Main questions of the topic.

1. Etiology and pathogenesis of diabetes.

2. Classification.

3. Diabetes clinic.

4. diagnostic methods.

5. Emergency medical care, including during the evacuation stages.

6. Correction of homeostasis disorders.

7. Indications and principles surgical treatment.

Dysphagia syndrome (impaired swallowing) is characteristic of all stenotic 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 motor function disorders that are accompanied by clinical symptoms, while 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 food transport is a reflex act. The vagus nerve carries out 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 displace the bolus of food down the esophagus. As the wave of contraction approaches, the esophagogastric 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 sections of the gastrointestinal tract, basal pressure is positive and much higher than atmospheric pressure. The sphincters separate the low pressure in the esophagus from the pressure in the pharynx and stomach. High pressure zones in the sphincters prevent air and saliva from entering the esophagus from the pharynx and gastric contents. 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.

Impaired motor activity.

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

The following diseases most often cause it: muscular dystrophy, myasthenia gravis, dermatomyositis. Swallowing disorders also occur with pharyngoesophageal diverticula. In this case, the normal relationship between contraction of the pharynx and contraction and relaxation of the pharyngoesophageal sphincter is disrupted. In these patients, contraction of the sphincter occurs before the contraction of the pharynx ends.

Pathology of the lower sphincter.

Esophageal achalasia (cardiospasm) is a disease of unknown etiology, characterized by the absence of esophageal peristalsis and disruption of the activity of the lower esophageal sphincter, which does not relax when swallowing. The incidence of achalasia ranges from 5 to 10% of all esophageal diseases. 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 plexus ganglion cells in the wall of the esophagus. Changes are detected at any level thoracic esophagus. Not only is the cause of ganglion cell damage unknown, but also at what level of the nervous system the primary disturbances occur.

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 underdevelopment of the intramural nerve plexus.

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

Pathological changes depend on the duration and stage of the disease. IN late stages the esophagus is expanded and elongated, the walls are thickened due to a sharp hypertrophy of the muscular layer of the esophagus. Inflammatory changes are observed in the mucous and submucosal membranes: first, hypertrophy of muscle fibers occurs, which are then replaced by connective tissue. In the intramural nerve plexus, phenomena of dystrophy are detected, in nerve cells - dissolution or wrinkling of protoplasm.

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

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

Stage 1. The patient's condition is satisfactory. Patients experience food retention, which is difficult to pass. Evacuation from the esophagus, although slow, is complete; regurgitation is not observed.

Stage 2. Along with more severe dysphagia, pressing pain appears behind the sternum. In the esophagus, increased peristalsis and antiperistalsis are observed, food masses are retained, and regurgitation is inconsistent. The diameter of the esophagus and cardia narrows somewhat.

In stage 3, organic changes appear in the esophagus in the form of a fibrous-scarring 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 peristalsis disorder, with segmental spasms and antiperistalsis. Patients experience weight loss and impaired ability to work.

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

Achalasia is characterized by a slow course with a gradual long-term 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 slight dilatation of the proximal part. As the disease progresses, characteristic radiographic signs appear. The esophagus is dilated, in the lower section it is conically narrowed over a short distance with a beak-shaped expansion in place of the narrowed segment. Although the X-ray picture of cardiospasm is quite characteristic, it is still necessary to differentiate it from cancer in the early stages of the disease, especially in people over 50 years of age.

Esophagoscopy has the greatest benefit in this. Confirmation of the clinical manifestations of the disease is the study of the motor function of the esophagus. Low pressure is detected in the esophagus with dilatation of its lumen and lack of peristalsis in the esophagus after swallowing. When swallowing, pressure rises throughout the entire esophagus. With achalasia, the esophageal sphincter does not open during the act of swallowing. In some patients, impaired peristalsis develops into diffuse spasm of the esophagus or repeated strong spasms occur in response to the act of swallowing.

Treatment. The disturbance of esophageal peristalsis that characterizes esophageal achalasia is difficult to treat with medication. Relief of the symptoms of the disease can be achieved by using a gentle diet, antispastic agents, vitamins, and sedatives. However, such therapy usually provides 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 they are the safest.

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 out, thus expanding the lumen of the esophagus. According to B.V. Petrovsky, ruptures of the mucous membrane or wall of the esophagus are observed when using an elastic dilator in 1% of cases, when using a mechanical one in 6%. In 80% of cases, dilation is successful and relieves the patient from the painful symptoms of the disease.

If there is no effect from dilatation, surgical treatment is used. Many operations have been proposed, including vagotomy, vagolysis, sympathectomy, transgastric retrograde dilation of the cardia, and esophagofundal anastomosis. Modern surgery is based on the proposal of Heller, who first performed bilateral cardiomyotomy in 1913. It consists of a longitudinal dissection muscle layers distal esophagus via transpleural access. The mucous membrane protruding through the incisions is covered with a flap of the omentum. Sometimes only 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 and, 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 excision of the muscular lining of the esophagus with a pedicled 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 using an abdominal approach.

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 esophageal spasm is extremely rare.

Clinically, this disease differs from achalasia in that pain occurs earlier, while dysphagia is rare or does not occur at all. The intensity of pain varies from a slight feeling of discomfort in the chest to severe pain radiating to the back and neck, similar to pain in the heart. The pain can occur while eating, but also at night when patients wake up from it. They are more pronounced in patients with an unstable nervous system. During attacks, despite the intensity of the pain, the disease does not seem severe.

Radiological signs are detected in less than half of the cases. The esophagus looks twisted in the form of a corkscrew, giving the impression of pseudodiverticulosis, and there are signs of muscle hypertrophy. Often these phenomena are combined with diaphragmatic hernia or epiphrenic diverticulum. The diagnosis is confirmed by studying the motor ability of the esophagus and its peristalsis. Peristaltic distortion is usually found in the lower half or lower third of the esophagus, where several peristaltic waves are detected simultaneously, continuously repeating. In most patients, the activity of the sphincter is not impaired, with the exception of the gastroesophageal sphincter, where the pressure increases to 140 cm of water column. In very severe cases of this disease, it is sometimes necessary to use a modified Geller operation. Before surgery, it is necessary to examine the patient to exclude other diseases. Muscle dissection must be carried out over a large area from the cardia to the aortic arch. If a diverticulum is present, 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 necessary.

Hypotension of the lower esophageal sphincter.

The slogan “The 20th century is the century of peptic ulcer disease, the 21st century is the century of gastroesophageal reflux disease” (GERD). Reflux esophagitis (RE) was first mentioned by Hunter (1786).

Definition: GERD is a clinical symptom complex that occurs as a result of the reflux of stomach contents into the esophagus.

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

Etiology and pathogenesis: the leading place in the pathogenesis is occupied by dysfunction of the antireflux barrier, which can occur as a result of a primary decrease in the tone of the lower esophageal sphincter (LES, normally 15-35 mm Hg). If the pressure in the lower esophageal sphincter is less than 12 cm of water, gastroesophageal reflux may occur. Increase in the number of spontaneous relaxations of the LES, structural changes LES (hiatal hernia - hiatal hernia); decrease in chemical, volumetric and esophageal clearance (reduction in the neutralizing effect of saliva and bicarbonates of esophageal mucus, inhibition and weakening of esophageal peristalsis, the ability to remove contents back into the stomach). Very high intra-abdominal pressure is also important. The causes are sphincter surgeries and collagen diseases such as scleroderma.

Other pathogenic factors are the damaging effect of refluxant, decreased resistance of the esophageal mucosa, impaired gastric emptying, and increased intra-abdominal pressure. Forced body position, smoking, alcohol.

Classification: There are 4 degrees of severity (Savari-Miller) EC: 1 – catarrhal esophagitis, less than 10% erosion of the distal esophagus; 2 – 50% of drainage erosion; 3 – circular erosion of almost the entire surface of the esophagus; 4 – peptic ulcer and stricture of the esophagus, 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 xiphoid process. External esophageal symptoms include pain, sometimes resembling angina, persistent cough, and dysphonia.

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

Diagnostics: The endoscopic method remains the “gold standard”. Endoscopic ultrasonography, which allows assessing the condition of the submucosal layer; histological examination; manometry (determining a decrease in the LES, hiatal hernia, 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 (determining the total number of refluxes, normally no more than 50 times a day); X-ray examination; bilimetry (identification of bile reflux) ; scintigraphy (clarification of the motor function of the esophagus); omeprazole test (significant reduction in the clinical symptoms of ER with daily intake of 40 mg of omeprazole) There is no direct connection between the hiatus and the esophagus.

Differential diagnosis: Cardiac syndrome of unknown origin, dysphagia, gastrointestinal 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, alcohol and carbonated drinks, giving up spicy and hot foods, sour fruit nipples, onions, garlic, pepper, fats, chocolate; last meal at 6 p.m.; raising the head of the bed by 15-20cm; refraining from stress associated with bending the body.

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) in Lately gave way to proton pump blockers (the most powerful antisecretory drugs) - omeprazole, lansoprozole.

Method surgical correction is a fundoplication combined 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 provided by the fundoplication developed by R. Nissen. In recent years, laparoscopic Nissen fundoplication has been developed. Indications: esophageal stricture, deep peptic ulcer, resistant to drug treatment.

Hiatus narrowing (OHN) is not necessary. With a short esophagus, the stomach cannot always be brought down into the abdominal cavity; in such cases, “mediastinilization” of the cardia is recommended, i.e. leave the fundoplication cuff in the posterior mediastinum.

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

It is currently noted that fundoplication in combination with SPV gives better results.

Thus, surgical treatment of patients with EC 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, careful study of the pathogenesis of the disease, immediate and long-term results of treatment, anti-reflux operations are now coming to the fore, taking into account, in addition to anatomical disorders, functional state esophagus, cardia, gastric secretion and motility, as well as the condition of other organs of the digestive system. With all this, the important question remains about the strict selection of patients for surgery, and therefore the correct conservative treatment of these patients.

Esophageal diverticula.

Esophageal diverticula are sac-like protrusions from the lumen of the esophagus. They can be classified depending on location, type of development, and also on origin - whether they are true or false. Depending on their anatomical position, they are divided into pharyngoesophageal, mesothoracic and epiphrenal. 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 amount of muscle tissue or none at all.

Pharyngoesophageal diverticula. Pulse diverticula of the esophagus develop due to increased pressure in the lumen of the esophagus. Pulsion diverticula include the Zenker diverticulum, located near the pharyngeal esophageal junction. This diverticulum is not truly esophageal because it is located 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 cricopharyngeus muscle. With normal neuromuscular coordination, the cricopharyngeal muscles relax as food passes from the larynx into the esophagus and the constrictor contracts. With impaired neuromuscular coordination, compression of the constrictor and non-relaxation of the cricopharyngeal muscles, protrusion of the posterior wall of the pharyngeal fossa appears. If this disorder is not eliminated, then the protrusion soon turns into a sac-like defect, and in the intermuscular space only the mucous and submucosal layers with very sparse muscle fibers bulge. There are several points of view on the occurrence of this diverticulum, however, the above is the most common.

Another reason could be chronic pharyngitis, which disrupts the normal relaxation of the sphincter and causes the formation of a protrusion. A possible reason may also be a wider anteroposterior diameter of the pharynx in men than in women, which causes higher pressure, which is indirectly confirmed by the frequent findings of diverticulum in men. Reflux esophagitis in hiatal hernia may also play an etiological role. At the stage of diverticulum formation, its sac, consisting of the mucous and submucosal membranes, is localized first on the posterior wall, then, as it grows, it shifts to the left. In the early stages 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 sac, the inlet remains small.

Men get sick three times more often than women. The overall incidence is 0.1%. In old age, weakening of the pharyngeal muscles may 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 occurs. In the third, symptoms of compression of the esophagus appear.

In most cases, symptoms increase gradually. Initially, patients experience irritation in the throat, drooling and a feeling of a foreign body when swallowing. Swallowing problems may occur even when drinking liquid. Sometimes there is a dry cough. As the diverticulum enlarges, regurgitation appears, especially at night, after a large meal or undigested food. With the onset of regurgitation, pulmonary complications may occur as a result of aspiration of the contents of the diverticulum. Sooner or later, obstruction of the esophagus occurs, which in rare cases is complete. Exhaustion and weight loss occur. Sometimes you can see bulging and swelling on the left side of the neck, but this is very rare. Symptoms in some cases develop quickly, over several months, sometimes over 10-15 years. The diagnosis is usually made by fluoroscopy with barium, sometimes without barium, if the level of fluid in the retrotracheal space can be seen. Fluoroscopy can determine the diameter of the diverticulum neck. Stagnation of food is observed in large diverticula, which is sometimes taken as a filling defect. For 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, as well as water after meals, but a cure can only be achieved with surgical treatment. Expansion of the lumen of the esophagus due to compression by a diverticulum is not recommended due to the risk of perforation of the diverticulum wall. Early surgery is necessary due to the risk of infection, mediastinitis, and pneumonia.

There are several methods of operation. One-stage resection of the diverticulum is most widespread. A skin incision is made along the anterior edge of the sternocleidomastial muscle. The diverticulum is exposed by retracting 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 laryngeal mucosa is sutured with separate interrupted sutures. The edges of the muscle layer are also carefully sutured. The operation does not pose any particular risk, and relapses are rare. For small diverticula, cricopharyngeal myotomy is suggested. The access is the same; an additional longitudinal incision is made through the cricopharyngeal muscles, 3-4 cm long. The rationale for this operation is the opinion that the origin of the diverticulum is due to discoordination of the pharyngeal-esophageal sphincter mechanism. Sometimes esophagoscopy is used to facilitate the search for a diverticulum and control the placement of sutures on the wall to avoid narrowing of the lumen of the esophagus.

For large border pharyngoesophageal diverticula, an operation of anastomosis between the bottom of the diverticulum and the thoracic esophagus using transpleural left-sided access in the fourth intercostal space was proposed [B. A. Korolev, 1953] and was successfully performed.

Diverticula of the midthoracic esophagus are much less common than in other areas. They are commonly called traction diverticula because they form due to tension on the wall of the esophagus. Typically, diverticula develop against the bifurcation of the trachea or left main bronchus. Due to inflammation of the lymph glands, adhesions are formed that stretch during swallowing, dragging the wall of the esophagus with them. Traction diverticula, when small in size, quickly fill and quickly empty. Their diameter is rarely more than 2 cm, and they are rarely accompanied by severe clinical symptoms. Complications in the form of mediastinal abscesses and esophago-bronchial fistulas are very rare, and partial obstruction of the esophagus is extremely rare. The presence of esophagitis in a patient threatens the development of an ulcer in the diverticulum, followed by perforation and the development of mediastinitis.

Epiphrenic diverticula are localized in the distal esophagus. They are sometimes called supradiphragmatic. 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. Diagnosis is usually made based on 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 ulcers, so the diagnosis must be confirmed by esophagoscopy. If the diverticulum is causing 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 appear at a younger age, grow over a long period of time and end with obstruction of the esophagus. Tumors can arise from any tissue of the esophageal wall - muscle, epithelial and others.

Based on their structure, tumors 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 intramural. Intraluminal tumors are more common in the upper part of the esophagus, intramural in the lower parts. The most common is 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 and its ability to compress the lumen of the esophagus and neighboring organs. The most common symptom is dysphagia. It appears when eating solid foods and progresses slowly over several years. Dysphagia is intermittent in nature, most often appearing with circular tumors on the stalk, hanging into the lumen of the esophagus. For large tumors that displace other organs of the mediastinum, the main symptom is pain. The pain is localized behind the sternum or in the epigastric region, radiating to the back and shoulder blade, but is never pronounced. Symptoms of compression also include cough, shortness of breath, palpitations, and arrhythmia. X-ray examination plays the main role in diagnosis. The esophagus in the area of ​​the tumor is dilated, there is a filling defect with smooth 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 normal structure. Sometimes you can see calcium inclusions in the tumor. Esophagoscopy determines the mobility of the tumor. If upon examination of the mucous membrane ulcerations are detected, then to clarify the nature of the disease it is necessary to take a biopsy. Treatment for leiomyomas is only surgical. Removal of the tumor prevents complications such as asphyxia, bleeding, and wall perforation. Access is determined by the location of the tumor. If the tumor is located in the upper or middle third of the esophagus, it is preferable to use a right-sided approach in the 5th or 6th intercostal spaces. If the tumor is localized in the lower third of the esophagus, it is better to use a left-sided approach in the 7th or 8th intercostal spaces. Some tumors located in the lower third of the esophagus can be removed during laparotomy, but this is technically more difficult. 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. Enucleation is not successful in large multinodular tumors that are closely associated with the muscular and mucous membranes of the esophagus. In these cases, it is necessary to resort to partial excision of the esophageal wall with suturing or resection. The removed leiomyoma is a whitish tumor with 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.

Cysts are the second most common type. They are acquired (retention) and congenital (bronchogenic or enterogenic). Retention 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 round and filled with light viscous material. liquid, lined from the inside with ciliated epithelium.

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

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

Burn scar stricture of the esophagus.

Damage caused by acetic acid is second only to caustic soda. 70% vinegar essence is especially dangerous. The scarring process occurs during the first 3-6 weeks (1.5 months). Periesophagitis and mediastinitis can join directly to the primary injury to the esophagus, but can also occur subsequently when the esophagus is injured by bougies. Such complications may initially occur hidden. It is indicated by a moderate increase in temperature and acceleration of ESR. Symptoms intensify when an abscess forms and breaks through into the pleural or abdominal cavities.

With 1st degree burn, the mucous membrane is affected; 2 tbsp. – submucosal layer; 3 tbsp. – all layers. Stenosis occurs only in grade 3. From the second week, acute inflammatory phenomena give way to ulceration. At 3st. 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 make it possible to establish 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 (upon admission or on days 3-5). If epithelization appears after three weeks, then the burn is 2 tbsp. You don't have to bougie.

Burn 3rd degree. detected only in 30% of children.

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

Complications during “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 using a metal conductor string with hollow bougies under local anesthesia. When forced bougienage under anesthesia, the esophagus should be intubated with a tube with a diameter of 11-13 mm and left for 2-4 weeks.

There are the following dangers and complications during bougienage:

Exacerbation of the inflammatory process after bougienage.

Obturation of the narrowed esophagus

Damage to the esophagus (during bougienage, tears, cracks occur, and an associated infection can penetrate the wall of the esophagus, sometimes it spreads to the peri-esophageal 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 scarred esophagus. Perforation during bougienage is one of the most common causes of death after chemical burns of the esophagus.

With perforation above the diaphragm, the perforation site is located on the right. Short annular strictures tend to be cured, but multiple strictures and total tubular strictures, on the contrary, often recur, requiring the use of bougienage “by a thread” through a gastrostomy.

According to our research, bougienage tactics allowed us to achieve good results in 84% of cases, satisfactory results in 6.3%, and unsatisfactory results in 8.7%.

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

Introductory part

1. Lesson topic: Dysphagia syndrome

2. Purpose of the lesson: To study clinical issues and diagnostics of dysphagia syndrome.

3. Timed lesson plan:

1. Attendance control 3 minutes.

2. Oral knowledge test 35 minutes.

3. Work in the dressing room for 25 minutes.

4. Output control 10 minutes.

5. Summary of the next topic 7 minutes

4. Literature

Kuzin M.I. "Surgical diseases", 2005

Clinical surgery. A reference guide for doctors, ed. Y.M. Pantsyreva, 1988

Surgery. Guide for doctors and students, ed. Y.M. Lopukhina and V.S. Savelyeva, 1997

Shalimov A.A., Saenko V.F. Surgery of the digestive tract. 1987.

Main part

Materials for work in class

Dysphagia is a violation of the act of swallowing, which is caused by an organic or functional obstacle to the movement of food through the esophagus. The symptom is often defined as a feeling of something stuck in the throat. With dysphagia, the patient cannot swallow food, first solid and then liquid. Most often, the cause of dysphagia is narrowing of the esophagus due to a burn or any other cause, damage to the muscles involved in the act of swallowing, compression of the esophagus by a tumor or lymph nodes. Temporary dysphagia occurs in hysterical neurosis.

I Anatomy of the esophagus

The esophagus is a hollow cylindrical tube connecting the pharynx to the stomach and located at the C 6 -Th 11 level. The length of the esophagus is approximately 25 cm (from the pharynx to the cardia). Cervical region - 5 cm, thoracic region - 15 cm, cardiac region 3-4 cm.

1. Cervical region. In adults, it extends from the level of the cricoid cartilage (C6) to the jugular notch of the manubrium (Th2). Length about 5-8 cm.

2. Thoracic region - from the jugular notch of the manubrium of the sternum to the esophageal opening of the diaphragm (Th10). Its length is 15-18 cm. From a practical point of view, the following topography is advisable in the thoracic esophagus:

· Top part- to the aortic arch.

· The middle part corresponding to the aortic arch and tracheal bifurcation;

· Lower part - from the bifurcation of the trachea to the esophageal opening of the diaphragm.

3. Abdominal section. Length 2.5 - 3 cm. The transition of the esophagus to the stomach, as a rule, corresponds to Th11.

Structure:

1. The mucous membrane of the esophagus along its entire length is lined with stratified squamous epithelium (except for the distal sections, where the inner surface of the esophagus is covered with single-layer keratinizing epithelium). The mucous membrane in a free state forms longitudinal folds. They give the lumen of the esophagus the shape of an asterisk on a cross section.

2. The submucosa contains the choroid plexuses and mucous glands. This shell is constructed from loose connective tissue, and therefore the muscular and mucous membranes are loosely interconnected.

3. The muscular layer consists of outer (longitudinal) and inner (transverse) layers. In the upper third of the esophagus, the muscular layer is built from striated muscles, in the lower third - from smooth muscle cells.

4.The connective membrane consists of loose fibrous connective tissue.

Motor innervation:

Parasympathetic (vagus nerves) and sympathetic nerve fibers take part in it. The esophagus, stomach and intestines have their own nervous apparatus, consisting of nerve plexuses located in the submucosal (Meissner's plexus) and muscular (Auerbach's plexus) membranes.

Esophageal lumen:

The esophagus has the following physiological narrowings:

1. Upper - at the junction of the lower part of the pharynx into the esophagus (C6-C7). The upper esophageal sphincter is located here, a muscle that relaxes when swallowing.

2. Average - at the intersection with the left bronchus (Th4-Th5).

3. Lower - at the point where the esophagus passes through the opening of the diaphragm (Th10). The lower esophageal sphincter is located here, preventing acidic gastric contents from refluxing into the esophagus.

II Physiology of the esophagus

2. The upper esophageal sphincter relaxes during swallowing.

3. Peristalsis increases towards the lower esophagus.

4. The lower esophageal sphincter relaxes 1-2.5 seconds after a swallow. After the bolus of food passes into the stomach, the tone of the lower esophageal sphincter is restored and it closes.

Diseases of the esophagus accompanied by dysphagia:

Esophageal motility disorders

Esophageal diverticula

Congenital membrane diaphragm of the esophagus

Benign tumors of the esophagus

· Esophageal carcinoma

Post-burn esophageal stricture

Foreign bodies of the esophagus

Reflux esophagitis

Etiology and diagnosis of dysphagia

Etiological factors	Diagnostic criteria	Research methods
Malformations of the oral cavity and pharynx	In newborns and children under 3 years of age	Examination, passing a catheter through the nose, nasopharyngoscopy
Atresia, esophageal stenosis	History of polyhydramnios during the mother's pregnancy, increased salivation, belching, vomiting immediately after the first feeding	X-ray contrast study, esophagoscopy
Compression of the esophagus by abnormal vessels (double aortic arch, left-sided right subclavian artery)	Possible acrocyanosis, shortness of breath, cough	FES, aortography
Neurogenic disorders	Clinical symptoms of intracranial birth injury. In children over 3 years old	Ultrasound
Reflux esophagitis	Increasing anemia, constant vomiting, sometimes mixed with blood, heartburn, chest pain	FES
Foreign body of the esophagus	Pain and sensation of a lump behind the sternum	X-ray examination, esophagoscopy
Cicatricial strictures of the esophagus	History of burn (thermal, chemical) or injury to the esophagus	X-ray examination, FES
Volumetric processes in the mediastinum	Possible respiratory manifestations	X-ray tomography
Varicose veins of the esophagus	Splenomegaly, bloody vomiting, hemorrhoids, chronic liver diseases	FES, splenoportography
Achalasia cardia	Vomiting and belching of undigested food, pain in the sternum after the first sips of food	X-ray examination, FES
Neuromuscular disorders	History of diphtheria, encephalitis, etc.	- II -
Psychogenic factors Inflammatory processes in the oral cavity and pharynx	More often in girls there is a sensation of a lump behind the sternum (hysterical lump), which is often accompanied by vomiting History, clinical picture. Consultations with a dentist and ENT doctor	Rhino- and pharyngoscopy

Esophageal motility disorders

Achalasia cardia

Achalasia cardia is a neuromuscular disease of the entire smooth muscle of the esophagus, manifested by erratic peristalsis of the esophagus, impaired passage of food masses into the stomach, persistent impairment of the reflex opening of the lower esophageal sphincter during swallowing, and dysphagia.

With achalasia cardia, the tone and peristalsis of the entire esophagus changes. Instead of peristaltic contractions spreading to the stomach, non-propulsive (not providing passage) waves appear, and segmental contractions of the esophageal wall join them. Food lingers in the esophagus for a long time and enters the stomach due to the mechanical opening of the lower esophageal sphincter under the influence of the hydrostatic pressure of the liquid column above it. Long-term stagnation of food masses, saliva and mucus in the esophagus leads to a significant expansion of its lumen, the development of esophagitis and periesophagitis, which aggravates disturbances in esophageal peristalsis.

Clinic. Achalasia is characterized by a triad of symptoms: dysphagia, regurgitation, pain. Dysphagia is the main and in most cases the first symptom of the disease. In some cases it occurs suddenly in the midst of complete health, in others it develops gradually. Increased dysphagia in most patients is noted after nervous excitement, during a hasty meal, or when eating dense, dry and poorly chewed food. In a number of patients, the degree of dysphagia depends on the temperature of the food: warm food passes with difficulty or does not pass, but cold food passes.

Patients gradually find techniques to facilitate the passage of food into the stomach (walking, gymnastic exercises, swallowing air and saliva, drinking large amounts of warm water, etc.). With achalasia cardia, regurgitation occurs several hours after eating and is provoked by bending the body forward or horizontal position bodies. Motility of the esophagus is depressed, and segmental contractions are absent.

Regurgitation in the supine position and with a strong forward tilt of the body is caused by mechanical pressure of the contents of the esophagus on the pharyngoesophageal (upper esophageal) sphincter and its stretching. Nocturnal regurgitation is associated with some decrease in the tone of the upper esophageal sphincter. However, in most patients, pain occurs when the esophagus is full and disappears after regurgitation or passage of food into the stomach. Some patients experience attacks of spontaneous chest pain similar to pain crises.

Frequent complications of achalasia include repeated aspiration bronchopneumonia, lung abscesses, and pneumosclerosis. These complications are especially common in children.

Diagnostics. Radiologically, with achalasia cardia, the terminal section of the esophagus usually has a rounded shape, its narrowed part is often located eccentrically, and the symptom of overhang of the esophageal wall over the narrowing is characteristic. Anticholinergics do not act on the cardia, and the onset of esophageal emptying depends on the height of the barium suspension column and occurs with an increase in hydrostatic pressure (positive Hurst test).

Esophagoscopy reveals thickened folds of the mucous membrane, areas of hyperemia, erosion, and ulceration. As a rule, the end of the esophagoscope can be passed through the narrowed area, which confirms the predominantly functional nature of the changes. The mucous membrane at the site of narrowing is most often unchanged.

Esophagotonocymography is the main method for early diagnosis of achalasia, since disorders of the contractility of the esophagus and lower esophageal sphincter occur much earlier than the clinical symptoms of the disease. The study is carried out with a multichannel probe with rubber balloons or “open” catheters that record contractions of the esophagus and changes in intraesophageal pressure. Normally, after the act of swallowing, a peristaltic wave propagates through the esophagus, the lower esophageal sphincter opens at this moment and the pressure in the esophagus drops. After the peristaltic wave passes, the sphincter closes again. With achalasia cardia, there is no reflex relaxation of the lower esophageal sphincter during swallowing and intraluminal pressure remains unchanged.

In doubtful cases, pharmacological tests are used to confirm the diagnosis of achalasia. Nitroglycerin and amyl nitrite in patients with esophageal motility disorders reduce the tone of the muscular lining of the esophagus and the lower esophageal sphincter, which facilitates the passage of the contents of the esophagus into the stomach. Introduction of cholinotropic medicines(acetylcholine, carbacholine) has a stimulating effect on the muscular layer of the esophageal wall and on the lower esophageal sphincter. In case of cardioesophageal cancer and organic stenosis of the esophagus, both tests are negative.

Treatment. Conservative therapy for achalasia is used only in the initial stages of the disease, and is also used as an addition to cardiodilation and in preparing patients for surgical treatment. Food should be mechanically and thermally gentle. Meals are fractional, the last meal is 3-4 hours before bedtime.

Reducing dysphagia in stages I-II of the disease can be achieved by using nitro drugs, ganglion blockers, calcium antagonists - nifedipine (Corinthard, or phenigidine), etc. For esophagitis, rinsing the esophagus with a weak solution of antiseptics is used.

The main treatment method for achalasia is cardiodilation using a balloon pneumatic cardiodilator. It involves forcibly stretching a narrowed section of the esophagus. Cardiodilation can be performed at any stage of the disease. Contraindications to its use are portal hypertension with varicose veins of the esophagus, severe esophagitis, blood diseases accompanied by increased bleeding.

A pneumatic cardiodilator consists of a radiopaque rubber tube-probe, at the end of which a dumbbell-shaped balloon is attached. The pressure in the cylinder is created with a bulb and controlled with a pressure gauge. At the beginning of treatment, smaller dilators are used and a pressure of 180-200 mm Hg is created in them. Art., subsequently use cylinders of larger diameter and gradually increase the pressure in them to 300-320 mm Hg. Art. The duration of the esophageal stretching procedure is 30-60 seconds, the interval between sessions is 2-4 days. Recently, dilatation has been used for 2 days, repeating this procedure 5-6 times. Relapse occurs in 10% of patients. Typically, during stretching, patients experience moderate pain behind the sternum and in the epigastric region. After the procedure, patients are prescribed bed rest and fasting for 2-3 hours until the pain disappears.

Surgical treatment is carried out for the following indications: 1) impossibility of cardiodilation (especially in children); 2) lack of therapeutic effect from repeated courses of cardiodilation; 3) early diagnosed esophageal ruptures that occur during cardiodilation; 4) amotylic form (III-IV stage according to B.V. Petrovsky); 5) suspicion of esophageal cancer. 10-15% of patients with achalasia are subject to surgical treatment.

Currently, extramucosal cardiomyotomy is used, i.e. extramucosal Geller cardiotomy from the abdominal approach: the muscular membrane of the terminal esophagus is longitudinally dissected with a probe over an area of ​​8-10 cm. Geller cardiotomy is combined with Nissen fundoplication to prevent the development of peptic esophagitis. In 90% of patients, the results of the operation are good.

Cardiospasm

It is believed that during cardiospasm the parasympathetic part of the autonomic nervous system is affected, mainly the intramural apparatus - the Auerbach plexus, as well as the fibers of the vagus nerve. As a result of damage to the neuro-reflex arc, the opening reflex of the cardia is disrupted. It should be noted that a violation of the cardia opening reflex and a violation of esophageal motility are two processes that occur simultaneously.

The clinic of cardiospasm is very typical. The onset of cardiospasm is often sudden, whereas with achalasia cardia, patients more often note a gradual development of the disease. Often there is an indication in the anamnesis that the onset of symptoms is related to mental trauma or difficult experiences. Typically, patients complain of dysphagia, which usually lasts a long time. In the initial stages of cardiospasm, dysphagia is intermittent, i.e. periodically goes away completely and reappears under the influence of various emotional stress and stress. Sometimes dysphagia is paradoxical, i.e. liquid does not pass and solid food passes well. Often, in order to overcome the obstruction, patients are forced to wash down food with water and resort to repeated swallowing movements. Dysphagia usually worsens with excitement. Complaints of regurgitation of undigested food are very common. Regurgitation at night can lead to aspiration of the contents of the esophagus into the respiratory tract with the development of bronchitis and pneumonia. Many patients complain of pain after eating, which is bursting and radiates to the back. The pain is more acute on an empty stomach, which is associated with segmental spasms of the esophagus.

Diagnostics. Characteristic radiological signs of cardiospasm are expansion to varying degrees of the esophagus and the presence of a “narrow segment” in the area of ​​the physiological cardia. The walls of the esophagus, including the narrowed part, remain elastic. In the presence of esophagitis, the folds of the mucous membrane in the suprastenotic region are rough, granular, and with ulceration they have a spotty character. Periodically, at a certain column of barium, opening of the cardia and emptying of the esophagus occur, unrelated to the act of swallowing. The cardia at this time appears to be quite wide with preserved folds of the mucous membrane. This once again suggests that the narrowing in the cardia region is functional in nature. If an organic narrowing is detected in the area of ​​the cardia, this indicates the presence of another pathology: a tumor of the esophagus, peptic stricture, etc. For the differential diagnosis of functional and organic narrowing, it is advisable to use a test with nitroglycerin.

If there is the slightest doubt about the diagnosis, as well as in cases where X-ray examination suspects the presence of a tumor in combination with cardiospasm, esophagoscopy is indicated. If the instrument manages to reach the vestibulumgastroesophageale (and this is not always easy with an S-shaped esophagus) and passes through the cardia into the stomach, it becomes clear that we are talking about cardiospasm. With esophagomanometry, cardiospasm is characterized by a high esophagogastric pressure gradient of more than 20 mmHg. A paradoxical increase in pressure on the pharynx is also characteristic.

Treatment. The main method of treating cardiospasm is the expansion of the physiological cardia with a pneumatic cardiodilator. In this case, repeated dilatations can cause paresis of the vfstibulumgastroesophageale and thus reduce the pressure gradient in the cardia and restore passive passage of food. Dilatation with a metal Stark dilator is very dangerous and is currently rarely used.

The most severe complication of dilatation is esophageal rupture, which occurs in approximately 0.5-1% of patients. Such a patient should be operated on immediately, the esophageal rupture should be sutured with a double-row suture and the suture line should be covered with a pedicled diaphragm flap according to Petrovsky or the fundus of the stomach.

In cases where the disease relapses too quickly and repeated dilatations do not lead to persistent positive result, and if it is impossible to carry out a dilator, surgical intervention should be resorted to. Many previously widely used operations (anastomoses of the esophagus with the stomach according to the Heyrovsky method, etc.) have now been abandoned due to frequent relapses and often severe reflux esophagitis developing after surgery.

The best results are obtained by two operations - cardioplasty with a diaphragmatic flap according to Petrovsky and cardioplasty with the fundus of the stomach, although these interventions are also not free from complications.

Cardioplasty with a diaphragmatic flap according to Petrovsky is performed from the left-side transthoracic approach. A rectangular pedicle flap is cut out from the dome of the diaphragm without cutting the esophageal opening of the diaphragm. On the anterior surface of the esophagus and cardia, a T-shaped incision is made in the muscle layer to the submucosa. Cross section runs along the anterior semicircle 6-7 cm above the cardia. The vertical incision should be continued to the cardia of the stomach (Fig. 2). Then the muscular layer of the esophagus and the seromuscular layer of the stomach are peeled off to the sides, the cardia is expanded with a finger, screwing the stomach wall into the lumen of the esophagus. A prepared flap of the diaphragm is sewn into the resulting muscle defect. The hole in the diaphragm formed after cutting out the flap is sutured.

Cardioplasty of the fundus of the stomach. A thoracotomy is performed in the seventh intercostal space on the left. As with the previous operation, the esophagus is mobilized and myocardiotomy is performed. The fundus of the stomach is sutured to the edges of the resulting defect in the muscular lining of the esophagus. To prevent the development of reflux esophagitis, the bottom of the stomach should cover at least 2/3 of the circumference of the esophagus. The stomach is sutured to the esophagus with separate silk sutures. Among the complications during surgery, the possibility of injury to the mucous membrane during myotomy should be noted. In such cases, the mucous membrane is sutured and the operation is completed as usual.

Esophagospasm

Esophagospasm is a disease of the esophagus caused by spastic contractions of its wall with normal function of the lower esophageal sphincter. In a number of patients, esophagospasm is caused by viscero-visceral reflexes and is combined with other diseases.

Clinic. With primary diffuse esophagospasm, dysphagia is permanent, sometimes having a paradoxical character: solid and rough food passes unhindered, while liquid and semi-liquid, on the contrary, can be delayed. Indirect signs include increased salivation, rapid loss of the patient’s body weight, increasing weakness and anemia. Intermittent pain in the chest, which has no definite relationship with food and disappears for a long time during periods of remission, is distinguished by clinical course diffuse esophagospasm from cardiospasm and achalasia of the cardia.

Diagnostics. On X-ray examination, the esophagus has deformation in the form of rosaries, pseudodiverticula, and corkscrew; its diameter above and below the constrictions is not changed, the walls are elastic, the folds of the mucous membrane are longitudinal, peristalsis is uneven and irregular. With repeated X-ray examinations, the same type of peristalsis disturbance usually persists.

Esophagoscopy is only useful to rule out organic diseases esophagus, it is often difficult due to severe chest pain that occurs during the examination.

Esophagotonocymography reveals spastic contractions of the esophagus in the form of waves of various shapes and amplitudes; peristaltic contractions are also recorded at the same time. Constant reflex relaxation of the lower esophageal sphincter is determined. Pharmacological test with acetylcholine and carbachol is negative.

The course of the disease is long, dysphagia either intensifies or disappears almost without a trace. With secondary (reflex) esophagospasm, symptoms usually go away when the underlying disease is cured. Working capacity, as a rule, is not impaired.

Treatment. In the conservative treatment of esophagospasm, a gentle diet, nitro group drugs, antispasmodics and sedatives, and vitamins are prescribed. In the absence of a positive effect from conservative therapy surgical treatment is performed - an esophagomyotomy is performed (like Heller's cardiomyotomy) to the level of the aortic arch. The results are usually insignificant.

Unlike cardiospasm and achalasia of the cardia, in primary diffuse esophagospasm, dysphagia is not eliminated by pneumocardiodilation, which at best does not reduce it, and in some cases even aggravates it. An effective method is only a complex of therapeutic measures, including:

Antispasmodic drugs - halidor 0.05 g 3-4 times a day, no-shpu - 0.04 g 3-4 times a day, 2% papaverine solution 2 ml intramuscularly 1 time a day, 0.2% platyphylline solution 1 ml 1 time per day intramuscularly;

Neuroleptics and tranquilizers - eglonil 100 mg intramuscularly 1 time a day for 7-10 days, motherwort tincture - 1 tablespoon 4 times a day;

Vitamins B 6 (5% solution 1 ml 1 time per day intramuscularly) and B 12 (0.01% solution 1 ml 1 time per day intramuscularly);

Acupuncture with influence on points of general and local influence - 7-10 procedures per course.

Esophageal diverticula

The most common diverticula of the thoracic esophagus are bifurcation diverticula, somewhat less common are Zenker diverticula. Among the patients, men significantly predominate. In most cases, the pathology occurs in mature age- from 40 to 60 years.

According to the mechanism of occurrence, pulsion, traction and mixed diverticula are distinguished. In fact, quite often a diverticulum, which initially formed as a traction one (a consequence of surgery, an inflammatory process), then develops according to a pulsation mechanism (an increase in intraesophageal pressure leads to the progression of protrusion).

Pharyngoesophageal (Zenker) diverticula with their mouth are located on the posterior wall of the pharynx at the level of the cricoid cartilage (Fig. 3), where there is an area (Limer-Heckermann triangle) not covered by muscles. Increased pressure in the pharynx and the “mouth” area of ​​the esophagus and incoordination of muscle function can lead to the formation of a diverticulum of significant size.

Bifurcation diverticula are located predominantly on the anterior or anterior right wall of the esophagus and are not as large in size as Zenker’s (Fig. 3). Inflammatory processes in the lymph nodes and other formations of the mediastinum lead to the development of adhesions, scarring and stretching of the esophageal wall. This mechanism of diverticulum formation is confirmed by surgical observations, in which dense adhesions of the diverticulum with the lymph nodes, trachea, and bronchus are always found. In the future, a pulsion mechanism can be added to the traction mechanism.

Epiphrenic diverticula are usually located on the anterior or right wall of the esophagus in the lower third of it and can reach significant sizes. These diverticula are pulsational. The main role in their formation is played by the congenital weakness of the esophageal wall in this area.

Relaxation (functional) diverticula are a consequence of impaired innervation of the esophagus and represent limited protrusions of the wall with increased pressure in the lumen of the esophagus (during the swallow). When the esophagus relaxes, they disappear.

Adhesive diverticula are of traction origin and are associated with inflammatory processes in the mediastinum. They are also usually detected during peristaltic activity of the esophagus and disappear with rest.

Clinic. Zenker's diverticulum in the initial stage can only manifest as vague “discomfort” (some awkwardness when swallowing, periodic “scratching” in the pharynx). As the size of the sac increases, the symptoms become richer. Due to food entering the diverticulum and compression of the esophagus, dysphagia, which is relieved after emptying the diverticulum. After eating, especially in the supine position, regurgitation of undigested food masses from the diverticulum is observed; patients appear bad smell from mouth. Regurgitation of food masses and mucus during sleep leads to the development of pulmonary complications. Other complications of diverticulum include ulceration and perforation of the esophagus, bleeding; in rare cases, cancer develops. With large Zenker's diverticula, an elastic tumor may be visible in the neck area, which, when pressed on the neck, may disappear as the sac empties.

Bifurcation diverticula , especially small ones with a wide neck, are asymptomatic, most often being an accidental radiological finding. The main symptoms of diverticula of the bifurcation of the esophagus are dysphagia, chest pain or back pain of varying severity. Dysphagia with small diverticula depends on segmental esophagitis in the neck and spasm of the esophagus. Pain can be caused by both diverticulitis and peridiverticulitis, as well as segmental esophagitis.

Epiphrenic diverticula with small sizes and a wide neck can be asymptomatic. With a significant size of the diverticulum and the occurrence of diverticulitis, patients complain of dysphagia, regurgitation, chest pain, heaviness in the chest after eating. In some cases, the pain resembles the pain of angina pectoris. In some cases, the clinical picture is very similar to that of cardiospasm or hiatal hernia. Diagnosis in this case is complicated by the fact that epiphrenic diverticulum is often combined with these diseases (up to 20% of cases).

Diagnostics. X-ray examination plays a major role in recognizing diverticula. A thorough, multi-axial examination is indicated in various positions sick. The task is not only to identify the diverticulum, but also to accurately localize it, determine on which wall it is located, what the neck is (narrow, wide), how long the barium suspension is retained, whether there is a violation of the patency of the esophagus and the phenomena of concomitant esophagitis. It is necessary to carefully examine the walls of the diverticulum, as it is possible that a polyp and cancer may develop in it. One should remember about the possibility of the formation of esophagomediastinal and esophagorespiratory fistulas.

Endoscopic examination is indicated if a fistula, cancer or polyp is suspected, to clarify the role of the diverticulum as possible source bleeding and in some cases to establish indications for surgical treatment in terms of identifying diverticulitis and ulceration of the diverticulum. Esophagomanometry can provide some assistance in diagnosis, in which a decrease in resting pressure is determined in the area of ​​the diverticulum. In the case of segmental esophagitis, a spasm of the esophagus may be recorded here in response to a swallow.

Treatment. Conservative treatment is indicated for small, rapidly emptying diverticula without symptoms of diverticulitis, with a poor clinical picture. Treatment should be aimed at reducing the possibility of developing diverticulitis (or eliminating it in cases where the patient is contraindicated for surgical treatment). Before each meal, it is recommended to consume a spoonful of vegetable oil. Food should not be too hot or cold. Spicy foods and alcoholic drinks should be avoided. Food must be chewed thoroughly. In some cases, it is advisable to temporarily prescribe the patient a semi-liquid diet. After eating, you should drink a few sips of water to mechanically cleanse the diverticulum. In cases where a diverticulum is combined with a hiatal hernia, treatment is prescribed to combat reflux esophagitis.

Surgical treatment is indicated for complications of esophageal diverticulum (diverticulitis, ulceration, fistulas, bleeding, cancer, etc.). For pharyngoesophageal diverticulum, currently only diverticulectomy from the cervical approach is performed as the most radical intervention for this disease.

For bifurcation and epiphrecal diverticula, diverticulectomy or intussusception of the diverticulum is performed. Diverticulectomy is performed from the right thoracic approach. The area of ​​localization of the diverticulum is specified and the mediastinal pleura is dissected. The esophagus is isolated only enough to allow the operation to be performed. In most cases there is no need to hold it. The diverticulum is isolated from the surrounding tissue up to the neck and excised. The hole in the esophagus is sutured, and separate sutures are placed on the mediastinal pleura. If the muscular lining of the esophagus is poorly expressed, then plastic covering of the sutures is required, which is best done with a diaphragm flap. Diverticulum intussusception is more likely to recur and is therefore used only for small diverticula, mainly during combined operations (for example, in the presence of an epiphrenic diverticulum and a hiatal hernia).

Congenital membrane diaphragm of the esophagus

The diaphragm consists of connective tissue covered with keratinizing epithelium. This diaphragm often has holes through which food can pass. It is almost always localized in the upper part of the esophagus, much less often in the middle part.

The main clinical manifestation is dysphagia, which occurs when solid foods are introduced into the child's diet. If there are significant holes in the membrane, food can enter the stomach. Such patients usually chew everything thoroughly, which prevents food from getting stuck in the esophagus. The membrane often becomes inflamed under the influence of food debris

Diagnostics:

· Clinical manifestations

Contrast study of the esophagus

Gradual expansion of the esophagus with probes of various diameters. If the diaphragm completely blocks the lumen, it must be removed under endoscopic control.

Benign tumors of the esophagus

Tumors in relation to the wall of the esophagus can be intraluminal (polyp-shaped) and intramural (intramural). Intraluminal tumors are most often located in the proximal or distal section esophagus, intramural - in the lower two thirds of it.

Clinic. The most common symptom is dysphagia that slowly increases over many years. With intramural tumors that surround the esophagus, dysphagia can be permanent; sometimes patients report pain, a feeling of pressure or fullness behind the sternum. With tumors of the cervical esophagus, tumor regurgitation may occur with the development of asphyxia. Due to compression of the mediastinal organs by the tumor, cough, shortness of breath, cyanosis and other disorders may occur.

For small polyps clinical manifestations may be very scanty or absent. However, when even small polyps are localized in the area of ​​the cervical esophagus (near the “mouth” of the esophagus) or at the level of the cardia, symptoms such as dysphagia and impaired swallowing may appear relatively early. Esophageal polyps can exist for a long time (years), sometimes reaching gigantic sizes. At the same time, in a significant proportion of patients they may not change significantly for many years. If we systematize all the clinical manifestations inherent in benign tumors of the esophagus, they can be divided into two groups: symptoms depending on damage to the esophagus, and symptoms inherent in mediastinal tumors. The most important and common symptom of the first group is dysphagia. More often it is observed with intraluminal tumors, especially large ones and with a long stalk. In such patients, complete obstruction of the esophagus may unexpectedly occur. Dysphagia in benign tumors is often intermittent, with slow progression. However, with large, especially intramural tumors that surround the esophagus, it can be permanent. Pain of varying intensity is often observed and is localized behind the sternum, in the back or in the epigastrium. They occur more often when eating and are almost never intense. Pain after eating, which is sometimes observed in such patients, depends more on concomitant diseases (hiatal hernia, etc.) than on the tumor itself. Bleeding and anemia are caused by traumatization of polyps due to their excessive mobility, with intramural tumors - damage to the stretched and anemized mucous membrane of the esophagus above the tumor, and sometimes (in cases of a tumor combined with a hiatal hernia) - with esophagitis. With a pedunculated tumor located in the cervical esophagus, regurgitation may be observed, which can lead to asphyxia.

Symptoms inherent in mediastinal tumors are a consequence of compression of the mediastinal organs (shortness of breath, cough, palpitations, cyanosis, arrhythmia, etc.). These symptoms are more common with large intramural tumors located in the bifurcation of the esophagus, where they can compress the left main bronchus and the left vagus nerve.

Diagnostics. The main method for diagnosing benign tumors of the esophagus is x-ray examination. The following radiological signs are characteristic: a clearly defined oval-shaped filling defect on one of the walls of the esophagus, preserved relief of the mucous membrane and elasticity of the walls of the esophagus in the area of ​​the defect, a clear angle between the wall of the esophagus and the edge of the tumor revealed in an oblique position (the “visor” symptom). The folds of the esophageal mucosa above the tumor often look flattened, but unlike cancer, they never break off in the area of ​​the filling defect, but go around it. The esophagus in the area of ​​the tumor may be moderately dilated, but barium retention, as a rule, does not occur, which is explained by the preserved elasticity of the walls of the esophagus. Ring-shaped and horseshoe-shaped tumors can sometimes cause a circular narrowing of the lumen of the esophagus, but even then the folds of the mucous membrane are clearly visible.

In the differential diagnosis of benign tumors and esophageal cysts, it is important to take into account functional signs that are best identified by X-ray television cinematography. The cyst changes its shape during different phases of breathing. Like leiomyoma, the cyst moves upward with the wall of the esophagus when swallowing. Clarifying the diagnosis benign neoplasm pneumomediastinum, inflation of the esophagus with air, and tomography can help determine the extent of the lesion.

The main radiological sign of an esophageal polyp is a filling defect with clear, often round, centrally located contours. Sometimes the filling defect has a cellular structure. The contrast mass seems to flow around the intraluminal formation. With wide-based polyps, the X-ray picture is very similar to the picture of an exophytic cancer tumor.

Esophagoscopy should be performed in all patients in whom a benign tumor is suspected. It is necessary to clarify the nature of the benign neoplasm and exclude malignancy, allows you to clearly determine its extent, carefully examine the mucous membrane of the esophagus and identify pathology that could go unnoticed during x-ray examination. Intraluminal tumors have a cauliflower-like appearance. Their color, as a rule, is the same as that of the surrounding mucous membrane of the esophagus. Often a round or elongated formation is determined, sometimes lumpy, covered, as a rule, with an unchanged mucous membrane. Endoscopy allows you to examine the pedicle and base of the polyp and make sure that there is no rigidity in the walls of the esophagus. For polyps, especially those in the form of cauliflower, a biopsy is indicated.

With intramural tumors, there is a distinct protrusion of the mucous membrane, which in this area can be smoothed, of normal color or pale. Sometimes with local esophagitis, moderate swelling and redness are noted. As a rule, even with circular tumors, it is possible to pass the instrument lower and examine the esophagus to the cardia.

Treatment. The diagnosis of an esophageal polyp is an indication for surgery to remove it due to the risk of complications such as malignancy and bleeding. Malignancy of polyps (even small ones) is often observed. Surgical intervention is also indicated for intramural tumors due to possible complications- malignancy, compression of surrounding organs, and in case of cysts - their suppuration and perforation. The only exceptions can be small intramural tumors, when there is complete confidence in their benign nature and when surgical treatment poses a significant risk due to concomitant diseases. In such cases, dynamic observation is indicated.

Surgery for polyps and intramural tumors is different. For small polyps on a thin long stalk, the tumor can be removed through an esophagoscope using a special loop with coagulation of the stalk to prevent bleeding. Wide-based polyps are excised, followed by strengthening the suture line with a pedunculated diaphragm flap. The main principle of surgical treatment of benign intramural tumors and esophageal cysts is the use of organ-preserving operations, i.e., their enucleation. The tumor is almost always removed without damaging the lining of the esophagus. In case of accidental damage to the mucous membrane, the rupture must be sutured with double-row sutures. The long-term results of the operations are good.

Esophageal cancer is one of the most common sites of cancer. The incidence of esophageal cancer increases with age; It most often affects people over 60 years of age. In men, esophageal cancer is observed 2-3 times more often than in women.

There are three main forms of esophageal cancer: ulcerative (saucer-shaped), nodular (mushroom-shaped, warty-papillomatous) and infiltrating (scirrhous) cancer.

Ulcerative cancer is the most malignant form esophageal cancer. Initially, a nodule forms in the mucous membrane of the esophagus, which quickly undergoes ulceration. An ulcer with dense protruding, undermined edges is formed. The ulcer has an oval shape, spreads along the length of the esophagus, grows into its wall, then spreading to the surrounding organs. The tumor metastasizes quite early. Nodular cancer often has the appearance of cauliflower and, growing, obstructs the lumen of the esophagus, leading to dysphagia quite early . When decaying, the tumor is not much different from the ulcerative form. Quite often, the cause of the inoperability of such a tumor is invasion of the trachea or aorta. Infiltrating cancer develops in the submucosal layer, circularly covering the esophagus. As the tumor grows, it engulfs all layers of the esophageal wall and obstructs its lumen. Subsequently, the tumor ulcerates, and perifocal inflammation develops around it.

In approximately 40-50% of cases of esophageal cancer, metastases occur. As a rule, they spread lymphogenously. There are four stages of esophageal cancer: stage I - the tumor is located within the mucous membrane of the esophagus, there are no metastases; Stage 11 - the tumor grows into the deeper layers of the esophageal wall, but not all of it; there are often single metastases to the nearest lymph nodes; Stage III - the tumor grows into all layers of the wall of the esophagus, often fused with surrounding organs, but does not grow into them, there are often regional metastases; Stage IV - distant metastases or tumor invasion of vital organs.

Clinic. In the clinical picture of esophageal cancer, two groups of symptoms can be distinguished - local, depending on damage to the walls of the esophagus and surrounding organs, and general. In most cases, the first symptom of esophageal cancer is dysphagia. However, although dysphagia is the first symptom in most patients, it is essentially late symptom. Only in some patients can it really be early sign diseases when a small tumor is located on one of the walls of the esophagus and dysphagia does not depend on the narrowing of the lumen by the tumor, but on spasm of the esophagus due to local esophagitis. In a number of cases, upon careful questioning, it is possible to find out that the patient has already had episodes of dysphagia in the past (he notes that he seemed to “choke” on a piece of food). This is usually associated with hasty eating and is soon forgotten. Only the repetition of dysphagia forces the patient to pay attention to this fact and consult a doctor. In older people, dysphagia may manifest itself only occasionally for a long time.

Esophageal cancer is characterized by a progressive increase in esophageal obstruction, which develops quickly in some patients and slowly in others. Coarse, poorly chewed food gets stuck first. Subsequently, even well-chewed food ceases to pass through and patients are forced to take semi-liquid and liquid food. The sometimes observed periods of improvement in the passage of food after a period of persistent dysphagia are usually associated with the disintegration of the tumor.

When the tumor is located in the cervical esophagus, patients usually first complain of a foreign body sensation, scratching, burning, and only later does dysphagia appear. Tumor growth into the upper area laryngeal nerve can lead to a disorder in the act of swallowing while the patency of the esophagus is still preserved. In case of cancer of the cardia with transition to the esophagus, dysphagia often appears late, already with a significant spread of the tumor. Often patients indicate the area where food is stuck is much higher than it actually is. Thus, with cancer of the cardia with a transition to the esophagus, patients often complain of a feeling of food retention in the area of ​​the cervical esophagus.

Pain in esophageal cancer, from mild, bordering on the definition of “unpleasant sensations,” to very strong, is often observed when swallowing food. Outside of food, they may not exist. With cardiac cancer, there may be ulcer-like pain that occurs after eating.

Increased salivation, which occurs with esophageal cancer, is often observed with stenoses of other etiologies. Esophageal vomiting and regurgitation indicate significant stenosis of the lumen of the esophagus and depend on the accumulation of food above the narrowing. With the slow development of the tumor, the esophagus above the stricture can expand significantly, sometimes reaching the same size as during cardiospasm Stage III. Belching for a long time may be the only symptom of cardia cancer and depends on the infiltration of the walls of the physiological cardia.

Hoarseness appears when the recurrent nerve is damaged and indicates advanced disease. Such general symptoms, such as weight loss, weakness, decreased performance, emotional depression, etc., are a consequence of intoxication and cannot be reference points for early recognition of the disease.

Diagnostics. The main role in the diagnosis of esophageal cancer belongs to X-ray method research. In the initial stages of cancer, a filling defect is detected in a limited area of ​​the esophagus, on one of its walls. These are the most difficult diagnostic cases, in which X-ray cinematography can be of great help, because frame-by-frame decoding of the X-ray film makes it possible to identify minimal changes in the wall of the esophagus. A distinctive sign of cancer, even in the early stages, is the loss of elasticity (rigidity) of the esophageal wall in the area where the tumor is located. If the tumor is localized on one of the walls of the esophagus, then its lumen in this area may even be somewhat expanded. Narrowing of the lumen occurs with circular growth of the tumor. With common tumors, characteristic symptoms of cancer are breakage of the folds of the mucosa in the area of ​​the pathological process, unevenness and corroded contours. With saucer-shaped carcinomas, a filling defect is determined in the form of an oval, elongated along the length of the esophagus, often with ulceration in the center. To clarify the spread of the tumor to neighboring organs, X-ray examination is used under pneumomednastinum conditions. If necessary, tomograms are made in direct and sagittal projections. Radioisotope research with 32 R can provide some assistance in diagnosis. In this case, a significant concentration of the isotope occurs in the area of ​​the malignant tumor, 1 1/2 –3 1/2 times higher than normal.

Esophagoscopy is indicated in all cases of suspected esophageal cancer. The objective of the study is not only to visually confirm the diagnosis of esophageal cancer, but also to obtain histological confirmation of the diagnosis, which is absolutely necessary, especially when conducting preoperative radiation therapy. Initial forms Esophageal cancer can look like a dense whitish tubercle or, with submucosal cancer, like a rigid area, which is revealed when pressing on the wall with the end of an instrument. With further progression of the exophytic tumor, whitish or pinkish masses are visible, often having the appearance of cauliflower.

In ulcerative and scirrhotic forms of esophageal cancer, when there is severe inflammation of the mucous membrane above the tumor, during esophagoscopy it is not always possible to see the tumor itself and specifically take a piece of it for histological examination. If unsuccessful, the biopsy should be repeated. During endoscopy, it is necessary to do a cytological examination of the contents of the esophagus and smears from the tumor area. A cytological examination in combination with a biopsy allows, in most cases, to confirm or reject the diagnosis of cancer at the first examination.

Treatment for esophageal cancer largely depends on the location of the tumor. Thus, cancer of the cervical and upper thoracic esophagus, located above the aortic arch, has an extremely unfavorable course - it grows into surrounding organs early and metastasizes early. Unsatisfactory results of operations forced surgeons to abandon esophageal resection in these patients in favor of radiation therapy. It is clear that in the early stages of cancer of these parts of the esophagus, radical surgery can and should be performed.

Currently, radical surgery is usually preceded by preoperative radiation therapy using a betatron or telegamma unit at a dose of 3000-3500 rad. Not only the tumor is exposed to radiation, but also possible ways metastasis. Preoperative radiation therapy aims to maximally suppress the main lesion and possible sites of metastasis in order to perform the operation more ablastically.

In some cases, radiation therapy allows the tumor to be converted from questionably resectable to resectable. For cancer of the midthoracic esophagus, as a rule, extirpation of the esophagus is performed according to Dobromyslov-Terek. In some cases, in strong young people, a one-stage operation of the Sweeta type with the imposition of a high esophageal-gastric anastomosis is permissible. For cancer of the lower thoracic esophagus, resection of the esophagus is performed and an esophagogastric anastomosis is performed.

Postoperative mortality in simultaneous operations is very high and reaches 30%. Currently, for cancer of the mid-thoracic region, most surgeons are inclined to favor a two-stage operation: first, extirpation of the esophagus according to Dobromyslov-Terek, and then (after 3-6 months), when the patient is strong enough, plastic surgery of the esophagus with the small or large intestine. In this case, esophagoplasty should be done in the simplest and most in a safe way, i.e. presternal.

Indications for surgery. When deciding on surgical treatment, it should be taken into account that surgery for esophageal cancer is extremely complex, traumatic and, despite the progress of surgery, anesthesiology and resuscitation, is accompanied by high mortality. It is necessary to distinguish between two concepts - operability and resectability. Operable means the ability to operate on a patient. Patients with esophageal cancer are inoperable for two reasons: 1) due to the prevalence of the lesion (distant metastases, esophagotracheal fistula, etc.); 2) due to general contraindications to major surgery (old age of patients combined with “frailty”, cardiopulmonary insufficiency, etc.).

Resectability is the ability to remove the tumor. The possibility or impossibility of tumor removal usually becomes clear only during surgery. Thus, the patient may be completely operable, but the tumor may be unresectable.

Palliative resections and operations. It should be based on the concept that if a tumor turns out to be resectable during surgery, then even if this operation was not considered radical for oncological reasons (solitary unremovable metastases, the need to leave a section of tumor tissue on any organ), the issue must be resolved in favor of resection, because Such an operation allows, firstly, to relieve the patient from dysphagia and, secondly, to carry out a repeated course of radiation therapy in the postoperative period, targeting the area of ​​the remaining tumor tissue. During surgery, the lesion can be marked with radiopaque material (tantalum, etc.). If the general condition of the patient allows, in case of an unresectable tumor accompanied by severe dysphagia, the application of bypass esophageal-gastric or esophageal-small intestinal anastomosis is indicated. For the same purpose, tumor recanalization can be performed with a lavsan prosthesis (endoprosthetics).

Endoprosthetics technique. After laparotomy or thoracotomy has determined that radical surgery is not feasible, a metal conductor with a spring at the end is passed through the tumor. Using this conductor, the tumor is bouged with bougies of increasing numbers. Then, when a channel of sufficient width has been made in the tumor, a hollow plastic tube is put on the bougie and passed with the bougie along a guide through the tumor. The tube, with its bell, firmly “sits” on the tumor. The bougie and guide are removed. If it is impossible to perform a palliative operation of this type, and the patient has severe dysphagia, it is advisable to apply a gastrostomy. The gastrostomy tube according to Witzel is the most sealed.

Radical operations. The most common radical operation was developed by V. D. Dobromyslov (1900-1902) on corpses and in experiments. In the clinic, this operation was successfully performed for the first time in 1913 by Terek. It consists of extirpation of the entire intrathoracic esophagus with the application of an esophagostomy in the neck and the formation of a gastrostomy.

The Dobromyslov-Torek operation is performed from the right-sided transthoracic approach in the fifth - sixth intercostal space. The mediastinal pleura is dissected from the level of the diaphragm to the dome of the pleura. The azygos vein is ligated and transected. The esophagus above and below the tumor is mobilized and held on holders (by pulling the holders, it is easier to mobilize the esophagus in the area of ​​the tumor). When isolating the esophagus with a tumor, the tissue and lymph nodes of the posterior mediastinum are widely removed. The vessels supplying the esophagus are ligated and divided. In this way, the entire thoracic esophagus is gradually mobilized. The esophagus is bluntly isolated on the neck. The esophagus is crossed in the region of the cardia and its end is immersed in a purse-string suture. The oral part of the esophagus is crossed using the UKL-40 apparatus in the upper third at the dome of the pleura. The resected section of the esophagus with the tumor is removed (it should not be removed to the neck due to the risk of implantation metastases). A rubber cap is put on the sutured oral part of the esophagus, the chest cavity is sutured, leaving drainage. Next, the oral part of the esophagus is isolated from an additional incision in the neck and an esophagostomy is formed. A gastrostomy tube is applied according to Witzel.

When resection of the esophagus with the imposition of an esophageal-gastric anastomosis in the postoperative period, one should be wary of the development of insufficiency of the sutures of the esophageal-gastric anastomosis. When this complication develops, the pleural cavity is drained and intensive care. Other possible complications are pleural empyema, pneumonia, cardiopulmonary failure, embolism pulmonary artery. 18-20% of radically operated patients survive the five-year period.

Post-burn esophageal strictures

Chemical burn of the esophagus

A chemical burn of the esophagus is most often the result of accidental or, less commonly, suicidal intake of acids (usually vinegar essence) or alkalis (usually caustic soda).

The clinical picture of a burn of the esophagus changes according to the development of pathological changes in its wall and can be divided into four periods: 1) acute, which lasts up to 2 weeks. and pathologically characterized by necrosis in the wall of the esophagus; 2) period imaginary well-being lasting 2-3 weeks, when necrotic tissue is rejected; 3) the period of formation of scar narrowing (from the 3-4th week), during which the development of granulations occurs, the processes of epithelization and stricture formation begin; 4) the period of formed scar stricture (from 2 to 6 months).

In the acute period, following the ingestion of a caustic substance, varying degrees phenomena of shock (poisoning clinic), as well as pain, vomiting, dysphagia, which can be pronounced due to spasm of the esophagus in the area of ​​the burn, and then swelling of the mucous membrane. With concomitant burns of the larynx and vocal cords, asphyxia may occur. In case of severe necrosis in the wall of the esophagus, purulent mediastinitis may develop, and with perforation of the stomach, peritonitis. Mortality in the acute period is 4-10%.

Diagnosis of a chemical burn of the esophagus is based on anamnestic data and the clinic.

Treatment. The main task is to start therapeutic measures as soon as possible. During the first hours, in case of acid burns, it is advisable to drink a 2% solution of sodium bicarbonate, burnt magnesia, almagel, and in case of alkali poisoning - 1-1.5% vinegar solution. Taking milk, egg whites, and activated carbon is also useful. Analgesics should be prescribed. Immediately after delivering the patient to the hospital, it is necessary to begin anti-shock measures. Such patients should be placed in an intensive care unit or a surgical hospital, because they constantly need monitoring: a tracheostomy may be required, and in the case of perforation of the esophagus or stomach, emergency surgery. It is necessary to establish intravenous administration of protein drugs, blood substitutes and fluids, taking into account the water and electrolyte balance. During this period, liquid foods are prescribed - milk, cream, juices, raw eggs, ice cream, butter. Before each meal you need to take a tablespoon of vegetable oil or fish oil. From the first days after the burn, hormonal therapy (hydrocortisone, cortisone, prednisolone) should be started, which helps reduce inflammatory changes in the esophagus. Broad-spectrum antibiotics are prescribed. Currently, the feasibility of early bougienage (starting from 8-10 days after the burn), which should be carried out within 1-1 1/2 months, has been proven. At the same time, lidase is prescribed by injection for 12 days.

Scar narrowing of the esophagus

Cicatricial narrowing of the esophagus most often occurs as a result of a chemical burn. Less commonly, it is caused by thermal burn when swallowing extremely hot food, peptic esophagitis, tuberculosis, syphilis and actinomycosis. In case of chemical damage to the esophagus, even with a large concentration of a caustic substance, the matter is often limited to necrosis of only the mucous membrane, as a result of which membranous strictures can form. When exposed to more concentrated alkalis and acids, all layers of the wall of the esophagus are affected, including the muscular layer, with the development of massive necrosis, which can lead to perforation of the wall of the esophagus and stomach and cause death. If this does not happen, then granulation tissue develops at the site of necrosis and the matter ends with intense fibrous changes, which leads to a narrowing of the lumen of the esophagus. A stricture often forms in areas of physiological narrowing of the esophagus: behind the cricoid cartilage, at the level of the aortic and supraphrenic segments. Multiple narrowings are common. The most severe burns occur from ingesting alkalis. Strictures can be complete or incomplete. The course of the stricture is often tortuous and eccentrically located. The suprastenotic section of the esophagus is often dilated, especially with sharp narrowings. In the area of ​​stricture, areas of ulceration covered with granulation tissue are identified. In terms of length, strictures can be short - up to 3 cm and long, often involving 2/3 of the esophagus or more, up to its total destruction.

The clinical picture of cicatricial stricture of the esophagus depends on the degree of obstruction. The main symptom of narrowing is dysphagia of varying degrees - from mild to complete obstruction of the esophagus. Increasing dysphagia occurs after a period of apparent well-being, starting from the 3-4th week after the burn. If measures are not taken, complete obstruction of the esophagus may develop. Dysphagia is accompanied by regurgitation, esophageal vomiting, and increased salivation. The free one is gradually depleted until cachexia develops. If congestive esophagitis occurs, then severe chest pain appears.

In the case of a combination of burn stricture with cardia insufficiency, there is a clinical picture of reflux esophagitis.

Diagnostics. Usually the diagnosis is made clinically based on anamnesis. X-ray examination and endoscopy make it possible to clarify the degree, location and extent of the narrowing.

The study begins with the introduction of a liquid barium suspension, and in case of sharp contractions - with water-soluble contrast agents (cardiotrast, etc.). In this case, the extent of the stricture, its course, the presence of suprastenotic expansion and complications (esophageal-mediastinal or esophageal-respiratory fistulas) are usually quite clearly determined. To select a treatment method, it is very important to determine the lower limit of the narrowing. In patients with complete strictures that are obstructed during radiographic examination, but who still have a gastrostomy tube, retrograde esophagoscopy should be performed. At endoscopic examination determine the condition of the suprastenotic part of the esophagus, the presence of esophagitis, scars, their nature, and the presence of pockets. By the way, in a number of such patients, saliva and water may periodically pass, which is associated with a change in the severity of the accompanying inflammation.

Bougienage is the main method of treating benign cicatricial strictures of the esophagus, which leads to lasting recovery in 90-95% of patients.

The best method of bougienage at present is dilation of the esophagus with radiopaque hollow plastic bougies over a metal guide. At the end of this conductor there is a metal spring, which allows you to pass the conductor through the narrowing without unnecessary injury.

Bougienage is indicated for all patients with burn strictures of the esophagus, when it is possible to pass a metal conductor through the narrowing, as well as in some cases of strictures of the esophageal-gastric and esophageal-intestinal anastomoses that developed after previous interventions on the esophagus, and in some patients with peptic strictures.

Bougienage is contraindicated in strictures complicated by esophageal fistulas (esophageal-mediastinal and esophageal-respiratory fistulas).

Surgery. Patients with complete burn strictures of the esophagus, as well as those in whom bougienage fails due to the impossibility of passing a metal string through the stricture, should undergo surgical treatment. The operation is also indicated in case of too rapid recurrence of narrowings that occur after expansion. Surgery is indicated for patients with esophageal fistulas. Preparing a patient for surgery is limited to treating the skin in cases where the patient has a gastrostomy with maceration around it. In 3 days. Before surgery, all patients are prescribed a slag-free diet (broth, juices, raw eggs, etc.) and a 25% solution of magnesium sulfate, 1 tablespoon 3 times a day. In the evening, cleansing enemas are given “to clean water.”

The choice of plastic surgery method depends on a number of conditions: age, general condition patient, localization of burn stricture. The stomach, small and large intestines are currently used as plastic material.

For very short strictures with a length of 1-1.5 cm, you can resort to local reconstruction, which can be of three types: 1) longitudinal dissection of the narrowing with a transverse suture; 2) submuscular resection of the stricture with separate suturing of the mucous-submucosal layers and muscular layer; 3) the application of a bypass esophageal-esophageal anastomosis, which is possible with a significant suprastenotic expansion of the esophagus and its wall overhanging in the form of a pocket. It is advisable to perform all these operations under magnification (special glasses or a microscope) using atraumatic needles. Unfortunately, local reconstruction is not often possible, since such narrowings are rare.

In case of extensive subtotal stricture of the esophagus, total plastic surgery with a presternal or retrosternal location of the graft is indicated, and an anastomosis is performed with the pharynx or, if there is a small free section of the esophagus, with the cervical esophagus. For segmental strictures, various types of partial plasties are indicated. If the stricture starts from the cardiac part of the stomach and involves part of the thoracic esophagus, it is possible to perform resection of the stricture with gastric plasty or plastic surgery using the type of bypass with the small or large intestine. If there is a free section of the esophagus above the cardia, then it seems possible to perform an esophageal bypass with the imposition of two anastomoses with the esophagus in pleural cavity. The graft is finally selected after laparotomy. First, you should always carefully examine the blood supply to the stomach, small and large intestines, and only then proceed to cutting out the graft.

Small intestinal esophagoplasty using the Roux-Herzen-Yudin method. The operation is based on the fact that in most people the first 5-7 intestinal arteries are connected to each other through vascular arcades. This allows, while forming a graft and crossing the vessels, to preserve the feeding arcade, which is sometimes located in two tiers (primary and secondary arcades). The first, second and, if necessary, third vessel are identified and clamped with soft clamps (test clamping). If the blood supply is good, the vessels are ligated and divided. The intestine is transected near the tritian ligament, and its distal end is sutured. The proximal end of the transected intestine is anastomosed with jejunum below the base of the graft. A strong thread is sewn along the mesenteric edge of the graft, which does not allow the graft to overstretch. The connection of the stomach to the small intestinal graft is carried out immediately or later, depending on how reliable the blood supply to the graft is. Then, according to the operation plan, the graft is inserted subcutaneously, retrosternally or intrapleurally and the issue of its immediate connection to the esophagus is decided. It is clear that with an intrapleural location of the transplant, it is necessary to immediately form an anastomosis, and with subcutaneous and retrosternal, if the blood supply to the intestine is in doubt, the connection of the esophagus with the graft can be postponed for a week.

Colonic esophagoplasty. The advantage of such plastic surgery over small intestinal plastic surgery is the possibility of easier creation of a graft of any length with a more reliable blood supply. To perform the operation, it is necessary to mobilize the entire colon, without crossing the supplying vessels and their arcades, up to the sigmoid colon. After this, using the same technique of preliminary clamping of the vessels with a soft clamp, a section of the intestine with the best vascular pulsation is selected and mobilized. A graft of sufficient length can be obtained from the right, colon and left half of the colon, both iso- and anti-peristaltically. The continuity of the intestine is restored, the graft is connected to the stomach and then, according to the plan, proceed in the same way as in the case of the small intestinal transplant.

Esophagoplasty with the stomach. It is necessary to distinguish between the use of the stomach for total and partial (intrapleural) plasty of the esophagus. In 1911, Zianu suggested using a flap of the stomach cut from its anterior wall for plastic surgery of the esophagus. In 1912, Ya. O. Galpern proposed cutting out a tube from the greater curvature of the stomach isoperistaltically. In 1959, Gavriliu modified the Jianu-Halpern technique: he cuts out the graft from the greater curvature antiperistaltically. This graft is fed by the splenic artery. Currently, Gavriliu's operation has gained many supporters, because in most cases, this method manages to obtain a graft of sufficient length to perform total gastric plastic surgery. In the case of strictures located in the lower third of the esophagus, resection of the narrowed area with the imposition of an esophageal-gastric anastomosis can be used, as is done for cancer.

Postoperative period. The most dangerous complication postoperative period is complete or partial necrosis of the graft, which, according to literature data, is observed in 10-12% of patients. To prevent necrosis in the first hours and days after esophagoplasty, it is advisable to conduct repeated sessions of hyperbaric oxygenation, which promotes adaptation and stabilization of blood circulation in the graft and helps to cope with the phenomena of transient ischemia, which are almost inevitable after mobilization of the intestine or stomach due to both surgical trauma and and changed conditions of the blood supply. If necrosis has developed, the graft must be removed completely or partially. This is easy to do if it is located subcutaneously and much more difficult (with a worse prognosis) if it is located substernally and especially intrapleurally.

Another serious complication is failure of the anastomotic sutures between the esophagus and the graft. In such cases, it is necessary to completely eliminate oral nutrition; The gastrostomy tube should be kept open for decompression purposes. The area of ​​pus accumulation is drained, a massive antibacterial therapy and complete parenteral nutrition.

Long-term results of reconstructive operations are good in most cases.

Foreign bodies of the esophagus

The reasons for the entry of foreign bodies into the esophagus can be: the habit of holding certain objects in the mouth (in small children, in workers of certain professions), carelessness in cooking and hasty eating, deliberate swallowing of various objects by mentally ill people. In more than 50% of cases, the foreign body freely passes through the esophagus and through other parts of the digestive tract and exits naturally. Sharp foreign bodies get stuck at the beginning of the esophagus, large ones linger in places of physiological narrowing. The retention of a foreign body in the esophagus is facilitated by pathological changes (tumor, benign stricture, diverticulum, etc.), as well as spasm of the esophageal muscles in response to irritation of the mucous membrane by a foreign body.

Clinic. Symptoms depend on the nature of the foreign body, the level of its retention in the esophagus, and the degree of damage to the esophageal wall. A common symptom is dysphagia, which is caused by a foreign body, the development of spasm of the esophageal muscles and the inflammatory reaction of the esophageal mucosa. The result is complete obstruction of the esophagus and regurgitation when taking liquid or food. Patients experience a feeling of fear, pressure or pain in the throat, in the area of ​​the jugular fossa or behind the sternum, which intensifies when swallowing saliva or liquid. If a large foreign body enters the area of ​​the entrance to the esophagus, instant death from asphyxia is possible. Perforation of the esophageal wall by sharp foreign bodies can lead to profuse bleeding from damaged adjacent large vessels - the common carotid artery, jugular vein, aorta, etc.; possible damage to the pleura, bronchi and lungs with the development of esophageal-tracheal or bronchoesophageal fistulas. Prolonged residence of a foreign body in the esophagus causes traumatic esophagitis, ulceration and perforation of the esophageal wall.

Diagnostics. During an emergency X-ray examination, metallic foreign bodies are detected; less contrasting foreign bodies are detected during examination of the esophagus with a water-soluble contrast agent. In case of perforation of the esophagus, the flow of the contrast agent beyond its contours and the presence of mediastinal emphysema are noted; in the development of fistulas, the penetration of the contrast agent into the tracheobronchial tree. Esophagoscopy is of great diagnostic importance, clarifying the nature of the foreign body and its location, allowing for its removal.

Treatment. If a foreign body of the esophagus is suspected, the patient must be sent to a surgical hospital at any time of the day. The foreign body is removed using a rigid esophagoscope and a set of special scratches. If it is impossible to remove a foreign body through an esophagoscope, an operation is indicated - dissection of the esophagus, removal of the foreign body and suturing of the esophageal wall.

Reflux esophagitis

The disease is caused by repeated prolonged exposure to the mucous membrane of the esophagus of gastric juice, bile, and pancreatic juice. The course of the disease is subacute or chronic. The cause of reflux esophagitis. Gastroesophageal reflux is associated with a violation of the closing function of the lower esophageal sphincter. Sometimes it occurs after various surgical interventions (cardia resection, esophagogastrostomy, gastric resection, gastrectomy, etc.) Reflux esophagitis is most often observed with hiatal hernias, as well as with gastric and duodenal ulcers, pylorospasm, pyloroduodenal stenosis, cholecystitis.

Clinic. Patients are concerned about heartburn, a burning sensation behind the sternum or along the entire esophagus, which arises or intensifies when the torso is tilted forward (gastric juice is thrown into the mouth), pain due to the effect of gastric juice and bile on the inflamed mucous membrane of the esophagus, and belching. The pain may be associated with strong spastic contractions of the esophagus. When regurgitating at night, aspiration of gastric contents into the respiratory tract may occur, which causes coughing. The return of contents from the stomach to the esophagus is facilitated by a lying position, bending the body forward, drinking alcohol, and smoking. Over time, dysphagia appears, which is first caused by functional disorders, and then by inflammatory swelling of the mucous membrane, peptic ulcer and the development of cicatricial changes in the esophagus.

If the disease occurs against the background of a peptic ulcer, hiatal hernia, etc., then the symptoms of the underlying disease may prevail in the clinical picture. Complications of esophagitis are bleeding, often hidden, cicatricial changes in the esophagus, its shortening and progression of hiatal hernia.

Diagnostics. The diagnosis of reflux esophagitis is established when patients have characteristic symptoms of the disease. X-ray examination (especially in the supine position) can detect gastroesophageal reflux and symptoms of esophagitis.

During esophagoscopy, several stages of inflammatory changes in the mucous membrane of the esophagus are noted: stage 1 – single erosions; Stage 2 – merging, but not circular erosions; Stage 3 – circular defects; Stage 4 – complications of reflux esophagitis (ulcers, strictures, short esophagus, columnar cell metaplasia of the epithelium).

When esophagotonocymography, a decrease in the tone of the lower esophageal sphincter, a violation of esophageal peristalsis such as esophagospasm, and gastroesophageal reflux, which can also be affected by intraesophageal pH-metry data (a decrease in pH to 4.0 and below), are noted.

Treatment. The primary measure is the treatment of the underlying disease that creates the conditions for gastroesophageal reflux (hiatal hernia, pyloroduodenal stenosis, pylorospasm). Conservative treatment is aimed at reducing reflux, reducing the manifestations of esophagitis, and preventing an increase in intraperitoneal pressure. Patients should strive to reduce body weight to the age norm and sleep with the head of the bed raised high. Depending on the stage of esophagitis, a mechanically and chemically gentle diet, split meals (4-6 times a day) are prescribed, the last meal is 3-4 hours before bedtime. H2 receptor blockers (cimetidine, ranitidine, etc.), alkalizing, enveloping, astringent, antispasmodic agents are prescribed; metoclopramide (tsirukal), local anesthetics, sedatives, antihistamines, vitamins; Drinking alcohol and smoking are not recommended. For stage 1-2 esophagitis, conservative treatment can be successful.

Surgical treatment is indicated for axial hiatal hernia, accompanied by stage 3-4 esophagitis, as well as bleeding and stenosis. Failure of conservative treatment may also be an indication for surgery. Currently, it is recommended to use operations in which the angle of His is corrected. More often, a transabdominal Nissen operation (fundoplication), a Belsay or Hill operation is performed. During a Nissen operation, the fundus of the stomach (fundus) is fixed with several sutures in the form of a cuff around the abdominal esophagus. In 85-90% of patients operated on using this technique, good and satisfactory results were obtained; in 5% of patients, excessive compression of the esophagus by the cuff causes supercontinence, in which belching becomes impossible. Recently, a plate using the round ligament of the liver (teres-plate) has been used to correct the angle of His. The round ligament is cut off from abdominal wall, passed around the esophagus through the angle of His and fixed to the stomach. This surgery corrects the angle of His and prevents reflux.

Dysphagia is a violation of the complex reflex swallowing act. This is not a separate nosology, but a syndrome that manifests itself in many diseases. Patients complain of difficulty swallowing food, pain in the retrosternal region, salivation, belching, and heartburn. If the act of swallowing is impaired, symptoms associated with food entering the respiratory tract are common, which is manifested by coughing and hoarseness. The doctor’s tactics are aimed primarily at identifying the causes.

For this purpose, pharyngoscopy, radiography of the esophagus with contrast, measurement of pH values ​​and manometry of the esophagus are used. After differential diagnosis and identification of a disease occurring with dysphagia syndrome, etiotropic conservative or surgical treatment is prescribed.

Esophageal dysphagia: symptoms

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

Acute esophageal dysphagia occurs as a result of:

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

Causes of esophageal dysphagia:

• Narrowing of the lumen of the esophagus causes esophageal cancer (stomach cancer localized in the cardia) and GERD also occur. Cicatricial narrowings occur after chemical burns and radiation therapy for thoracic oncology.
• When the esophagus is compressed by tumors of the chest organs (lung cancer, bronchi), enlarged mediastinal lymph nodes, paraesophageal, cardiac pathology with severe myocardial hypertrophy.
• Violation of coordinated contraction of the esophageal muscles can be a sign of achalasia, total spasm of the esophagus, diabetes mellitus, and scleroderma.
• Disturbance of esophageal peristalsis can lead to infectious diseases(tuberculosis), uncontrolled use of certain drugs (calcium antagonists, nitrates).

Symptoms of esophageal dysphagia:

• in the initial stage of the disease, patients complain of;
• retrosternal pain, drooling, often heartburn, dry cough, hoarseness appear;
• As the symptoms progress, the symptoms increase, and difficulties appear when swallowing soft foods and then liquids.

Types of dysphagia

All diseases occurring 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 movement into the pharynx, in this case the initial swallowing movements are disrupted.

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

• cough;
• nasal regurgitation;
• attacks 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 to the stomach. The causes of the disease are narrowing or compression of the esophageal tube, as well as impaired motility.

In addition, all dysphagia is divided into:

• spicy;
• chronic

According to the nature of the flow:

• intermittent;
• permanent;
• progressive, with increasing clinical symptoms.

Dysphagia - what is it?

Dysphagia (Greek dys - denial, phagein - is) 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 disrupted.

Oropharyngeal dysphagia syndrome includes the following symptoms:

• difficulty at the very beginning of swallowing;
• return of food through the nasal passages;
• cough;
• attack of suffocation;
• 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 esophageal tract.

• various infectious processes (sore throats, pharyngitis, abscesses);
• enlargement of the thyroid gland (thyromegaly);
• various lymphadenitis;
• Zenker's diverticulum;
• various types of myositis and fibrosis;
• cervical osteochondrosis;
• oropharyngeal malignancy;

1. Disturbance in the conduction of nerve impulses to muscle fibers:

• diseases of the central nervous system (brain tumors, stroke, Parkinson's disease);
• disorder of nerve impulse transmission to smooth muscles (ACD dysfunction).

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

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

• degenerative diseases of the central nervous system;
• past illnesses (stroke, head injury, gastrointestinal diseases);
• oncological diseases;
• the presence of severe chronic diseases (diabetes mellitus, ischemic heart disease, hypertension).

Dysphagia in children

Dysphagia in children has some features. 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, common to which is damage to the brain structures 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 injuries, kernicterus.
3. Various congenital pathologies of the 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 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. An entire rehabilitation program for patients with cerebral palsy has been developed. Rehabilitation measures begin almost from the first days of life (carry out drug therapy, massage, exercise therapy, physiotherapeutic procedures). From the age of three, a speech therapist is involved in treatment.

Dysphagia after fundoplication

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

Functional dysphagia

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

• suspicious;
• anxious;
• are susceptible to various types of phobias.

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

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

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

Diagnosis of dysphagia

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

1. Pharyngoscopy is a method that allows you to identify the causes of oropharyngeal dysphagia: glossitis, tonsillitis, neoplasms, foreign bodies. Pharyngoscopy is complemented by indirect laryngoscopy; the method allows identifying pathology of the epiglottis.
2. allows you to identify esophageal motility disorders.
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 environment inside the esophagus is the most reliable method for identifying GERD; esophageal manometry is performed (to determine disturbances in the functioning of the esophageal esophagus).
5. Laboratory research methods are nonspecific:

• in peripheral blood, slight leukocytosis, anemia, and increased ESR may be detected;
• in venous blood, a decrease in total protein, dysproteinemia, is most often observed;
• testing stool for occult blood.

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

• CT scan of the brain;

If cardiac or pulmonary pathology is suspected, the following is carried out:

• chest x-ray;
• echocardiography.

Dysphagia is treated after the final diagnosis.

Dysphagia grades

Based on the severity of the clinical picture, the following degrees of dysphagia are distinguished:

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

Treatment

The doctor’s tactics in the treatment of dysphagia are determined by the cause of the disease and the severity of the syndrome. The efforts of doctors are aimed at quickly restoring the act of swallowing and preventing aspiration complications.

Acute cases of dysphagia require urgent care:

• the foreign body is urgently 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. For degenerative diseases, dopamine agonists and precursors, central H-anticholinergic blockers are prescribed. For strokes, membrane stabilizers, neuroreparants, and neuroprotectors are widely used.
2. Calcium antagonists. The medicine reduces the concentration of intracellular calcium, thereby eliminating spasm of muscle fibers (diffuse esophageal spasm, achalasia), thereby improving the passage of food.
3. Antisecretory drugs. These drugs are used for GERD and eosinophilic esophagitis with dysphagia. Antacids, PPIs, and IGRs are used.
4. For infectious etiology of the disease (sore throat, abscesses, pharyngitis), antibacterial therapy is indicated.
5. Traditional medicine is widely used in the treatment of functional swallowing disorders.

In some cases, elimination of dysphagia is only possible through surgery. For neoplasias that cover the lumen of the esophagus or compress 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 only be treated in surgery; timely cricopharyngeal myotomy practically cures dysphagia.

Dysphagia is a syndrome (complex of symptoms) manifested in the form of difficulty passing a bolus of food or liquid when swallowed.

A similar phenomenon can be observed both at the initial stages of the act of swallowing (oropharyngeal dysphagia) and at the final stages (esophageal dysphagia). One in 17 people worldwide experiences symptoms of dysphagia at least once.

However, there is no trend toward a decrease in incidence.

What it is?

Esophageal dysphagia is a symptom of the disease that involves difficulty swallowing solid and liquid foods. This condition can occur both due to diseases of the larynx, pharynx, esophagus and adjacent organs, and as a result of neurological diseases, since it is the central nervous system that regulates the process of eating.

Classification

Depending on the location of the disorders that cause difficulty swallowing, the following types of dysphagia are distinguished:

• oropharyngeal (or oropharyngeal) - caused by difficulty in the entry of a bolus of food into the lumen of the esophagus, caused by pathologies of the muscles of the pharynx, peripharyngeal tissues or nervous system;
• pharyngoesophageal - provoked by a violation of the rapid swallowing phase and difficulty in entering the bolus into the esophagus;
• esophageal (esophageal) - occurs when there are disturbances in the slow phase of swallowing, making it difficult for the food bolus to enter the esophagus, divided into lower and middle.

Depending on the causes, swallowing disorders may be:

• functional – caused by nervous and psycho-emotional disorders;
• organic - provoked by diseases or other lesions of the mouth, pharynx or esophagus.

In dysphagia, there are 4 degrees of problems with swallowing food:

• 1st degree – swallowing impairment is observed only when trying to eat certain types of solid food;
• 2nd degree – the problem manifests itself when trying to swallow any solid food;
• Grade 3 – difficulty swallowing soft food;
• Stage 4 - there is practically no possibility of swallowing soft food, and even liquids (this condition is often observed with stage 4 cancer).

Causes

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

• Mechanical obstruction. Disruption 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 adhesion. Narrowing of the upper digestive tract is also observed with malignant neoplasia of the oral cavity, pharynx, larynx, and 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 circulatory disorders. Half of the patients with parkinsonism have clinical symptoms of impaired oropharyngeal swallowing, and in another 45% of patients, latent signs of the disorder are detected instrumentally. Dysphagia is complicated by multiple sclerosis, amyotrophic lateral sclerosis, and pseudoparalytic myasthenia gravis.

Esophageal swallowing disorders are often caused by esophageal pathology, chronic diseases of the gastrointestinal tract, and mediastinum. Acute forms of dysphagia occur with allergic Quincke's edema, sudden obstruction of the esophageal body and gastroesophageal junction by foreign bodies. The normal passage of solid and liquid food through the esophagus into 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 damage to the cardiac region, and complicated gastroesophageal reflux disease. Cicatricial stenosis develops after radiotherapy for thoracic cancer, chemical burns with caustic compounds, potassium chloride, salicylates, and some other drugs. Signs of dysphagia are observed when the organ lumen narrows to less than 12 mm.
• External compression of the esophagus. The passage of food is obstructed by space-occupying formations that put pressure on the esophageal wall. Esophageal dysphagia is often found in tumors (lung cancer, bronchial cancer, thymoma), enlarged mediastinal lymph nodes, substernal goiter, infectious diseases (tuberculosis, histoplasmosis), paraesophageal hernia. Difficulties in swallowing are detected in cardiac pathology - mitral valve defects, vascular compression.
• Disorders of contractile activity of the esophagus. Esophageal swallowing disorders complicate achalasia, diffuse spasm of the esophagus, and corkscrew deformation of the organ. Pathological changes in motility are observed in patients with systemic scleroderma, Chagas disease, and diabetes mellitus. Disorders of contractions of the esophageal muscles that interfere with the swallowing process occur when taking nitrates, estrogens, methylxanthines, and calcium channel blockers.

Symptoms

If there is dysphagia, symptoms can appear either sporadically or on a regular basis, it all depends on the reasons that provoked the pathology. The disease manifests itself in different ways and all its symptoms are quite unpleasant:

1. “Lump in the throat” condition. Despite the absence of obstacles to the passage of food through the esophageal canal, the patient may feel a bolus of food stuck in the pharynx or esophagus. Often the patient cannot determine the exact place where the food masses are stuck.
2. Heartburn and belching are frequent accompaniments of dysphagia. These processes occur as a result of the reflux of food from the stomach into the oral cavity.
3. Pain syndrome in the upper abdomen and behind the sternum. Chest pain can be quite sharp and tend to increase.
4. The occurrence of asthma attacks that appear due to blockage respiratory tract food masses.
5. The appearance of a strong reflex cough, which is a consequence of the reflux of food masses into the larynx and trachea.
6. Increased salivation.
7. Hoarseness and hoarseness of voice.

Diagnostics

The doctor must find out in which part of the esophagus the disorder occurs, whether swallowing is accompanied pain syndrome, whether there is a cough and heartburn, how much weight the patient loses, how long the attack lasts. The doctor should be interested in the consistency of food, which can cause dysphagia, if the patient has any other concomitant diseases. It will be necessary to examine the pharynx for inflammation, check the condition of the thyroid gland, find out whether the patient suffers from cardiomegaly, or whether the trachea is deviated.

If necessary, an x-ray should be taken. Endoscopy will also not be superfluous, which will make it possible to examine in detail the lumen of the esophagus, the mucous membrane and the upper parts of the duodenum. If esophageal dysmotility is suspected, the patient will be advised to undergo esophageal manometry. When performing it, you can evaluate the work of the upper and lower sphincters, as well as monitor the peristalsis of the esophagus.

Dysphagia leads to aspiration into the trachea, as a result of which pneumonia can occur, which will eventually become chronic. The disease is dangerous due to malnutrition and weight loss.

How to treat dysphagia?

Therapy for dysphagia syndrome should be based on a differentiated approach, because has both functional and organic causes.
With functional dysphagia, the patient should be explained the cause of the pathology, the conditions for a favorable prognosis, and given recommendations on preventing trigger factors, proper nutrition (chew food thoroughly) and changing any psychological situations that can provoke dysphagia syndrome.

In patients with dysphagia caused by nervousness, the use of antidepressant drugs and psychotherapeutic methods is recommended.
There is the possibility of applying an empirical extension. For spastic disorders that cause the development of dysphagia, it is recommended to use muscle relaxants, botulinum toxin injections, and dilation of the esophagus using the pneumatic method.

The first step in the treatment of dysphagia of organic etiology is to influence impaired motor skills and eliminate causative factors.

Correction of motility is carried out with the help of medications that have a stimulating or inhibitory effect on the muscular apparatus of the esophagus.

1. Treatment with drugs that have an stimulating effect (prokinetics): selective - domperidone and non-selective drug - metoclopramide. Metoclopramide enhances the muscle tone of the lower esophageal sphincter, its peristalsis, causing the fastest passage of food from the stomach and throughout the intestines. The average dosage of metoclopramide is 10 mg. three times a day, the drug is taken half an hour before meals. Sometimes a fourth dose of metoclopramide can be added. If the drug is prescribed parenterally, the dose will be 10 mg. 1-2 times a day. Another drug that has a selective mechanism of action is domperidone. The effects of the drug are the same, except for the effect on the large and small intestines. Side effects much less than metoclopramide. Dosage 10 mg. three times a day, take 30 minutes before meals or before bed.
2. If a patient's dysphagia is accompanied by hypermotility of the digestive system, it is advisable to begin treatment with antispastic medications. These include non-selective anticholinergics, calcium channel blockers, nitrates and myotropic antispasmodics. Best effect has a selective anticholinergic blocker of M1 receptors - gastrocepin. Take 50 mg. twice a day. Of the calcium channel blockers, dicetel is most often used at a dose of 50-100 mg three times a day. Of the nitrates, preference is given to prolonged ones - isosorbide mononitrate (0.01-0.02 g twice a day), isosorbide dinitrate (0.005-0.01 three or four times a day). Of the myotropic antispasmodics, it turns out to be quite effective but-shpa(0.04 g), nikoshpan tablet, duspatalin 0.2 g twice a day.
3. Treatment of each type of dysphagia has certain subtleties, for example, the main treatment for esophageal achalasia is the balloon pneumocardiodilation method. Less commonly used is a technique based on botulinum toxin - it is injected into the thickness of the lower sphincter of the esophagus. If conservative treatment turns out to be ineffective, they resort to surgical methods, most often myotomy operations.

Treatment of dysphagia in most cases is impossible without prescribing a diet. This is required by the following diseases: gastroesophageal reflux disease, Barrett's esophagus, esophagitis. Asymptomatic hiatal hernias do not require treatment; if there are signs of strangulation, hernia treatment is surgical. If a patient is found to have Helicobacter pylori contamination of the mucosa, treatment should begin with eliminating the infection. In case of a complicated course of the underlying disease (recurrent gastroesophageal bleeding, the presence of strictures), as well as insufficient effect of conservative treatment methods, surgical intervention (resection) or endoscopic methods of therapy (methods of laser and photodynamic coagulation of metaplastic areas of the mucosa) are indicated.

Nutrition

Compliance with a chemically, mechanically and thermally gentle diet is an important part of the treatment of dysphagia. The nutrition of a patient suffering from dysphagia should follow the following principles:

• It should be fractional: that is, the patient should eat little by little, but often (at least five times a day).
• The food consumed should be pureed, warm and lightly salted. When preparing it, you must use olive oil or butter. The use of pork fat is strictly contraindicated.
• The patient is prohibited from eating dry food or hastily. Any food should be chewed very thoroughly.
• To avoid regurgitation (esophageal vomiting), the patient must refrain from any (especially forward) body bending for two hours after eating.
• The last meal should take place at least a couple of hours before departure for the night.

The diet of a person suffering from dysphagia should be as follows:

• The optimal cooking method is boiling, baking and steaming.
• Smoked, fatty, fried, salted, spicy and canned foods are completely excluded from daily diet. The consumption of fast food, any carbonated and alcoholic drinks, foods containing large amounts of coarse plant fiber, as well as strong coffee and tea are also strictly prohibited.
• The diet should be predominantly egg-milk-vegetable, containing cereals (semolina, oatmeal, buckwheat, rice) and mucous soups.
• The patient benefits from consuming dairy and fermented milk products, meat (preferably white) and lean fish, boiled or steamed vegetables.

Prevention

Measures aimed at preventing dysphagia:

• periodic contact with medical specialists for examination;
• correction of chronic pathology;
• proper nutrition;
• active lifestyle;
• rejection of bad habits.

Dysphagia most often begins with “harmless” symptoms, and not everyone is alarmed by choking while eating or difficulty swallowing food (especially hard and dry food). Considering the numerous causes of the syndrome, at the first complaints you should immediately consult a doctor. This will help not only avoid serious complications, but also save the lives of some patients.

Forecast

Probability full 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 gastric juice and other conditions that respond well to drug therapy

Relevance of the topic: Differential diagnosis of dysphagia syndrome is one of the important and complex problems in gastroenterology. 2-5% of the population of industrialized countries complain of swallowing disorders. Dysphagia is the reason for 3-4% of visits to general medical practitioners and 10% of visits to a gastroenterologist. In 25% of patients presenting such complaints, the pain turns out to be functional, and in other cases it is organic, and moreover, every 10th situation is considered to require surgical intervention.

Thus, the general practitioner will often have to resolve issues of tactics and strategy regarding dysphagia syndrome. A number of patients (with tumors, strictures, hernias) may require assistance in surgical or hospital settings. Another category of patients with a chronic variant of dysphagia syndrome requires reasonable conservative treatment.

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

Dysphagia is terminologically defined as difficulty or discomfort when swallowing. The patient perceives this as a feeling of food being “stuck” as it passes through the oral cavity, pharynx or esophagus.

Normal transport of the food bolus through the swallowing canal depends on the size of the bolus, the diameter of the canal, 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 those cases where it cannot stretch beyond 1.3 cm in diameter, a swallowing disorder will be obligatory. A 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 impaired swallowing due to 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 inhibition of the swallowing center leads to motor dysphagia.

The causes of dysphagia are many and varied. Of the main goals, namely, timely diagnosis and prescription adequate treatment This implies the need 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 distinguished (see table).