11. Obstruction of the esophagus. Clinic Congenital obstruction of the esophagus is caused by its atresia. This complex developmental defect is formed in the early stages of intrauterine life of the fetus. With atresia, in most cases, the upper end of the esophagus ends blindly, and

12. Obstruction of the esophagus. Diagnostics With exhaustive completeness and reliability, the diagnosis is made on the basis of an X-ray examination of the esophagus using a contrast agent, which is carried out only in surgical hospital. Received

Diseases of the esophagus Need to know Esophageal cancer. The structure of the mucous membrane of the esophagus, explaining the development of epidermoid carcinoma and the possibility of metaplasia with possible development adenocarcinomas. Syntopy of the esophagus from the perspective possible defeat those around

Bleeding from the veins of the esophagus Fresh blood in the vomit occurs when the veins of the esophagus dilate and rupture. Observed when abnormal development vessels of the liver or spleen, as well as in those suffering from cirrhosis of the liver. Blood streaks may also appear in vomit after

Esophageal cancer Esophageal cancer in Russia accounts for 3% of all malignant neoplasms and ranks 14th in the structure of cancer incidence. Nevertheless, esophageal cancer is a highly malignant tumor and is characterized by early lymphogenous metastasis.

Examination of the esophagus The essence of the method: the method is simple, painless, but its information content and diagnostic value are many times inferior to fibrogastroscopy - endoscopic examination esophagus and stomach. The most common indication for using the method is fear and

Recognition of esophageal abnormalities is based mainly on radiographic findings. The research plan is based on the anamnesis and clinical picture of the disease. Initially, fluoroscopy and radiography of the chest and chest organs are always performed. abdominal cavity, and then resort to artificial contrast of the esophagus. The tasks of the radiologist are obvious: he must establish the presence and type of anomaly, morphological and functional state esophagus, its relationship with neighboring organs.

Aplasia of the esophagus. With this anomaly, the only radiological symptom is the absence of gas in the digestive canal. Contrast of the esophagus is not possible.

Esophageal atresia. Radiological manifestations of atresia are numerous (Fig. 6). However, its symptoms are entirely determined by the type of anomaly. In the case when the esophagus is obliterated for some extent and its proximal section is a blind sac, a tubular structure containing gas and liquid appears on radiographs of the neck and upper chest. When the body is in a vertical position, the liquid forms a horizontal level. Artificial contrast allows you to accurately determine the position, extent and outline of the preserved part of the esophagus. If this part is connected by a fistula to the trachea, then the child, as a rule, has multiple foci of aspiration pneumonia. In this case, the use of barium sulfate is unacceptable. A thin rubber catheter is inserted into the patient's esophagus. 1-2 ml of contrast agent is poured through it under fluoroscopy, determining the location, caliber and direction of the fistula. The fistula usually opens in the trachea 1-3 cm above the bifurcation (less often in the bronchus). The lumen of the esophagus above the fistula is expanded. The study is carried out with the patient lying on his stomach, since the opening of the anastomosis is always located on the anterior wall of the esophagus.

With another type of atresia, the upper and lower pouches of the esophagus are connected to the trachea by a wide common anastomosis, or each of the pouches is connected to the trachea by a separate fistula. Such patients have gas in the stomach. The most common option (more than 80 % cases) is atresia, in which the proximal esophagus is blind, middle section It is a fibrous-muscular dense cord, and the lower one is connected by a fistula to the trachea (see Fig. 6). Radiographs show gas and a horizontal fluid level in the proximal region, as well as gas in the stomach and intestines. Sometimes it is possible to identify the fistula itself as a narrow light strip between the trachea and the esophagus.

Tracheoesophageal fistula. IN In rare cases, it occurs without esophageal atresia. Artificial contrast is carried out with a water-soluble drug, paying attention to the nature of the anastomosis and the presence of narrowing of the esophagus at this level.

Duplication of the esophagus. It can be complete or partial (see Fig. 6). Easily recognized full doubling, doubling of the upper, middle or lower parts of the esophagus (the latter is combined with doubling of the stomach). Some difficulties may arise if the accessory esophagus ends blindly and is small in size, i.e. there is a congenital diverticulum. In this case, the main esophagus empties normally, although sometimes it is deformed and somewhat narrowed, while the contrast mass is retained in the accessory cavity.

Congenital esophageal cyst. This anomaly is a variant of esophageal duplication. It is located in the submucosal layer or between the esophagus and trachea and does not connect to the lumen of the esophagus. If the cyst is large enough, it causes a semi-oval defect in the shadow of the contrast-enhanced esophagus. The outlines of the defect are smooth and arched. The folds of the mucous membrane bypass it or are smoothed out. Computed tomography allows you to determine that the content pathological formation is a liquid.

Dilatation of the esophagus. General dilatation or enlargement of part of the esophagus is easily detected by X-ray examination, but is described as a congenital anomaly very rarely.

Congenital narrowings. They meet often. These include short stenoses 1-2 cm long, mainly in places of physiological narrowings, narrowings up to 5-10 cm long (segmental stenoses) and membranous stenoses, in which there is a narrow membrane in the esophagus, which to one degree or another reduces its lumen (see. Fig. 6). The radiologist determines the location, extent and degree of stenosis, as well as the amount of suprastenotic expansion. It is important to carefully examine the contours of the shadow of the esophagus in the area of ​​narrowing. With congenital stenoses, they are smooth and sharp, and the folds of the mucous membrane are preserved (unlike those with scar and tumor lesions). Unlike the circular membrane, the impression from the cricopharyngeal muscle has the shape of a small notch on back wall cervical part of the esophagus, and retraction with iron deficiency anemia(Plumer-Wilson syndrome) - on the anterior wall.

Congenital short esophagus. This anomaly is well known. Such an esophagus has the form of a straight tube, which at the level of the tracheal bifurcation or somewhat distally passes into the stomach. The place of their junction is marked by a short narrow segment, in which the folds of the mucous membrane are invisible. When changing body position, the picture does not change. A significant part of the stomach

ka or all of it is in chest cavity. Gastroesophageal reflux is usually observed in the patient's supine position.

Islands of the gastric mucosa. IN esophagus they may be delayed in the process embryonic development. These dystopic islands sometimes cause a mild narrowing of the lumen of the organ and, in addition, serve as a factor predisposing to the occurrence of esophageal ulcers.

Almost 50% of patients with malformations of the esophagus have abnormalities of other organs, in particular the heart and blood vessels. This helps in diagnosis and at the same time should not be missed when analyzing radiographs. After surgical intervention checks are carried out regarding the anomaly X-ray examination.

4.2. ESOPHAGUS DIVERTICULAS

Based on the X-ray picture, three types of esophageal diverticula should be strictly distinguished: 1) diverticulosis (intrawall pseudodiverticula); 2) pulsion diverticula (single and multiple); 3) traction diverticula (Fig. 7). The first are associated with the penetration of the contrast agent into the mouths of the mucous glands. The images show numerous very small accumulations of barium on both sides of the esophagus, most often in its lower section. This phenomenon is extremely rare. In its genesis, it is common with similar formations observed in the bronchi, colon and gallbladder(Aschoff-Rokitansky sines).

Pulse diverticula are saccular protrusions of the mucous and submucosal membranes through the cracks of the muscular layer. They can develop in any part of the esophagus, but mainly in the area of ​​the pharyngoesophageal junction, at the level of the aortic arch and tracheal bifurcation and in the supraphrenic segment. In any case, an X-ray examination should be carried out in different projections and positions of the patient’s body. It is necessary to make the base (neck) of the diverticulum edge-forming, carefully examine the mucous membrane and contours of the esophagus along its entire length, determine the period of emptying of the diverticulum from the contrast mass, and evaluate the function of the esophagogastric junction.

The pharyngoesophageal (borderline, Zenker) diverticulum is formed between the lower fibers of the lower pharyngeal constrictor and the cricopharyngeus muscle and slightly hangs over the latter. Its neck is always located in the midline on the posterior wall of the esophagus at the level VII cervical vertebra. If the diverticulum is small in size (0.2-0.5 cm), it is noticeable only in the lateral projection during swallowing movements and does not affect the passage of barium sulfate through the esophagus. The picture changes with large diverticula. The contrast mass often first enters the diverticulum and only then into the esophagus. The diverticulum has the appearance of a large round formation with smooth contours, shifting upward during swallowing (Fig. 8).

It can cause depression on the wall of the esophagus, making it difficult to pass the contrast mass. The latter sometimes lingers in the diverticulum. At inflammatory complications the contours of the diverticulum become uneven, and displacement during swallowing is limited.

A diverticulum that has developed in the interaortobronchial segment usually originates from the left side wall between the lower contour of the aortic arch and the left main bronchus. The diverticulum of the subbronchial segment, on the contrary, lies on the right side wall. Under the pressure of the contrast mass, such diverticula increase, and as they are emptied, they decrease, which indicates the preservation of the elasticity of the walls (Fig. 9). The folds of the mucous membrane of the esophagus are not thickened and enter directly into the neck of the diverticulum. Supradiaphragmatic (epiphrenic) diverticula are rare. Such a diverticulum is localized mainly on the posterior surface of the esophagus, less often on the anterior one, and has a round shape and smooth outline (Fig. 10). It is filled with a contrast mass from the esophagus, in contrast to a paraesophageal hernia, which may externally resemble a diverticulum, but is filled after the barium sulfate passes through the cardia into the stomach.

Traction diverticula without any particular reason are called protrusions of the esophageal wall that arise as a result of cicatricial traction from surrounding tissues. They do not have a neck and have an elongated or triangular shape. The contrast mass, as a rule, does not linger in them. In such cases, it is more correct to talk about limited deformation of the esophagus due to periesophageal adhesions. However, according to some data, a traction diverticulum can eventually turn into a traction-pulsion diverticulum.

The development of diverticulitis changes the x-ray picture: deformation of the diverticulum, unevenness of its contours, rigidity of the walls, retention of contents are determined. In case of perforation, the contrast agent enters the media-astinal tissue through the perforated hole.

Esophageal atresia, the most common congenital malformation digestive system. The clinic appears immediately after the birth of the baby. Foamy, copious mucus is released from the nose and mouth; after suctioning, it appears again, as a result of which aspiration pneumonia inevitably develops. If the diagnosis is not made in time and the child begins to be fed, the child’s general condition deteriorates sharply, signs of pneumonia and respiratory failure increase. The children are coughing and restless. Episodes acute disorder general condition baby coincide with feeding. breast milk flows out through the mouth and nose. The condition of children is even more severe if this defect is combined with a lower tracheoesophageal fistula.

Tracheoesophageal fistula, isolated, without esophageal atresia is extremely rare, and even less often it is diagnosed in a timely manner, immediately after birth. Clinical picture, depends on the width of the fistula itself and its connection between the trachea and the esophagus. The wider the fistula, the greater the signs of defect, for any width of the fistula clinical manifestations identical, but different in intensity, these are breathing disorders that occur during feeding: shortness of breath, cyanosis skin, choking. And it is precisely this connection with the act of sucking that should alert a neonatologist to the presence of a tracheoesophageal fistula in a child. With a sufficiently wide fistula, the child’s condition is very serious and sometimes requires transfer to artificial ventilation lungs. Suction of gastric contents from the trachea is the main diagnostic criterion. To clarify the diagnosis, it is enough to transfer the child to feeding through a tube and his condition improves. This type of nutrition is important not only for diagnosis, but for the treatment of the child. To clarify the diagnosis, tracheobronchoscopy is performed.

Congenital intestinal obstruction, This frequent occasion for hospitalization of a child in surgical departments for newborns. The reasons can be divided into three groups: disruption of the formation of the intestine itself, its tube (its absence, stenosis, or the presence of a membrane); anomalies of intestinal rotation and fixation; vices from others internal organs leading to compression of the intestines (tumors, abnormal development of the pancreas, etc.). It should be pointed out that there is a so-called “benign” intestinal obstruction, this is meconium ileus. Blockage of the intestinal lumen with very thick meconium, the cause is still unknown.

Intestinal obstruction manifests itself acutely, from the first days, and sometimes even hours, of the baby’s life. It happens low and high , depends on the level of congenital malformation. High vices include those that are at level 12 duodenum, and to low ones, below it. This division is associated not only with a different clinical picture, but with further prognosis. Low intestinal obstruction is more severe and the prognosis is more unfavorable. Life-threatening complications may develop for the baby: perforations small intestine, which leads to peritonitis, but it can develop without perforation; the survival rate of children after such complications is not high. With high obstruction, such complications are not observed. Its clinical picture is characterized by the accumulation of food in the stomach and 12 intestines, which is released through vomiting or regurgitation.

Leading symptom high intestinal obstruction , is vomiting, it is profuse, sometimes with an admixture of bile, not frequent once every 3-4 hours, appears for the first day after birth, and sometimes for the first time hours of life. If after birth an obstruction was not suspected, and the child began to be fed, then vomiting always associated with feeding, occurs immediately after it, the volume of vomit corresponds to the amount of food. The condition of children quickly deteriorates, dehydration occurs and aspiration pneumonia develops with the formation of respiratory failure. Meconium (the first stool) passes for a long time over 5-6 days, but subsequently it does not, this passage is explained by the lack of intestinal motility, the abdomen is distended. With partial high intestinal obstruction, the clinical manifestations are “smoothed out”, vomiting may appear on the 2-3rd day of life, not profusely. Dehydration develops more slowly, meconium passes faster, and even partially there is stool, in small portions, and then its quantity decreases.

Clinical picture low intestinal obstruction , is varied and depends on which part of the intestine is affected. It is rarely partial and its manifestations are acute. Most often, a rotation disorder occurs; it can occur both in utero and after birth. It is based on constriction of intestinal loops, which leads to impaired circulation, which, in turn, causes peritonitis. The clinic is the same for almost all forms. The baby's paroxysmal restlessness for no apparent reason, associated with intestinal motility, comes to the fore. Abdominal bloating is noted immediately after birth and does not disappear even after the stomach has been emptied. Vomiting mixed with intestinal contents and blood occurs later than with severe obstruction, usually by the end of the 2nd to the beginning of the 3rd day, and is not profuse. There is no meconium, sometimes there are only lumps of mucus with a greenish tint. Severe intoxication, intestinal loops can be palpated, and in severe cases can be visible to the eye.

Anomalies in the development of the digestive system, if possible, should be diagnosed in utero, so that one can prepare for the birth of an “unusual” baby into the world, the mother and medical personnel. Such births should take place in specialized institutions, just as a child after birth should receive qualified surgical care. And if it is not possible to diagnose during pregnancy, maximize the diagnosis during the first hours of life.

TO congenital defects development of the esophagus include: complete absence esophagus

(aplasia or complete atresia), complete obstruction of the esophagus (atresia),

stenosis, tracheoesophageal fistula, duplication of the esophagus, congenital short esophagus,

congenital chalazia (insufficiency) of the cardia.

Frequency - 1:1000 newborns.

Atresia is the complete absence of lumen of the esophagus in any part of it or on

all along. In 40% of cases, atresia is combined with other developmental defects. IN

In the first hours and days after birth, newborns experience constant discharge

saliva and mucus from the mouth and nose may occur severe cough, shortness of breath and cyanosis in

as a result of aspiration of the contents of the esophagus into respiratory tract. With the beginning

During feeding, the milk is regurgitated and enters the mouth uncurdled.

Esophageal stenosis can be a result of hypertrophy of the muscular layer, the presence of

wall of the esophagus fibrous or cartilaginous ring, mucosal formation

a shell of thin membranes. Minor stenoses long time are leaking

asymptomatic and manifest dysphagia only when eating rough food. At

In severe stenosis, dysphagia and regurgitation during and after meals are noted.

Gradually, suprastenotic dilatation of the esophagus develops,

food masses linger in it and undergo rotting, putrefactive

bad breath.

Congenital broncho-, tracheoesophageal fistulas (see section "Inflammatory

diseases of the trachea").

Duplication of the esophagus - rare anomaly. The lumen of doublings can be isolated

or have a connection with the main canal of the esophagus. Clearance of isolated duplications

filled with secretion secreted by their mucous membrane, sometimes they look like cysts, in others

cases communicate with the trachea or bronchus. As cysts grow, they develop

symptoms of compression of the esophagus and respiratory tract, patients develop dysphagia,

cough and shortness of breath appear.

Congenital chalazia (insufficiency) of the cardia is a consequence of underdevelopment

neuromuscular apparatus of the physiological cardia or straightening the angle of His.

The clinical picture is similar to those of congenital short esophagus.

Congenital short esophagus. With this malformation, part of the stomach turns out to be

located above the diaphragm. The clinical picture is due to insufficiency

cardia accompanied by gastroesophageal reflux. After feeding

children experience regurgitation, vomiting sometimes mixed with blood as a result of development

esophagitis.

Complications of malformations of the esophagus. The most common complication of congenital

atresia, stenosis, esophageal-respiratory fistulas is aspiration

pneumonia. Esophageal atresia can lead to starvation of a child, if

stenosis develops congestive esophagitis. Increasing bronchial compression

double esophagus causes repeated pneumonia, development of bronchiectasis,

possible suppuration and breakthrough of the cyst into the respiratory tract or pleural cavity.

The lining of cysts from ectopic gastric mucosa may be subject to

ulceration with the development of bleeding and perforation. With congenital short

esophagus and cardia insufficiency, reflux esophagitis occurs, develops

peptic ulcer followed by esophageal stricture, a common complication is

aspiration pneumonia.

Diagnosis congenital anomaly development of the esophagus is established using

X-ray examination, in which into the lumen of the esophagus along a thin

1-2 ml of iodolipol is injected into the catheter. The study reveals the blind

the end of the esophagus, the level of its location, the length and magnitude of the narrowing,

suprastenotic dilatation of the esophagus, the presence of communication between the lumen of the esophagus and

bronchi or trachea. When the esophagus is doubled, an additional shadow is noted with

with clear contours, adjacent to the shadow of the mediastinum and pushing aside the esophagus. At

the short esophagus has no bends, and part of the stomach is located above

diaphragm. Cardia insufficiency is manifested by gastroesophageal reflux

contrast agent during the study. A major role in the diagnosis of defects

development of the esophagus is played by esophagoscopy and bronchoscopy.

Treatment: features surgical treatment esophageal atresia is determined by its

view. If the diastasis between the separated ends of the esophagus does not exceed 1.5 cm,

a direct end-to-end anastomosis is performed. With significant diastasis of the ends

of the esophagus, its proximal part is brought out to the neck in the form of an esophagostomy,

gastrostomy tube to feed the child, and subsequently esophagoplasty is performed.

The choice of type of surgery for congenital esophageal stenosis depends on the extent

narrowing. When narrowing to 1.5 cm, a longitudinal dissection of the wall of the esophagus is performed

with cross-suturing of the wound edges over the catheter. If the narrowing area is not

exceeds 2.5 cm in length, it is possible to perform resection of the esophagus with

end-to-end anastomosis. If the narrowing is significant, it is indicated

esophagoplasty. When the narrowing is localized in the area of ​​the physiological cardia

perform extramucosal myotomy (Geller operation) with fundoplication or

plastic surgery with a diaphragm flap.

Treatment of tracheo- and bronchoesophageal fistulas involves cutting the fistula

the course and suturing of the resulting defects in both organs When the esophagus is doubled

enucleation or resection of the diverticulum-like area is indicated.

In case of congenital short esophagus and the absence of complications, conservative treatment is performed.

treatment. In cases of severe reflux esophagitis, pyloroplasty or

transpleural fundoplication leaving the stomach in the chest cavity.

Congenital cardia failure is treated conservatively. Usually over time

normalization of cardial function occurs.

Congenital esophageal atresia and esophagotracheal fistulas.

Occurrence:

occurs in 1 case per 7-8 thousand newborns. The most common is complete atresia of the esophagus in combination with a tracheobronchial fistula: the proximal end of the esophagus is atretic, and the distal end is connected to the trachea. Less common is complete atresia of the esophagus without tracheobronchial fistula.

Clinic:

the disease manifests itself immediately after birth. When a newborn swallows saliva, colostrum, or liquid, respiratory distress and cyanosis immediately occur. With complete atresia without esophagotracheal fistula, belching and vomiting occur at the first feeding.

Diagnostics:

• Clinical manifestations;
• Probing of the esophagus;
• Contrast study of the esophagus with gastrografin;
• Plain X-ray of the chest and abdominal cavity: signs of areas of atelectasis, signs of pneumonia (aspiration), absence of gas in the intestines. There may be gas in the intestines if there is a connection between the lower segment of the esophagus and the trachea (fistula).

Treatment:

• If there are no signs of atelectasis or pneumonia, a one-stage operation is performed to close the esophagotracheal fistula and anastomose the upper and lower segments of the esophagus.
• If the disease becomes more complicated aspiration pneumonia, atelectasis in the lungs is then carried out next treatment: at the beginning a gastrostomy tube is placed, intensive care until the condition improves and then the fistula is closed and an anastomosis is made between the upper and lower segments of the esophagus.
• In case of multiple malformations, in severely weakened newborns, the proximal end of the esophagus is brought out to the neck to avoid the accumulation of saliva in it, and a gastrostomy is placed for feeding. After a few months, the anastomosis is performed. If it is impossible to compare the upper and lower segments, esophagoplasty is performed.

Congenital stenosis of the esophagus.

As a rule, stenosis is located at the level of the aortic narrowing.

Clinic: hiatal hernia, esophagitis, achalasia. With significant narrowing of the esophagus, suprastenotic dilatation of the esophagus occurs. Symptoms usually do not appear until administration food ration baby solid food.

Diagnostics:

• Clinical manifestations;
• Fibroesophagogastroscopy;
• Contrast study of the esophagus;

Treatment: in most cases, expansion of the esophagus by dilatation or bougienage is sufficient. Surgical treatment carried out in case of unsuccessful conservative treatment.

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. Almost always localized in upper section esophagus, much less often - in the middle section.

Clinic: 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

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

Congenital short esophagus.

It is believed that during intrauterine development, the development of the esophagus proceeds more slowly, and part of the stomach, penetrating through the diaphragm, forms lower section esophagus. Congenital short esophagus occurs in Marfan syndrome, and familial cases of the disease occur.

Clinic: clinical manifestations are similar to those of a sliding hiatal hernia - pain in chest after eating, heartburn, maybe vomiting.

Diagnostics:

• Clinical manifestations
• Often, it is possible to differentiate a congenital short esophagus from a sliding hiatal hernia only during surgery
• Fibroesophagogastroscopy

Treatment: for symptoms - surgical; as a rule, in the absence of fusion of the esophagus and aorta, the normal position of the esophagus and stomach can be restored by stretching it.

Congenital esophageal cysts.

Cysts are located intramurally, paraesophageal. Such cysts are lined with bronchial and esophageal epithelium.

Clinic: in children, cysts can cause dysphagia, cough, respiratory distress, and cyanosis. In adults, cysts are usually less than 4 cm, if more than 4 cm then clinical symptoms the same as for leiomyomas. Cysts can be complicated by mediastinitis during infection, bleeding and malignancy.

Treatment: removal of the cyst using fibrogastroscopy.

Vascular abnormalities.

Congenital anomalies of the aorta and large vessels may compress the esophagus and cause dysphagia. For example, abnormal right subclavian artery. As a rule, dysphagia manifests itself in the first 5 years of life. Occasionally occurs double arc the aorta, which surrounds the trachea and esophagus and when eating, cyanosis and cough occur, and later dysphagia occurs

Treatment consists of removing the connective tissue ring connecting the vessel and the esophagus without interfering with the vessels.