His angle is normal. Glossary of Special Terms

Hiatal hernia, or hiatus hernia, is a very common condition. Experienced radiologists who correctly examine patients find it in 5-10% of all those subjected to fluoroscopy of the stomach for “stomach” complaints.”

The first major domestic work devoted to the study of hiatus hernia was the candidate's dissertation of radiologist E. M. Kagan, defended in 1949. The features of hiatal hernias in children are well covered in the works of S. Ya. Doletsky (1958, 1960).

We began to operate on patients with this type of diaphragmatic hernia from the late 40s, and in 1959 we instructed our employee N.N. Kanshin to study this problem in more detail. In 1963 he defended his candidate's dissertation, and has now completed his doctorate. Employees of our clinic also defended candidate dissertations on the study of hiatal hernias with shortening of the esophagus (A.F. Chernousov, 1965) and the diagnosis of peptic esophagitis complicated by hiatus hernia (V.M. Arablinsky, 1966).

A comprehensive study of this problem has allowed our clinic to gain significant experience in the diagnosis and treatment of hiatal hernias, which is summarized in a number of works.

Before moving on to the consideration of hiatal hernias, it is necessary to recall some anatomical and physiological features of the exophagocardial region.

Normally, the esophagus flows into the stomach below the diaphragm, having first passed through a special opening - hiatus oesophageus, formed by the medial legs of the lumbar part of the diaphragm. The esophagus is fixed in this opening by means of the esophageal-phrenic membrane, which is a continuation of the fascia covering the diaphragmatic crura.

The fusion of the esophagus with the stomach occurs at an acute angle (angle of His), corresponding to the apex of which folds of the mucous membrane protrude into the lumen of the stomach, acting as a cardiac valve (Gubarev valve) (Fig. 123).

In addition to the valve, there is also a sphincter in the area of ​​the cardia, but anatomically it is poorly expressed. There is no clear thickening of the muscle bundles, as is observed, for example, in the pyloric zone, and the role of the sphincter is played by the circular layer of the muscular membrane of the terminal part of the esophagus. The last 3-4 cm of the esophagus is called the gastroesophageal vestibule (vestibulum gastrooesophageale), or physiological cardia.

The circular layer of the muscular layer in the area of ​​the physiological cardia outside the act of swallowing is moderately spastically contracted. This contraction, together with the action of the Gubarev valve, prevents the flow of gastric contents. During the act of swallowing, the esophagocardial sphincter reflexively relaxes and the cardia becomes passable. Then the sphincter contracts again, which also leads to the closure of the Gubarev valve.

In recent years, it has been established that the diaphragm (i.e., its muscle bundles that form the edges of the hiatus oesophageus) does not take part in the closure of the cardia and is not the external sphincter of the latter. By measuring intraperitoneal pressure, it was established that the force of contraction of the esophagocardial sphincter is very insignificant, but the zone of increased pressure in the area of ​​the physiological cardia in healthy people is very clearly identified. In a state of physiological rest, the highest pressure is in the esophagocardial region, and in the stomach and esophagus it is lower; immediately after the swallowing movement, the cardia reflexively opens.

There are several types of hiatal hernias. The first classification, which formed the basis for all subsequent ones, was proposed in 1926 by Åkerlund. He divided them into three types:

1. hernias with congenital shortening of the esophagus, paraesophageal hernias,
2. the remaining hiatal hernias (later called sliding hernias).

Our clinic has adopted the following classification (Fig. 124).

Sliding hiatal hernias are more common. They are called so not because the hernial contents can move up and down, but by analogy with the corresponding type of femoral and inguinal hernias. The fact is that the posterior wall of the upper part of the cardia of the stomach is not covered by the peritoneum, as a result of which, when the cardia is displaced upward into the mediastinum, this part of the gastric wall participates in the formation of a hernial sac. On this basis, the hernia is classified as sliding. Sliding hiatal hernias are sometimes also called axial hernias, since the displacement occurs along the axis of the esophagus.

With paraesophageal hernias, the cardia remains fixed under the diaphragm, and one or another abdominal organ is displaced into the mediastinum next to the esophagus. Therefore, the hernia is called paraesophageal, i.e. paraesophageal.

Sliding hernias can be fixed or non-fixed. In the latter case, they are independently reduced when the patient is in an upright position. Large hernias (cardiofundal and giant) are always fixed due to the suction effect of the chest cavity. Fixation of the hernia is associated with shortening of the esophagus. The latter may be congenital, depending on an abnormality of embryonic development. Patients with a congenital “short esophagus” are usually observed by pediatric surgeons. In adults, shortening of the esophagus in the vast majority of cases is acquired. We will dwell on the reasons for the development of this pathology below. Shortening of the esophagus is divided into two degrees. When shortening the first degree, the cardia is fixed no higher than 4 cm above the diaphragm. More significant shortening is classified as grade II.

We have given names to individual types of hiatal hernias depending on which organ or part of the organ is involved in the formation of the hernia. Thus, when the cardia with a small adjacent area of ​​the stomach is displaced into the mediastinum, we speak of a cardiac hiatal hernia. If, in addition to the cardia, the fundus of the stomach also prolapses through the hernial orifice, then we call such a hernia cardiofundic. We previously identified subtotal and total gastric hernias as a separate type - giant hernias, but it is more correct to classify them as sliding ones, since they are a consequence of a further increase in cardiofundal hernias. Thus, the name of the hernia alone gives a very clear idea of ​​its pathological essence.

Regarding origin of hernias esophageal opening, then, like hernias of other localizations, they can be congenital and acquired. Acquired hiatus hernia is observed much more often, and age-related changes play a significant role in their origin. In the vast majority of cases, these hernias, according to our observations, are observed after the age of 40 years. In addition to the expansion of the hiatus oesophageus caused by age-related involution and the weakening of the connection between the esophagus and the diaphragm, a hereditary constitutional predisposition to hernia formation is of great importance. It depends on the congenital weakness of the mesenchial tissue. In such patients, in addition to hiatus hernia, hernias of other locations, flat feet, and varicose veins of the lower extremities are often observed.

The weakening of the connection between the esophagus and the diaphragm, caused by one reason or another, is the background against which a hernia develops. In the direct mechanism of formation, two types of factors can be distinguished: pulsion and traction.

Pulse factor- this is an increase in intra-abdominal pressure, with heavy physical activity, overeating, flatulence, constipation, pregnancy, wearing tight belts and corsets, with large tumors and cysts of the abdominal cavity.

Traction factor associated with increased contraction of the longitudinal muscles of the esophagus.

Numerous researchers have experimentally established that irritation of the branches of the vagus nerves or the organs innervated by them causes a reflex longitudinal contraction of the esophagus. In this case, the cardia is pulled upward. In various chronic diseases of organs innervated by the vagus nerves, such a tendency of the esophagus to longitudinal contraction can lead to the development of a traction hiatal hernia. Longitudinal contraction of the esophagus is also necessary for the act of vomiting. Therefore, frequent vomiting also contributes to the development of a hiatal hernia.

It is the spastic longitudinal contraction of the esophagus that we attach special importance to in the origin of the acquired shortening of this organ. The second reason for shortening of the esophagus is the development of scar tissue in its wall as a result of peptic reflux esophagitis.

Clinic. The clinical picture of sliding hiatal hernias depends mainly on the resulting disorder of the valvular function of the cardia. When the cardia moves upward, the angle of His becomes obtuse, which leads to smoothing of the folds of the mucous membrane, which act as a valve. The weak tone of the esophagocardial sphincter becomes unable to withstand intragastric pressure, and the contents of the stomach begin to flow into the esophagus, i.e. so-called gastroesophageal reflux occurs. In this case, peptically active gastric juice burns the mucous membrane of the esophagus. Often such patients complain of painful heartburn, belching, and regurgitation. These symptoms intensify after eating and with body positions that promote reflux, which also causes pain behind the sternum or high in the epigastric region and left hypochondrium. At the same time, in many patients, especially with achylia, the hernia may not give almost any symptoms.

Constant exposure of the esophageal mucosa to peptically active gastric juice leads to the development of reflux esophagitis, which in some cases becomes erosive and even ulcerative. Due to inflammatory edema and scarring, peptic stricture of the esophagus can occur until its lumen is completely closed. We observed a similar complication in 16 patients. The inflamed mucous membrane of the esophagus is easily injured, which is accompanied by bleeding. In some patients this leads to the development of hypochromic anemia.

Proof that all of the listed symptoms depend specifically on gastroesophageal reflux is the fact that a completely similar clinical picture develops in patients who undergo esophagofundostomy due to cardiospasm. We were forced to completely abandon this operation due to the development of gastroesophageal reflux after it. Currently, such an intervention should be considered antiphysiological and unacceptable for cardiospasm.

Reflux most often occurs with a cardiac hernia, especially if it is combined with a shortening of the esophagus. With cardiofundal hernia, due to the often occurring recovery in the mediastinum of the acute angle of His, reflux is observed less frequently. But with this form of hernia, due to venous stagnation in the supracardial part of the stomach, bleeding per diapedesin into the lumen of the organ can occur, leading to the development of hypochromic anemia.

Sliding hiatal hernias are never strangulated. This depends on the fact that the cardia is displaced above the diaphragm, and if some compression of the stomach occurs in the hernial orifice, then complete venous stasis in the supradiaphragmatic part of the stomach does not occur, since the outflow of blood will be carried out through the veins of the esophagus, and the emptying of the cavity of the supradiaphragmatic part of the stomach occurs through the esophagus. Thus, with sliding hiatal hernias there are no conditions necessary for the development of strangulation, while paraesophageal hernias can cause strangulation just as easily as ordinary ventral hernias.

Diagnosis. When recognizing hiatal hernias, you should pay attention to the patient’s complaints: those with features of gastroesophageal reflux. They can be defined quite clearly.

X-ray examination is necessary to diagnose hiatal hernia. It begins with the patient in an upright position. With a cardiofundic or giant gastric hernia, part of the gas bubble of the stomach is found in the posterior mediastinum. A contrast study confirms that the detected clearing refers to the stomach displaced upward.

A cardiac hernia can be detected only when the patient is transferred to a horizontal position, although even in a standing position it is manifested by a number of indirect radiological signs that make it possible to suspect it. These include a decrease in the size of the gas bubble of the stomach, up to its complete absence, shortening of the abdominal esophagus, an obtuse angle of His and thickening of the folds of the mucous membrane of the cardiac part of the stomach. These phenomena are associated with insufficiency of the valvular function of the cardia and injury to the stomach, which periodically penetrates the relatively narrow hernial orifice. In a horizontal position, part of the cardiac part of the stomach extends into the posterior mediastinum.

In diagnosing complications of hiatal hernias, we carefully use x-ray cinematography, which allows us to identify very subtle changes.

Gastroesophageal reflux is often detected radiographically, but most often it can be detected by probing the esophagus with the introduction of a colored liquid into the stomach, as well as esophagomanometry, which also allows one to determine the degree of decompensation of the esophagocardial sphincter.

Let us present the medical history of a patient with a pronounced clinical picture of a cardiac hernia of the esophageal opening of the diaphragm.

Volnaya Sh., 37 years old, was admitted with complaints of pain in the epigastric region that is not associated with food intake, a burning sensation in the lower third of the esophagus, heartburn and belching after eating, periodic vomiting, weight loss (5 kg). I have been suffering from pain in the epigastric region for about 5 years. Over the past year, heartburn and pain in the right and left hypochondrium began to bother me. No dysphagia noted. The patient's condition is satisfactory. No pathological changes were detected in blood and urine tests. Urine diastasis 64 units. Based on the complaints, a hiatal hernia, complicated by reflux esophagitis, was suspected. An X-ray examination in the Trendelenburg position revealed a cardiac hiatal hernia (Fig. 125). When esophagomanometry in the terminal part of the esophagus, its spasm is determined, caused by terminal esophagitis, and gastroesophageal reflux is expressed.

Treatment. Treatment of patients with a sliding hiatal hernia should begin with conservative measures. First of all, these include appropriate nutrition and diet. Patients should eat food often, in small portions, which helps reduce reflux. The diet for normal gastric secretion should be close to anti-ulcer. Under no circumstances should you eat at night. The last meal should be 3-4 hours before bedtime. You should not lie down to rest after eating, as this also makes reflux easier. After eating, it is advisable to take a short walk or sit, reclining somewhat. Patients should also sleep with the head end of the bed raised, on two pillows. If the symptoms of reflux esophagitis are pronounced, drug treatment can be prescribed, which should be combined with antiulcer drug therapy aimed at reducing gastric secretion and relieving spastic phenomena on the part of smooth muscles.

Only in the absence of effect from conservative therapy should patients with severe symptoms of reflux esophagitis be recommended to undergo surgery. Surgical treatment is also indicated for a number of complications: bleeding leading to anemia, peptic stenosis of the esophagus, volvulus of the stomach, almost entirely displaced into the chest cavity, and if the development of a malignant tumor is suspected. It should be noted that hiatal hernias are often combined with esophagocardial carcinoma. In less than 10 years, we observed 35 such patients. There is an opinion that a hernia leading to a chronic inflammatory process contributes to the development of cancer. It is very difficult to diagnose a tumor developing in the displaced esophagocardial region. Therefore, patients with unrejected suspicion of cancer should always undergo surgery.

For paraesophageal hernias due to strangulation, surgical treatment is also indicated.

Of more than 600 patients with a sliding hiatal hernia who applied to our clinic, 109 were operated on. It should be taken into account that patients with the most severe clinical picture of reflux esophagitis come to the surgical facility.

In the surgical treatment of hiatal hernia, transperitoneal and transthoracic approaches can be used. Preference should be given to the less traumatic transperitoneal approach. The transpleural approach in the clinic was used mainly in cases where the hernia was combined with shortening of the esophagus. Surgery for a sliding hiatal hernia should be aimed not only at eliminating the hernia itself, but primarily at restoring the valvular function of the cardia.

There are several types of operations.

Reduction of the stomach into the abdominal cavity and plastic surgery of the hernial orifice. The main stage of the intervention, which can be performed either through the abdomen or transpleurally, is suturing the medial legs of the diaphragm behind the esophagus to each other, thereby narrowing the hernial orifice. This operation is usually called crurorrhaphy. Other methods of hernial orifice repair have been described, including those using alloplastic materials. We have developed a technique for hernial orifice repair with wrapping the esophagus with a pedicled diaphragmatic flap. This operation, performed transthoracically, virtually eliminates the possibility of a hernia recurrence.

Unfortunately, after simply moving the stomach into the abdominal cavity, gastroesophageal reflux does not always disappear. This is due to the fact that in some patients the angle of His remains unfolded. In addition, with a long course of the disease, decompensation of the esophago-cardiac sphincter occurs (due to frequent overstretching during reflux). Therefore, we recommend that crurorrhaphy be performed only in combination with one or another intervention specifically aimed at restoring the valvular function of the cardia.

To restore the cardiac valve, esophagophundoraphy , i.e. suturing the fundus of the stomach with the esophagus, thereby restoring the acute angle of His. We perform this operation with partial envelopment of the terminal part of the esophagus with the wall of the fundus of the stomach (Fig. 126).

Esophagofundorraphy is effective only in the absence of severe decompensation of the esophagocardial sphincter, the functional state of which we determine using esophagomanometry. If the function of this sphincter is significantly impaired, then one should resort not to esophagofundoraphy, but to the fundoplication proposed by Nissen.

Fundoplication consists of completely enveloping the terminal part of the esophagus with the wall of the fundus of the stomach (Fig. 127). In this case, a screw valve is created in the area of ​​the cardia, which functions even with complete decompensation of the esophagocardial sphincter. In 64 patients who underwent this operation in our clinic, gastroesophageal reflux completely disappeared. We recommend that fundoplication, like all other operations aimed at restoring the valvular function of the cardia, be supplemented with pyloroplasty, since after manipulations in the area of ​​the cardia, where the trunks of the vagus nerves pass, pylorospasm phenomena may subsequently be observed.

When a hernia is combined with a shortening of the esophagus of the first degree, in our clinic, after fundoplication, without eliminating the hernia, they perform an additional expansion of the hernial orifice, cutting the diaphragm anteriorly and suturing the stomach with separate sutures to a fairly wide esophageal opening of the diaphragm. This detail of the operation is called mediastinalization of the cardia due to the fact that the latter remains firmly fixed in the mediastinum.

This proposal is due to the fact that if, when the esophagus is shortened, the stomach is brought down into the abdominal cavity and crurorrhaphy is performed, then the continuing tendency of the esophagus to longitudinal spastic contraction can lead to a recurrence of a traction hernia, which we observed in our practice. It is the contraction of the longitudinal muscles of the esophagus in response to certain chronic irritations of the receptors of the vagus nerves that is one of the leading causes of acquired shortening of the esophagus. Therefore, recurrences of hernia with a short esophagus are very frequent. If the stomach moves into the mediastinum along with the fundoplication cuff, then reflux in such patients does not resume, but spastic pain caused by compression of the stomach in the narrow hernial orifice is usually significant.

With mediastinalization of the cardia, combined with fundoplication, reflux disappears due to the creation of a screw valve, and compression of the stomach does not occur, since the hernial orifice becomes wide enough. Fixing the stomach to the edges of the hernial orifice prevents its further displacement into the mediastinum. Our clinic has 24 cases of mediastinalization of the cardia performed through laparotomy, and no complications associated with leaving the cardia in the mediastinum were noted.

In case of shortening of the esophagus of the second degree, when the cardia is fixed above the diaphragm higher than 4 cm, it is not possible to perform fundoplication from a laparotomic approach. In such cases, Nissen (1960) suggested performing fundoplication transpleurally. If it is impossible to bring the stomach completely under the diaphragm due to significant shortening of the esophagus, Nissen leaves its upper section in the pleural cavity, as is done during resection of the cardia of the stomach with intrapleural esophagogastroanastomosis. However, due to the fact that a significant part of these patients are elderly, traumatic transpleural surgery does not completely solve the problems of surgical treatment of a shortened esophagus of the second degree.

We have developed an intervention that allows us to operate through the abdomen in case of shortening of the esophagus of the second degree. This operation, called valve gastropplication, involves creating a valve from the stomach wall while simultaneously lengthening the esophagus through the stomach. It works as follows. After mobilization of the cardia of the stomach and a small sagittal diaphragmotomy, the upper part of the cardia of the stomach is transformed into a tube forming a continuation of the esophagus using collecting sutures. A cuff is formed from the gastric wall around this tube, similar to a Nissen fundoplication (Fig. 128). As observations of 9 patients operated on in the clinic showed, valve gastropplication completely relieves patients from reflux esophagitis.

To illustrate, we present the medical history of a patient who underwent this operation 3 years ago.

Patient M., 61 years old, was admitted to the clinic on August 28, 1964 with a diagnosis of a tumor of the cardia. He complained of difficulty passing through the esophagus, painful heartburn, and pain in the epigastric region. Heartburn and pain in the epigastric region appeared soon after eating and became more intense if he was in a horizontal position. Ill since 1956. All this time he was treated for hyperacid gastritis. Due to heartburn, I took large amounts of baking soda. Dysphagia arose in May 1964. The feeling of food retention was localized at the level of the xiphoid process. Upon admission to the clinic, the condition was satisfactory. Based on the patient's complaints, a hiatal hernia with pronounced reflux esophagitis was suspected. Fluoroscopy revealed a cardiofundal hiatal hernia with shortening of the esophagus (Fig. 129). The diagnosis of a cardinal tumor was rejected. Esophagoscopy revealed symptoms of pronounced peptic esophagitis with a scarring ulcer on the anterior wall of the terminal esophagus. During esophagoscopy, it was possible to observe the reflux of gastric contents into the esophagus. Due to the fact that targeted treatment for a hiatal hernia was never carried out, the patient was discharged home on 19/IX for conservative therapy, which, however, turned out to be ineffective, and on 9/XII 1964 he was hospitalized again. A control X-ray examination confirmed the diagnosis of cardio-fundal hernia with shortening of the esophagus of the II degree. In the terminal section of the esophagus, an area of ​​intermittent spasm is identified, corresponding to which there is a spot of contrasting mass with folds of the mucous membrane converging towards it and a partial narrowing of the esophagus. Gastroesophageal reflux is clearly expressed. Clinical diagnosis: cardio-fundal hiatal hernia, II degree shortening of the esophagus, ulcerative reflux esophagitis, initial stage of peptic stricture of the esophagus. On January 6, 1965, the operation was performed under endotracheal anesthesia. From the upper, middle laparotomy access, valve gastropplication was performed with mediastinalization of the cardia and extramucosal pyloroplasty. The postoperative period proceeded without complications, 26/1 patients were discharged home in satisfactory condition. His condition to this day (3 years after the operation) remains quite satisfactory. All complaints, including dysphagia, disappeared after the operation. X-rays reveal a well-functioning cardiac valve formed from the stomach wall. The esophagus is freely passable. There is no gastroesophageal reflux. It was also not detected during probing of the esophagus and esophagomanometry.

A hiatal hernia often occurs in elderly and debilitated patients, i.e. in individuals for whom surgery poses significant risk. With painful symptoms of reflux esophagitis in such cases, palliative intervention is sometimes recommended, namely transection of the left phrenic nerve in the neck.

We have 5 similar observations. In 3 patients this operation was effective. How can one explain the positive effect of frenicotomy? The fact is that paralysis of the left dome of the diaphragm, firstly, reduces intra-abdominal pressure, and, secondly, the paralyzed dome of the diaphragm, rising upward, drags along the bottom of the stomach, which leads to independent reduction of the hernia and restoration of the acute angle of His. It should, however, be remembered that it is almost pointless to perform this operation when the esophagus is shortened, since the hernia in such cases is firmly fixed in the mediastinum and will not correct itself.

In conclusion, we should once again emphasize the high frequency of the pathology we have considered, the need for a serious study of the diagnosis, clinical picture and complications of this type of hernia and the correct, strictly differentiated and individually applied therapeutic measures.

Literature [show]

1. Doletsky S. Ya. Diaphragmatic hernias in children. M., I960.
2. Multivolume manual on surgery. T. 6, book. 2. M., 1966.
3. Petrovsky B.V., Kanshin N.N., Nikolaev N.O. Diaphragm surgery. L., 1966.

Source: Petrovsky B.V. Selected lectures on clinical surgery. M., Medicine, 1968 (Educational literature for student medical institutes)

Hiatal hernia ( HH) is characterized by the penetration of part of the stomach into the chest cavity through the esophageal opening of the diaphragm. The frequency of this type of hernia increases with age: among patients aged 50-60 years, it is detected in approximately 60% of those examined. Four out of five patients are over 40 years of age. Hernias account for 90% of all diaphragmatic hernias. The frequency in girls and boys is the same, however, in women it is more common (pregnancy and childbirth, predisposition to obesity, longer life expectancy) than in men.

Classification of hernias:

1. Traumatic and non-traumatic.
2. False (absence of a hernial sac, for example, traumatic) and true.
3. Congenital and acquired.
4. Hernia of the diaphragm itself:
   - hiatal hernia;
   - hernia of the anterior diaphragm;
   - relaxation of the diaphragm (there is no defect, but part of the diaphragm protrudes due to insufficiency of the diaphragm muscle).

Etiology

There are congenital hiatal hernias (in children) and acquired ones (in adults). The main factors for acquired hernias are weakness of connective tissue and increased intra-abdominal pressure.

Anomalies of the musculotendinous apparatus of the cardia fixation of congenital and acquired age origin (involutive hernias) are important. The expansion of the diaphragmatic ring with the possibility of inserting 1-3 fingers into it explains the possibility of freedom of movement (Halter). Often combined with hernias of other localizations, varicose veins, flat feet, diverticula, visceroptosis.

Significant changes in intra-abdominal pressure (flatulence and constipation, overeating, ascites, physical labor) are a provoking factor!

Pathogenesis

There are sliding (axial) and paraesophageal (paraesophageal) hernias. Sliding hernias develop with increased intra-abdominal pressure, longitudinal contractions of the esophagus and weak attachment of the esophagogastric junction to the diaphragm. As a result, the fundus of the stomach and this connection are displaced upward.

The essence of a hiatal hernia is the sequential prolapse of the abdominal esophagus, cardia and upper stomach. Analogous to intussusception. It should be distinguished from a paraesophageal hernia, in which the upper part of the stomach prolapses without displacement of the cardia and esophagus.

With a sliding hernia, the anatomical connection of the stomach and esophagus lies above the diaphragm, and the angle between the esophagus and the fundus of the stomach is lost. With paraesophageal hernias, the esophagogastric junction remains in its normal position, and the fundus of the stomach and the greater curvature are wrapped above the diaphragm.

There may be a combination of axial and paraesophageal. Some experts believe that this condition is an advanced development of a paraesophageal hernia with pronounced traction of the cardia, leading to the occurrence of an additional sliding hernia.

Hernias grow slowly over the years, but progress steadily according to the laws of hernias. The vagus nerve is secondarily involved, leading to functional disorders. The consequence of hernias is reflux esophagitis. Reflux esophagitis (peptic esophagitis) occurs due to the reflux of stomach contents into the esophagus due to dysfunction of the lower esophageal sphincter.

The pathological process with hiatal hernia proceeds as follows: compression and bending of the abdominal organs in the hernial orifice → compression of the lung and bending of the mediastinum → dysfunction of the diaphragm.

Symptoms

There are two large groups of symptoms: gastrointestinal and cardiorespiratory. The clinic depends on various combinations of the type of prolapsed organs, the degree of their filling, as well as the size and location of the hernial orifice.

Clinical manifestations for small sliding hernias are usually absent. But with large hernias, symptoms may be caused primarily by reflux esophagitis. Gastroesophageal reflux is detected in many patients, but not everyone develops esophagitis. The result depends on the ratio of mucosal resistance and gastric juice aggressiveness.

Most often, patients complain of pain of varying intensity associated with eating, but it can also be independent. The pain is retrosternal and can be localized in the area of ​​the xiphoid process. Reflex angina with hiatal hernia is associated with food intake or exacerbation of reflux esophagitis. Often, hiatal hernias are accompanied by heartburn, belching and, in severe reflux esophagitis, dysphagia and bleeding.

Paraesophageal hernias are formed during normal fixation of the esophagogastric junction, and the gastric vault is displaced into the posterior mediastinum through the diaphragm next to the esophagogastric junction. Unlike sliding hernias, paraesophageal hernias can be strangulated and strangulated. Paraesophageal hernias usually have no characteristic symptoms. Only some patients develop dysphagia, pain in the epigastric region and behind the sternum, and belching after eating.

Hiatal hernias are usually easily identified by X-ray examination. Sliding hernias are formed above the diaphragm, have an oval shape, and folds of the gastric mucosa are often visible in them, going through the esophageal opening of the diaphragm. Detection of cardia under the diaphragm is a pathognomonic sign of sliding hernias. Indirect signs of these hernias include expansion of the lower third of the esophagus, a widened obtuse angle of His with a high confluence of the esophagus into the stomach and a decrease in the gas bubble of the stomach.

The consequence of hernias is reflux esophagitis, often disguised as signs of diseases such as gastric and duodenal ulcers, cholecystitis, pancreatitis, duodenitis, colitis, coronary artery disease (the so-called " upper abdominal masquerade"(C.Harrington)). However, it should be remembered that reflux esophagitis is often combined with other diseases of the digestive tract. In this case, the symptoms of reflux esophagitis are included in the overall clinical picture as part. However, 10-20% of patients are asymptomatic.

Complications

Strangulated hernias occur rarely and are usually paraesophageal. Complications of reflux esophagitis:

• erosions and ulcers of the esophagus, bleeding from them,
• esophageal strictures,
• laryngitis,
• pulmonary aspiration,
• replacement of the stratified squamous epithelium of the esophagus with a single-layer cylindrical epithelium (Berreth's esophagus),
• precancer with a risk of developing adenocarcinoma.

Diagnostics

The basis of diagnosis is x-ray examination. Paraesophageal hernias are detected mainly by X-ray examination. Plain X-ray of the chest reveals a round clearing against the background of the shadow of the heart in the posterior mediastinum. When taking barium, the location of the cardia in relation to the diaphragm is clarified and the relationship of the part of the stomach prolapsing into the hernia with the esophagus is studied. The key is a contrast multiplanar examination while lying down with increased intra-abdominal pressure (without fanaticism). Direct sign: reflux of barium suspension from the stomach into the esophagus. In addition: flattening or absence of the angle of His, “thickening” of the gastric vault, changes in the gas bubble of the stomach, displacement of the esophagus during breathing by more than 3 cm.

Endoscopic research methods (esophagoscopy and gastroscopy) are of no importance in the diagnosis of hiatal hernia; however, endoscopy provides additional information. For diagnosis, it is important to see the hernial cavity starting behind the gaping cardia displaced in the oral direction. The combination of the following signs is important:

• decreasing the distance from the incisors to the cardia (39-41 cm in men and 38-39 in women);
• the presence of a hernial cavity;
• gaping of the cardia;
• gastroesophageal reflux with stomach contents;
• distal esophagitis.

At the slightest suspicion of cancer, bleeding, peptic structure of the esophagus and ulcers, with which differential diagnosis is carried out, esophagoscopy with biopsy and esophageal manometry are indicated. If you have a clinical picture of reflux esophagitis, you should start thinking about the hiatal hernia.

A congenitally short esophagus with a “thoracic” stomach has symptoms similar to those of hiatal hernia. Anamnestic data indicating the presence of a similar condition from early childhood allows one to suspect a congenital disease.

Treatment

Asymptomatic hiatal hernias do not require any treatment. If sliding hernias are accompanied by reflux esophagitis, it should be treated. The criterion for the effectiveness of conservative treatment is positive changes in the endoscopic picture of the esophageal mucosa.

For paraesophageal hernias, due to the risk of strangulation, surgical treatment should be performed. Indications for surgery:

1. Complicated reflux esophagitis (overt and hidden bleeding and anemia, ulceration, strictures), regurgitation.
2. Giant hernias with anemic, hemorrhagic and compression syndromes.
3. Paraesophageal types of hernias due to the risk of strangulation.
4. Concomitant diseases of the upper abdominal cavity requiring surgical treatment.

The goal of surgical treatment is to restore the obturator mechanism of the cardia, eliminate the peptic factor. Dozens of types of operations have been proposed. Collective experience has shown that the abdominal approach is more gentle. Moreover, patients are people in the second half of life. Currently, the most common method is R. Nissen (1955), performed from the abdominal approach in combination with vagotomy for high acidity of the stomach. The laparoscopic version of the Nissen technique is becoming increasingly widespread.

His angle (W. His, 1863-1934, German anatomist)

the angle between the walls of the esophagus and stomach; G. value affects the speed of passage of food from the esophagus to.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary of Medical Terms. - M.: Soviet Encyclopedia. - 1982-1984.

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Gastroesophageal reflux disease (GERD) is a disease caused by the development of inflammatory changes in the distal esophagus and/or characteristic symptoms due to regularly repeated reflux of gastric and/or duodenal contents into the esophagus.

EPIDEMIOLOGY

The true prevalence is unknown, which is associated with the wide variability of clinical symptoms: from occasional heartburn to clear signs of complicated reflux esophagitis. The true prevalence of GERD is much higher than official statistics due to the existing difficulties in using diagnostic methods. In addition, less than 1/3 of GERD patients see a doctor.

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

In the United States, 10-20% of adults experience heartburn (the main symptom of GERD) weekly.

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

CLASSIFICATION

According to ICD-10, GERD is divided into GERD with esophagitis and GERD without esophagitis. In clinical practice, different terminology is accepted:

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

Endoscopically positive reflux disease, or reflux esophagitis.

Rice. 39-1. Severity of reflux esophagitis.

Table 39-1. Classification of reflux esophagitis

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

Complications of GERD include:

Peptic strictures;

Esophageal bleeding;

Barrett's esophagus.

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

ETIOLOGY AND PATHOGENESIS

The reasons for the development of GERD include the following.

Weakening the function of the antireflux barrier (the obturator mechanism of the cardia of the stomach).

Reduced esophageal clearance.

Reduced resistance of the esophageal mucosa to damaging factors.

Increased production of hydrochloric acid and pepsin in the stomach, and the entry of bile into the stomach.

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

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

The mechanisms that support the functionality of the esophagogastric junction (cardia obturator mechanism) include:

Lower esophageal sphincter;

Diaphragmatic-esophageal ligament;

Mucous “socket”;

Acute angle of His, forming Gubarev's fold;

Intra-abdominal location of the lower esophageal sphincter;

Circular muscle fibers of the cardia of the stomach.

LOWER ESOPHAGAL SPHINTER

The main role in the obturator mechanism belongs to the state of the lower esophageal sphincter. At rest in a healthy person it is closed. Normally, transient relaxations last for 5-30 seconds and help relieve the stomach of excess air swallowed during meals. In patients with GERD, these spontaneous episodes of lower esophageal sphincter relaxation are frequent and prolonged. The reason for this is a violation of esophageal peristalsis, fast and heavy meals, when a large amount of air is swallowed.

The tone of the lower esophageal sphincter is reduced:

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

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

Lesions of the vagus nerve (vagal neuropathy in diabetes mellitus, vagotomy).

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

A decrease in the function of the antireflux barrier can occur in three ways:

Primary decrease in pressure in the lower esophageal sphincter;

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

Complete or partial destruction of the sphincter, for example, with a hiatal hernia, scleroderma, after surgery, pneumocardiodilation.

GIS ANGLE

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

REDUCED CLEARANCE

The esophagus is equipped with an effective mechanism that eliminates pH shifts to the acidic side - esophageal clearance. In 50% of patients with GERD, esophageal clearance is reduced. In this case, the following options for esophageal clearance are affected:

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

Volumetric - due to inhibition of secondary peristalsis and decreased tone of the wall of the thoracic esophagus.

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

RESISTANCE OF THE ESOPHAGUS MUCOSA

Provided by preepithelial, epithelial and postepithelial factors.

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

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

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

CLINICAL PICTURE

A special feature of GERD is that the severity of clinical symptoms (heartburn, pain, regurgitation) does not depend on the severity of changes in the mucous membrane of the esophagus. Symptoms of the disease do not allow differentiating non-erosive reflux disease from reflux esophagitis.

All symptoms can be combined into two groups: esophageal (heartburn; belching of sour, bitter or food; regurgitation; dysphagia; odynophagia; chest pain) and extra-esophageal (cough, asthma attacks, shortness of breath, hoarseness or hoarseness of voice, dry throat, drooling, caries, signs of anemia).

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

HEARTBURN

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

BUPPING AND regurgitation of food

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

RETROSTERMAL PAIN

It spreads to the interscapular region, neck, lower jaw, left half of the chest and can simulate angina pectoris. When differentially diagnosing the origin of pain, it is important to establish what provokes and relieves pain. Esophageal pain is characterized by a connection with food intake, body position and its relief by taking alkaline mineral waters and antacids.

DYSPHAGIA

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

DIAGNOSTICS

The main methods used to detect gastroesophageal reflux are:

X-ray examination;

Endoscopic examination;

Daily monitoring of esophageal pH;

Study of motor function of the esophagus;

Histological examination.

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

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

Chromoendoscopy detects metaplastic and dysplastic changes in the epithelium of the esophagus by applying substances to the mucous membrane that stain healthy and affected tissues differently. In addition, you can see prolapse of the gastric mucosa into the lumen of the esophagus, especially noticeable during gagging movements; true shortening of the esophagus with the location of the esophagogastric junction above the diaphragm. Assessing the closure function of the cardia is difficult, since it can open in response to the introduction of an endoscope or insufflation of air.

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

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

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

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

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

COMPLICATIONS

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

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

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

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

Esophagus Barrett(See section 39.2 Barrett's esophagus).

TREATMENT

The choice of treatment method is related to the characteristics of the course and the cause of GERD. Treatment of GERD can be therapeutic or surgical.

THERAPEUTIC TREATMENT

Avoid loads that increase intra-abdominal pressure: do not wear tight clothes and tight belts, corsets; do not lift weights exceeding 8-10 kg with both hands; avoid physical activity associated with abdominal strain.

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

Sleep with the head of the bed raised.

Stop smoking.

Normalize body weight.

Medication treatment

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

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

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

In the treatment of reflux esophagitis, drugs containing sodium alginate have proven themselves to be effective. It forms a foamy antacid suspension floating on the surface of the gastric contents, and, entering the esophagus in the case of gastroesophageal reflux, gives a therapeutic effect.

Blockers N 2 -receptors histamine. For reflux esophagitis, ranitidine and famotidine are widely used, which significantly reduce the acidity of the refluxed gastric contents, which helps relieve the inflammatory and erosive-ulcerative process in the mucous membrane of the esophagus.

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

SURGICAL TREATMENT

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

FORECAST

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

39.2. BARRETT'S ESOPHAGUS

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

Barrett's esophagus with intestinal metaplasia occurs in approximately 10-20% of people with GERD. The risk of developing adenocarcinoma in Barrett's esophagus is 1 in 200 to 400 patients per year. Barrett's esophagus is 10 times more likely to develop in men (especially older adults) than in women.

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

Clinical painting Barrett's esophagus is no different from that of GERD. In this regard, it is necessary to exclude the presence of Barrett's esophagus in any patient with a long history of GERD (more than 5 years).

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

Treatment

If low-grade dysplasia is detected, high (double) doses of proton pump inhibitors are prescribed. After 3 months, a repeat histological examination is performed. If low-grade dysplasia persists, treatment with proton pump inhibitors is continued in the same doses, performing control histological examinations after 3 and 6 months, and then annually.

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

39.3. ESOPHAGITES

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

INFECTIOUS ESOPHAGITES

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

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

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

Fungal esophagitis. With fungal esophagitis, white or yellowish deposits on the hyperemic mucous membrane of the esophagus are endoscopically detected. During bacteriological and histological examination of biopsy specimens, filamentous forms of the fungus are determined. Patients suffering from fungal esophagitis and immunodeficiencies are recommended to take oral medications that include imidazole derivatives (bifonazole, oxiconazole). Patients with granulocytopenia due to the high risk of dissemination of fungal infection are prescribed amphotericin B intravenously.

DRUG-DRUG ESOPHAGITES

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

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

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

39.4. ACHALASIA OF THE CARDIA

Achalasia (Greek) A- - absence, chalasis- relaxation) of the cardia - a disease of the esophagus in which reflex relaxation of the lower esophageal sphincter during swallowing is absent, and the tone and peristalsis of the thoracic esophagus are impaired.

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

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

Clinical painting. A characteristic symptom of achalasia cardia is dysphagia. At the beginning of the disease, dysphagia occurs only when eating solid food, then gradually dysphagia occurs when drinking liquid. In some cases, dysphagia is remitting. As a result, patients require significantly more time to eat. To speed up the emptying of the esophagus, patients often resort to certain techniques, for example, drinking a glass of water in one gulp.

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

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

A large amount of esophageal contents;

Impaired evacuation of contrast agent into the stomach;

Moderate or significant (spindle-shaped or S-shaped) dilatation of the esophagus with narrowing in the distal part (symptom of “mouse tail”, “carrot tip” or “bird beak”);

No gas bubble in the stomach.

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

Manometrically, with achalasia cardia, hypertonicity of the lower esophageal sphincter, the absence of its reflex opening, as well as impaired peristalsis of the thoracic esophagus are detected.

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

Treatment. The main method of treatment for achalasia cardia is pneumocardiodilation (expansion of the cardial opening of the stomach using an inflated rubber balloon, resulting in a partial rupture of the muscles of the lower esophageal sphincter). The rate of good results of this treatment method is 86-100%. The effect lasts for 2-8 years or more; if dysphagia recurs, repeat courses of cardiodilation are performed.

Long-acting nitrates and calcium channel blockers reduce pressure in the lower esophageal sphincter and improve esophageal emptying, but are not a complete replacement for cardiodilation.

Patients with achalasia cardia should be monitored by a gastroenterologist. They are advised to undergo X-ray and endoscopic examination of the esophagus at least once a year.

Forecast. The prognosis without treatment is serious: the disease progresses and can lead to death from exhaustion. The prognosis is worsened by the high probability of esophageal cancer (2-7% of cases) and aspiration pneumonia.

39.5. TUMORS OF THE ESOPHAGUS

MALIGNANT TUMORS OF THE ESOPHAGUS

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

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

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

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

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

Achalasia cardia;

Alcohol abuse;

Smoking;

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

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

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

Progressive dysphagia.

Regurgitation of gastric contents.

Chest pain.

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

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

Painful cough, wheezing when the tumor invades the trachea and large bronchi.

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

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

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

Diagnostics. X-ray examination plays an important role in the diagnosis of esophageal cancer. When the tumor grows exophytically with disintegration and ulceration, a filling defect with uneven, corroded contours is revealed. The most informative method for diagnosing esophageal cancer is FEGDS.

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

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

Differential diagnostics. It is performed with the following diseases characterized by symptoms of dysphagia:

Peptic and burn scar strictures of the esophagus;

Esophagospasm;

Achalasia cardia;

Benign tumors and diverticula of the esophagus;

Lymphogranulomatosis, lymphosarcoma (characterized by enlargement of the cervical and mediastinal lymph nodes);

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

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

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

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

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

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

BENIGN TUMORS OF THE ESOPHAGUS

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

Benign tumors are subject to surgical treatment to avoid malignant degeneration and complications (bleeding, inflammation, etc.).

Gastroesophageal reflux disease develops as a result of insufficiency of the closure function of the cardia, manifested by signs of pathological gastroesophageal reflux (acid or alkaline) with the subsequent development of peptic reflux esophagitis of varying severity, extraesophageal manifestations caused by the direct effect of the refluxant on the organs (laryngitis, pharyngitis, bronchopneumonia) , and those that occur reflexively when refluxed gastric contents enter the esophagus (reflex angina).

There is a wide prevalence of gastroesophageal reflux disease and reflux esophagitis among the population. GERD is detected in 5.8%-10.7% of patients undergoing endoscopic examination, and in frequency is second only to peptic ulcer disease, detected in 14.7%. The true prevalence of the disease has been little studied, which is due to the wide variability of clinical manifestations - from occasional heartburn to clear signs of complicated reflux esophagitis, and only a quarter of patients consult doctors about this.

5.1. Factors determining the closing function of the cardia

The reasons influencing the development of GERD are diverse, among them: blunting of the angle of His, a decrease in the mucous-muscular fold in the area of ​​the esophageal-gastric junction - Gubarev valve, an increase in the distance between the crura of the diaphragm, a shortening of the length of the abdominal esophagus, a decrease in the tone of the lower esophageal high pressure zone, decrease in the esophageal-gastric pressure gradient, disappearance of the stretching of the self-tightening muscle loop in the cardia area.

The angle of His, formed by the fundus of the stomach and the left rib of the abdominal esophagus, is normally 30-40 degrees. The authors believed that with a sliding hiatal hernia, dystopia of the cardiac part of the stomach into the chest cavity occurs, which promotes straightening of the angle of His, and sometimes its complete disappearance. This leads to a decrease in the role of the gas bubble in the valve mechanism of the cardia and the occurrence of pathological gastroesophageal reflux.

The development of reflux esophagitis due to blunting of the His angle, which occurred after gastrectomy or selective proximal vagotomy for peptic ulcer disease, was observed in 50.5% by V.P. Petrov et al. . Restoration of the acute angle of His for prophylactic purposes in patients who underwent gastric resection according to Hofmeister-Finsterer allowed A.I. Gorbashko et al. reduce the incidence of reflux esophagitis from 48% to 10%.

V.A. Kuznetsov on corpses proved the valve action of the mucous-muscular fold in the area of ​​the esophageal-gastric junction (Gubarev valve).

A.S.Balalykin et al. ; A.G. Khitaryan et al. ; Pzicolo R. believed that the acute angle of His contributes to the formation of a gas bubble of sufficient size in the stomach, which presses the Gubarev fold to the right wall of the esophagus and thereby prevents gastroesophageal reflux. In this regard, during operations for pathological gastroesophageal reflux and always after selective proximal vagotomy in patients with peptic ulcer disease, they restored the acute angle of His, which made it possible to avoid gastroesophageal reflux in most patients.

At the same time, experiments on dogs by A.G. Zemlyanaya et al. showed that esophagofundoplication with a degree of coverage of the esophagus of 180 degrees, in fact, the creation of an acute angle of His, does not provide a full antireflux effect in GERD. K.V.Lapkin et al. Referring to the results of their research and the German scientists U. Kunath and W. Spalteholz, they established that blunting of the angle of His does not lead to GERD.

Our radiological and intraoperative determination of the His angle in 271 patients with GERD who had various chronic diseases of the abdominal organs showed that when GERD was combined with hiatal hernia, every second person had an obtuse or right angle of His, and in patients with GERD combined with CGD and cholelithiasis - the angle of His was acute. We have not established any relationship between the size of the hiatal hernia and the value of the His angle. When comparing the value of the His angle with the severity of reflux esophagitis, confirmed by endoscopic examination, a statistically unreliable tendency was noted for the more frequent detection of severe morphological changes in the esophagus in patients with an obtuse and right angle of His.

Since the gas bubble of the stomach is of decisive importance in the formation of the His angle, we believe that the size of the His angle depends on its volume. In patients with GERD, frequent emptying of the gas bladder (belching air) leads to blunting of the angle of His. Most likely, it is not the value of the His angle that determines the closure function of the cardia, but insufficiency of the cardia function contributes to its blunting. Since GERD almost always accompanies patients with hiatal hernia, and the clinical picture of NDFC is most pronounced in them, blunting of the His angle is more often observed in this group of patients.

According to V.Kh.Vasilenko et al. ; A.I.Gorbashko et al., A.V.Kalinin; A.G. Khitaryan et al. ; Mittal R.K. et al. the closing action of the legs of the diaphragm is especially evident during deep inspiration, when, due to the contraction of the latter, the esophagus narrows and is pulled to the right and upward, which leads to its bending and closure in the area of ​​the esophageal opening of the diaphragm (hiatal loop). Measurements of the size of the esophageal opening of the diaphragm carried out by A.I. Gorbashko et al. showed that normally in the transverse direction it ranges from 1.9 cm to 3 cm, in the longitudinal direction - from 3.5 cm to 6 cm, and when a thick gastric tube No. is inserted into the esophagus. 36 the index finger should pass between the edge of the inner leg of the diaphragm and the wall of the esophagus. The authors believed that with an increase in the distance between the legs of the diaphragm, which often occurs with hiatal hernia, the obturator mechanism of the cardia is disrupted, which is the cause of its insufficiency.

Meanwhile, according to E.M. Masyukova, V.G. Thun, wide sagittal diaphragmotomy according to A.G. Savinykh in patients and intersection of the crura of the diaphragm in the experiment of U. Kunath, do not lead to insufficiency of the closure function of the cardia. In addition, the operation of cutting the diaphragmatic legs, proposed by some surgeons for the treatment of achalasia cardia, as a rule, did not affect the function of the cardia and was ineffective.

We measured the distance between the legs of the diaphragm intraoperatively in 397 people. with GERD, of which 216 patients had open and 181 people. in closed versions of operations. In more than half of the patients (253 people, 63.7+2.4%), the distance between the legs of the diaphragm was unchanged and corresponded to 3.5-4 cm. If there was an enlargement of the esophageal opening of the diaphragm, it usually did not exceed 4-7 cm. More than 7 cm. The distance between the diaphragmatic legs was noted in only 7 patients (1.8%). Dilation of the esophageal opening of the diaphragm was more typical for patients with hiatal hernia, which can serve as an intraoperative diagnostic sign of this disease. The relationship between the severity of reflux esophagitis and the distance between the legs of the diaphragm was not observed.

D.X. Baron, F.G. Moody considered shortening the length of the abdominal esophagus to be the leading cause of NDFC. The distal portion of the esophagus, located in the positive pressure sphere of the abdominal cavity, forms an insulating tube and functions as a valve in response to increased intra-abdominal pressure. The degree of consistency of the cardia provided by the intra-abdominal segment of the esophagus directly depends on its length.

N.Y. Laurie, O.S. Radbil; A.L. Grebenev, A.A. Sheptulin; A.V. Vukolov, V.A. Kubyshkin believed that the lower esophageal zone of high pressure is the main factor ensuring the consistency of the cardia. Others believe that the tone of the LESVD alone is not capable of reliably preventing the flow of gastric contents into the esophagus, therefore, in the mechanism of closure of the cardia, both valvular (angle of His, Gubarev valve, abdominal esophagus) and pectoral functions (USVED) are distinguished. V.G. Sakhautdinov, O.V. Galimov, A.G. Khitaryan et al. In addition to these two functions, a diaphragmatic component was added.

Based on numerous studies by A.F. Chernousov et al. proved that the main indicator of the functional state of the cardia is the gradient of esophageal-gastric pressure, which normally corresponds to 14.6 mmHg.

Meanwhile, K.V. Lapkin et al. pointed out the inconsistency of generally accepted ideas about the functioning of the esophagocardial junction, based on the separation of the cavities of the stomach and esophagus (cardiac sphincter, gas bubble of the stomach, angle of His, contraction of the crura of the diaphragm). They supported U. Kunath's theory that the closure of the cardia is ensured by the physiological tension of the esophagus. Thanks to the helical structure of the esophageal muscles, a self-tightening loop is formed in the cardia area, which, when the length of the esophagus decreases, as happens with a hiatal hernia, leads to the release of the closure zone and the opening of the entrance to the stomach (gaping). In our opinion, the weak point in this theory is that it does not explain the development of GERD in other diseases of the abdominal organs in the absence of a hiatal hernia.

Quite a lot of observations have been published in the literature that GERD often accompanies many common chronic diseases of the abdominal organs. However, the reasons for the development of GERD in certain diseases are poorly understood and remain insufficiently clarified.

V.M. Buyanov et al. , Yu.M. Pantsyrev et al. , P.Ya. Grigoriev et al. , believed that dysfunction of the esophageal-gastric junction is largely due to an increase in intragastric pressure caused by increased gastric motility and a violation of its evacuation function, which in ulcer patients is directly dependent on the severity of deformation of the pylorus and duodenal bulb. D.I. Tamulevichute et al. described the development of NDFC with hypermotility and impaired gastric evacuation due to pylorospasm in patients with gastroduodenal ulcers, cholecystitis, hepatitis, duodenitis, etc. Along with this, V.K. Ilinich et al. Based on the results of a survey of 1738 patients, we came to the conclusion that duodeno-gastric reflux and impaired antrum-pyloroduodenal motility are not significant in the formation of gastroesophageal reflux. K.Ruchauer et al. proved that the pressure of the intragastric pressure decreases during peristalsis of the esophagus and increases with an increase in intragastric pressure. A hiatal hernia, according to the authors, is not the cause of esophagitis.

There are conflicting opinions in the literature about the development of reflux esophagitis depending on the acidity of the refluxant. V.P. Salupere et al. It was believed that the frequent combination of reflux esophagitis with duodenal ulcer is due to the high acidity of gastric juice in these patients. The authors observed that reflux of aggressive gastric contents into the esophagus was more common with increased rather than decreased acidity of gastric juice. V.V. Utkin, G.A. Ambalov, E.D. Palmer, Z. Szymanski doubted the significant role of hydrochloric acid in the genesis of reflux esophagitis. E.B.Vygodner et al. proved that reflux esophagitis can occur with both increased and normal or decreased secretory and acid-forming functions of the stomach.

Our analysis of the results of a study of the acid secretion function of the stomach in 252 patients with GERD did not reveal a correlative dependence of the severity of reflux esophagitis on the volume of gastric secretion and the acidity of gastric juice. Consequently, indicators of the acidity of gastric juice in patients with GERD are not decisive in the development of reflux esophagitis; what is more important is the presence of gastrointestinal tract, its intensity, height and duration of refluxant retention in the esophagus.

The combination of GERD and chronic cholecystitis was explained by J. Foster, K. Kuntson as a complex of congenital and acquired defects of the sphincter of the cardia and sphincter of Oddi. A.V. Kalinin noted that in case of cholelithiasis, reflux esophagitis is often caused by reflux of duodenal contents into the esophagus. Along with this, T. Larmi et al. in an experiment on dogs, he discovered that the rapid introduction of bile into the stomach increases the tone of the NSAID.

The presented literature data indicate that the closing function of the cardia is ensured by many factors, but the significance of each of them has not been sufficiently clarified. The reasons for the development of GERD in chronic diseases of the abdominal organs have not been disclosed.