, the tactics of bougienage made it possible to achieve good results in 84% of cases, satisfactory - in 6.3%, unsatisfactory results were 8.7%.

If bougienage fails, they resort to surgical treatment - esophagoplasty, replacing the esophagus with segments of the small, large intestines or stomach.

1. Definition
2. Introduction and main points
3. Disease manifestation and epidemiology
4. Causes of dysphagia
5. Clinical diagnostics
6. Choice of treatment
7. Literary references
8. Useful Websites
9. Reader comments and feedback

1. Definition

Dysphagia is defined as a difficulty for a person to start swallowing (commonly defined as oropharyngeal dysphagia) or as a sensation of obstruction in the passage of food or liquid from the mouth to the stomach (commonly defined as esophageal dysphagia).

Dysphagia is thus the sensation of having an obstruction to the normal passage of ingested food.

2. Introduction and main points

Fundoplication

Infectious esophagitis

Antibiotics (nystatin, acyclovir)

Absent

Pharyngoesophageal

(Zenker's) diverticulum

Absent

Endoscopic or external (traditional) recovery after crico-pharyngeal myotomy

Ring of Shatsky

soft food

Dilatation

6.2.1. Peptic stricture

Peptic stricture is usually the result of gastroesophageal reflux disease (GERD) and may be caused by certain medications.

At differential diagnosis must be excluded:

• caustic stricture after ingestion of a corrosive substance
• stricture caused by drug
• postoperative stricture
• fungal stricture

After confirmatory endoscopy, dilation is the method of choice, and its methodology is given below.

Esophageal strictures should be dilated in a vigorous manner with Savary elastic bougies or balloons. The choice of the type of dilator should be based on the experience of using it at the given institute and the experience of the operator, as well as the convenience of its use, since the literature does not make it possible to determine the advantage of one type of dilator over another.

If dilatation is performed with bougies, the diameter of the first bougie should be approximately equal to the identified diameter of the stricture. The increase in the diameter of the inserted bougies is carried out until the moment when the resistance to insertion reaches the value at the first introduction, after which two more subsequent bougies can be additionally inserted during one procedure. If a balloon dilator is used, the initial dilatation should be limited to a diameter of no more than 45F. The degree of initial dilatation of the stricture does not appear to affect either recurrence or the need for re-dilation, so the concept of aggressive dilatation to prevent recurrence finds little support. The degree of dilation in each patient should be based on the response of the patient to the treatment and the difficulties that arise in the implementation of dilation. Experience shows that in most patients, good relief of dysphagia is achieved with a diameter between 40F and 45F. Strictures should generally not expand to a diameter greater than 60F.

Vigorous antireflux therapy with proton pump inhibitors or fundoplication improves dysphagia and reduces the need for subsequent esophageal dilatation in patients with peptic esophageal strictures. In patients with persistent dysphagia or in cases of relapse of the disease after first dilation and antireflux therapy, endoscopic confirmation of the cure of reflux esophagitis should be performed before re-dilatation. In case of receipt positive effect treatment, the need for subsequent dilation is decided empirically. Patients who experience only short-term relief after dilatation can be taught self-boosting techniques. In the presence of refractory strictures, an attempt to introduce hormones into the strictures may be considered. Rarely, true refractory strictures require esophageal resection and reconstruction. In exceptional cases, in the presence of benign strictures, endoluminal prosthetics may be recommended (17). The risk of perforation is about 0.5%. In cases of obvious perforation, there are usually indications for surgical treatment.

Below is an algorithm for choosing a treatment method.

Medical therapy nitrates or calcium channel blockers are often ineffective or poorly tolerated. Botulinum toxin injections may be used as initial therapy in patients at low risk for surgery when there is suspicion that drug therapy or bougienage will be poorly tolerated by them. Botulinum toxin injections are a safe procedure that can induce remission for at least 6 months in about 2/3 of achalasia patients. However, most patients will need repeat injections to maintain remission, and only 2/3 of patients in remission at 6 months will go into remission for up to 1 year despite repeated injections of the toxin. When this type of treatment fails, the clinician and patient must decide whether the benefits of pneumatic dilatation or myotomy outweigh the risks in elderly or debilitated patients. A feeding gastrostomy is a safe alternative to pneumatic dilatation and myotomy, but many neurologically intact patients find life with a gastrostomy unacceptable.

7. References

1. Dysphagia - ABC of the upper gastrointestinal tract. William Owen BMJ 2001;323:850-853 Pubmed-Medline
2. A Technical Review on Treatment of Patients with Dysphagia caused by benign disorders of the distal esophagus Gastroenterology. 1999 Jul; 117(1): 233-54. PubmedMedline
3. Oesophageal motility disorders Joel E Richter The Lancet ; 8 September 2001; 358/9284;823-828. PubmedMedline
4. Current concepts expandable metal stents for the treatment of cancerous obstruction of the gastrointestinal tract Baron Todd H New England Journal of Medicine; 2001 31 May; 344(22);1681-1687 Pubmed-Medline
5. Plummer-Vinson syndrome Atmatzidis-K, Papaziogas-B, Pavlidis-T, Mirelis-Ch, Papaziogas-T. Diseases of the Esophagus 2003, 16/2 (154-157) Pubmed-Medline
6. Dysphagia in patients with nasopharyngeal cancer after radiation therapy: A videofluoroscopic swallowing study. Chang-Y-C, Chen-S-Y, Lui-L-T, Wang-T-G, Wang-T-C, Hsiao-T-Y, Li-Y-W, Lien-I-N. DYSPHAGIA, 2003, Vol/Iss/Pg. 18/2 (135-143). PubmedMedline
7. Morphological findings in dynamic swallowing studies of symptomatic patients. Scharitzer-M, Pokieser-P, Schober-E, Schima-W, Eisenhuber-E, Stadler-A, Memarsadeghi-M, Partik-B, Lechner-G, Ekberg-O. M. Scharitzer European Radiology EUR-RADIOL, 01 MAY 2002, 12/5 1139-1144). PubmedMedline
8. Visualization of swallowing using real-time true FISP MR fluoroscopy. Barkhausen-J, Goyen-M, von-Winterfeld-F, Lauenstein-T, Debatin-J-F European Radiology 01 JAN 2002, 12/1 (129-133). PubmedMedline
9. Early assessments of dysphagia and aspiration risk in acute stroke patients. Ramsey-D-J-C, Smithard-D-G, Kalra-L. Stroke 01 MAY 2003, 34/5(1252-1257). PubmedMedline
10. Real-time remote telefluoroscopic assessment of patients with dysphagia. Perlman-A-L, Witthawaskul-W. Dysphagia 2002, 17/2(162-167). PubmedMedline
11. Videofluoroscopic studies of swallowing dysfunction and the relative risk of pneumonia. Pikus-L, Levine-M-S, Yang-Y-X, Rubesin-S-E, Katzka-D-A, Laufer-I, Gefter-W American Journal of Roentgenology 01 JUN 2003, 180/6 (1613-1616). PubmedMedline
12. Tolerance of early diet textures as indicators of recovery from dysphagia after stroke. Wilkinson-T-J, Thomas-K, MacGregor-S, Tillard-G, Wyles-C, Sainsbury-R. Dysphagia, 2002, 17/3(227-232). PubmedMedline
13. Effect of citric acid and citric acid-sucrose mixtures on swallowing in neurogenic oropharyngeal dysphagia. Pelletier-C-A, Lawless-H-T. Dysphagia 2003, 18/4(231-241). PubmedMedline
14. Aspiration pneumonia and dysphagia in the elderly. Marik-P-E, Kaplan-D. Chest 01 JUL 2003, 124/1(328-336). PubmedMedline
15. Predictors of Feeding Gastrostomy Tube Removal in Stroke Patients With Dysphagia. Ickenstein-G-W, Kelly-P-J, Furie-K-L, Ambrosi-D, Rallis-N, Goldstein-R, Horick-N, Stein-J. Journal of Stroke and Cerebrovascular Diseases 2003, 12/4 (169-174).
16. Quality of life following surgical treatment of oculopharyngeal syndrome. Gervais-M, Dorion-D. Journal of Otolaryngology 2003, 32/1(1-5). PubmedMedline
17. Relapsing cardial stenosis after laparoscopic Nissen treated by esophageal stenting. Pouderoux-P, Verdier-E, Courtial-P, Bapin-C, Deixonne-B, Balmes-J-L. Dysphagia 2003, 18/3 (218-222) Pubmed-Medline

8. Useful websites

1. Medical Position Statement on the Management of Oropharyngeal Dysphagia; Gastroenterology 1999; 116; 452-478 Link
2. Diagnosis and Management of Achalasia. practice guidelines. The American Journal of Gastroenterology; 1999; 94/12;3406-3412. Link
3. ACR Appropriateness Criteria for imaging recommendations for patients with dysphagia - Radiology 2000 June; 215 (suppl) 225-230. Link
4. management of patients with stroke; III Identification and management of Dysphagia ; SIGN Guideline No. 20; pilot edition november 1997; Link
5. Diagnosis and treatment of swallowing disorders (dysphagia) in acute care stroke patients. (ACHPR-99-E023. Rockville: AHCPR, 1999). Link
6. M. Louay Omran, Dysphagia. Link
7. Clinical Use of esophageal manometry; AGA Medical Position Statement; reviewed 2001. Link
8. Practice guidelines for preoperative fasting and the use of pharmacological agents to reduce the risk of pulmonary aspiration. American Society of Anesthesiologists Anesthesiology 1999 Mar;90(3):896-905. Link

9. Reader comments and feedback

Invitation to comment

The Guidelines Drafting Committee welcomes comments and suggestions from readers. If you think that some aspects of the problem are not covered enough, if you have good experience in solving these problems, then share it with the authors of the guide. Together we can make it even better!