Hiatal hernia and reflux esophagitis. Clinic and diagnostics

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 health care. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

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In healthy people, gastroesophageal reflux can occur mainly during the day after meals (postprandial), between meals (interprandial) and much less often at night (at horizontal position), but in these cases the intraesophageal pH decreases to less than 4.0 for no more than 5% of the total time of esophageal pH monitoring.

The results of intraesophageal pH monitoring during the day in healthy volunteers showed that episodes of gastroesophageal reflux occur no more than 50 s total duration no more than 1 hour normal conditions in the lower third of the esophagus the pH is 6.0. During gastroesophageal reflux, the pH either decreases to 4.0 when acidic stomach contents enter the esophagus, or increases to 7.0 when duodenal contents mixed with bile and pancreatic juice enter the esophagus.

Normally, to prevent damage to the mucous membrane (MU) of the esophagus, the following protective mechanisms are activated:

1. Antireflux barrier function gastroesophageal junction and lower esophageal sphincter.
2. Esophageal cleansing (clearance).
3. Resistance of the esophageal mucosa.
4. Timely removal of gastric contents.
5. Control of the acid-forming function of the stomach.

Violations in the coordination of the first three mechanisms have highest value in the development of reflux disease.

The most common reasons for a decrease in the function of the antireflux barrier are:

1. Hernias hiatus diaphragm (more than 94% of patients with reflux esophagitis have a hiatal hernia).
2. Increased frequency of spontaneous relaxations (relaxations).
3. Decreased pressure in the lower esophageal sphincter.

The action of the antireflux mechanism is ensured by the following factors:

• the length of the abdominal part of the esophagus;
• angle of His (an acute angle at which the esophagus enters the stomach; normally its dimensions range from 20 to 90 degrees depending on the person’s constitution);
• legs of the diaphragm;
• Gubarev's fold, formed by the mucous rosette of the cardia.

An important place in fixing the esophagus in the esophageal opening of the diaphragm is occupied by the Morozov-Savvin ligament (diaphragmatic-esophageal ligament). It resists upward traction of the cardia, allowing movements in the esophagus during swallowing, coughing, and vomiting. The peritoneum also contributes to the fixation of the esophagus: on the right, the abdominal section of the esophagus is held by two peritoneal layers forming the hepatogastric ligament, and at the back by the gastro-pancreatic fold of the peritoneum. Paraesophageal fatty tissue, the gas bubble of the stomach and the left lobe of the liver also contribute to fixation of the esophagus. Atrophy of muscle fibers in the area of ​​the esophageal opening of the diaphragm, and, first of all, the Morozov-Savvin ligaments that occurs with age or due to other reasons, leads to expansion of the esophageal opening of the diaphragm, the formation of a “hernial orifice,” increased mobility of the esophagus and predisposes to the development of a hiatal hernia.

Hiatal hernia (HH) is a chronic recurrent disease associated with displacement of the abdominal esophagus, cardia, upper stomach, and sometimes intestinal loops through the esophageal opening of the diaphragm into the chest cavity (posterior mediastinum). The first descriptions of the hiatal hernia belong to the French surgeon Pare Ambroise (1579) and the Italian anatomist G. Morgagni (1769). The frequency of detection of hiatal hernia ranges from 3% to 33%, and in old age up to 50%. Hiatal hernias account for 98% of all hiatal hernias. It is important to note that in 50% of patients it does not cause any clinical manifestations and, therefore, is not diagnosed.

Highlight congenital hernias, the formation of which is associated with uneven development of the muscles and openings of the diaphragm, incomplete descent of the stomach into the abdominal cavity, obliteration of the air-intestinal pouches, weakness connective tissue in the esophageal and aortic openings of the diaphragm. Most hiatal hernias in adults are acquired and are formed as a result of the combined influence of various factors, of which the main role is played by the weakness of the connective tissue structures and atrophy of the muscle fibers that form the esophageal opening of the diaphragm, increased intra-abdominal pressure and upward traction of the esophagus in dyskinesias of the digestive tract and diseases of the esophagus.

According to N. Bellmann et al. (1972), the hiatal hernia is a common symptom generalized weakness of connective tissue (small collagenosis). It is assumed that the pathogenesis is due to insufficient absorption of ascorbic acid and impaired collagen synthesis. Observations indicating frequent combinations Hernia with hernias of other localization: inguinal, umbilical, white line of the abdomen, varicose veins lower limbs, diverticulosis of the gastrointestinal tract, confirm this hypothesis.

An increase in intra-abdominal pressure is observed with pronounced flatulence, persistent constipation, pregnancy, especially repeated, indomitable vomiting, severe and persistent cough (it is known that 50% of patients with chronic obstructive bronchitis with a long history of the disease have a hiatal hernia), ascites, if abdominal cavity large tumors, with severe degrees of obesity. Hernias often form after heavy physical exertion, especially in untrained individuals. This mechanism of hernia development is observed in young people. Also, in the pathogenesis of hernia formation, some authors attach importance to trauma and abdominal surgery, in particular gastric resection.

Functional disorders (dyskinesia) of the esophagus often occur with peptic ulcers of the stomach and duodenum, chronic cholecystitis, chronic pancreatitis and other diseases of the digestive system. With hypermotor dyskinesia of the esophagus, its longitudinal contractions cause the esophagus to be pulled upward and contribute to the development of the hiatal hernia. The Castena triad (HH, chronic cholecystitis, duodenal ulcer) and Saint's triad (HH, chronic cholecystitis, colon diverticulosis) are known. A.L. Grebenev identified chronic cholecystitis and cholelithiasis among patients with hiatal hernia in 12% of cases, and duodenal ulcer - in 23%.

There is no uniform classification of hiatal hernia. According to the classification based on anatomical features Hernia, a sliding (axial, axial) hernia is distinguished, characterized by the fact that the abdominal part of the esophagus, cardia and fundus of the stomach can freely penetrate into the chest cavity through the enlarged esophageal opening of the diaphragm and return back to the abdominal cavity. And also paraesophageal, in which the terminal part of the esophagus and cardia remain under the diaphragm, and part of the fundus of the stomach penetrates the chest cavity and is located next to the thoracic esophagus. With a mixed variant of hernia, a combination of axial and paraesophageal hernias is observed.

According to radiological manifestations, depending on the size of prolapse (eventration) of the stomach into the chest cavity I.L. Tager and A.A. Lipko (1965), there are three degrees of hiatal hernia.

In case of stage I hiatal hernia, the abdominal esophagus is located in the chest cavity above the diaphragm, the cardia is located at the level of the diaphragm, and the stomach is elevated under the diaphragm. Excessive displacement of the abdominal segment is considered an initial hernia (vertical displacement normally does not exceed 3-4 cm). With stage II hiatal hernia, the vestibule and cardia lie under the diaphragm, and folds of the gastric mucosa are visible in the diaphragmatic opening. With hiatal hernia III degree together with the abdominal segment of the esophagus and cardia, part of the stomach (body, antrum) also falls into the chest cavity.

According to clinical classifications Hernias (V.Kh. Vasilenko and A.L. Grebenev, 1978, B.V. Petrovsky and N.N. Kanshin, 1962) distinguish between fixed and non-fixed hernias. According to N.N. Kanshina, fixation of the hernia in the mediastinum is caused not by the adhesive process, but by negative intrathoracic pressure. The fixation and size of the hiatal hernia are in an inverse relationship - the smaller the hernia, the greater its mobility and tendency to grow, and vice versa, the larger the hernia, the more often it is fixed and stable in size. Hernias are divided depending on the organs that make up the hernial sac(esophageal, cardiac, fundal, antral, subtotal and total gastric, intestinal, omental), the congenital short esophagus (thoracic stomach) is isolated. In addition, there is a classification of hernias depending on the complications that arise as a result of the presence of a hernia, the first place of which is reflux esophagitis. A vicious circle arises when the hernia leads to reflux esophagitis, and the latter contributes to an increase in the hernia due to the traction mechanism, as well as shortening of the esophagus as a result of the scar-inflammatory process.

The main role in the mechanism of cardia closure is played by the lower esophageal sphincter (LES). The LES is a smooth muscle thickening located at the junction of the esophagus with the cardia of the stomach, 3-4 cm long, with a specific autonomous motor activity, own innervation, blood supply. These features make it possible to distinguish the lower esophageal sphincter as a separate morphofunctional formation. Relaxation of the lower esophageal sphincter is stimulated by the vagus nerve through preganglionic cholinergic fibers and postganglionic noncholinergic and nonadrenergic nerve fibers. Sympathetic impulses increase the tone of the lower esophageal sphincter. In addition, the myogenic properties of the smooth muscles of the lower esophageal sphincter are influenced by various humoral factors: gastrin, motilin, histamine, bombesin, vasopressin, prostaglandin F 2 a alpha-adrenergic agonists, beta-blockers - increase the tone of the lower esophageal sphincter, and secretin, glucagon, cholecystokinin, neurotensin, gastric inhibitory polypeptide, progesterone, prostaglandin, alpha-blockers, beta-adrenergic agonists, dopamine - reduce the tone of the lower esophageal sphincter. At rest, the muscle fibers of the esophagus are in a state of tonic constriction, therefore, under resting conditions in a healthy person, the esophagus is closed, while a pressure of 10 to 30 mm Hg is created in the lower esophageal sphincter. Art. (depending on the breathing phase). The minimum pressure of the lower esophageal sphincter is determined after eating, the maximum at night. During swallowing movements, the muscle tone of the lower esophageal sphincter decreases and after food passes into the stomach, the lumen of the lower part of the esophagus closes. With GERD, hypotension or even atony of the lower esophageal sphincter occurs; pressure in the lower esophageal sphincter rarely reaches 10 mm Hg. Art.

The pathophysiological mechanisms of spontaneous (or transient) relaxation of the lower esophageal sphincter are not yet entirely understood. Perhaps this depends on a violation of the cholinergic effect or on an increase in the inhibitory effect of nitric oxide. Normally, relaxation of the lower esophageal sphincter lasts 5-30 s. Most patients with GERD experience repeated episodes of spontaneous relaxation of the lower esophageal sphincter that cannot be adequately controlled. Transient relaxations of the lower esophageal sphincter can be a response to incomplete swallowing and bloating, so reflux episodes often occur after eating.

Relaxations of the lower esophageal sphincter may be associated with swallowing, which is observed in 5-10% of reflux episodes, their cause is impaired esophageal peristalsis. It should be noted that modern prokinetics are not effective enough in reducing the number of episodes of lower esophageal sphincter relaxation. In the future, we still have to decipher the mechanisms regulating the function of the lower esophageal sphincter and implement them into clinical practice new prokinetic drugs.

Reasons leading to more frequent episodes of spontaneous relaxation (relaxation) of the lower esophageal sphincter:

• disturbance of esophageal peristalsis (esophageal dyskinesia), leading to smoothing of the esophagogastric angle, decreased pressure on bottom part esophagus in the chest. This often contributes to neurotic state patient or diseases such as systemic scleroderma, diaphragmatic hernia;
• hasty, fast and plentiful meals, during which a large amount of air is swallowed, which leads to an increase in intragastric pressure, relaxation of the lower esophageal sphincter (overcoming its resistance) and reflux of stomach contents into the esophagus;
• veteorism;
• peptic ulcer (especially with localization of the ulcer in the duodenum), while gastroesophageal reflux is observed in 1/2 of the patients;
• duodenostasis of any etiology;
• excessive consumption of fatty meat, refractory fats (lard), flour products (pasta, noodles, butter cookies, bread), spicy seasonings, fried foods (these types of food contribute to prolonged retention of food masses in the stomach and increased intra-abdominal pressure).

These factors cause the reflux of gastric or duodenal refluxate containing aggressive factors - hydrochloric acid, pepsin, bile acids, which causes damage to the mucous membrane of the esophagus. Such damage develops with sufficiently long contact of refluxate (more than 1 hour per day) with the mucous membrane of the esophagus, as well as with insufficient functioning of protective mechanisms.

The second factor in the pathogenesis of GERD is a decrease in the clearance of the esophagus, consisting of a chemical - a decrease in the content of bicarbonates in saliva and a decrease in the production of saliva as such, and a volumetric - inhibition of secondary peristalsis and a decrease in the tone of the wall of the thoracic esophagus.

The esophagus is continuously cleansed by swallowing saliva, ingesting food and liquids, secretions from the glands of the submucosal lining of the esophagus, and gravity. With GERD, prolonged contact (exposure) of aggressive factors of gastric contents with the mucous membrane of the esophagus is observed, a decrease in the activity of esophageal clearance and an extension of its time (normally it averages 400 s, with gastroesophageal reflux disease 600-800 s, that is, it is almost doubled) . This occurs as a result of esophageal dysmotility (esophageal dyskinesia, systemic scleroderma, and other diseases) and dysfunction of the salivary glands (the amount and composition of saliva in healthy people is regulated by the esophageal salivary reflex, which is disrupted in older people and with esophagitis). Insufficient salivation is possible with organic and functional diseases of the central nervous system, endocrine diseases (diabetes mellitus, toxic goiter, hypothyroidism), scleroderma, Sjögren's syndrome, diseases of the salivary glands, during radiation therapy of tumors in the head and neck area, during treatment with anticholinergics.

Resistance of the esophageal mucosa is determined by protective system, consisting of three main parts:

• preepithelial protection (salivary glands, glands of the submucosal lining of the esophagus), including mucin, non-mucin proteins, bicarbonates, prostaglandin E 2, epidermal growth factor;
• epithelial protection - normal regeneration of the mucous membrane of the esophagus, which can be divided into structural (cell membranes, intercellular junctional complexes) and functional (epithelial Na + /H + transport, Na + -dependent transport CI-/HCO3; intracellular and extracellular buffer systems; cell proliferation and differentiation);
• postepithelial protection (normal blood flow and normal tissue acid-base balance).

Based on the above, it can be argued that GERD occurs when there is an imbalance between aggressive factors of gastric contents and protective factors with a clear predominance of aggressive factors.

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.

Behind last years It has been established that the diaphragm (i.e., its muscle bundles forming 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 most high pressure appears 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 back wall 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. Hernias large sizes(cardiofundal and giant) are always fixed due to the suction effect of the thoracic 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.

Titles certain species hiatal hernias are given 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.

Concerning origin of hernias esophageal opening, then, like hernias of other localizations, they can be congenital and acquired. Acquired hiatus hernia are observed much more often, and a significant role in their origin is played by age-related changes. 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 localizations, flat feet, varicose veins veins of the lower extremities.

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 severe 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 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 may 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.

Cardiac hernia can be detected only when the patient is transferred to a horizontal position, although in a standing position it manifests itself in a number of indirect radiological signs, allowing her to be suspected. 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.

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. Diet at normal gastric secretion should be close to antiulcer. 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. For severe symptoms of reflux esophagitis, you can prescribe drug treatment, which should be combined with antiulcer drug therapy aimed at reducing gastric secretion and relieving spastic phenomena on the part of smooth muscles.

Only if there is no effect from conservative therapy patients with severe symptoms For reflux esophagitis, surgery should be recommended. 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 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 in 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 pleural cavity, as is done during resection of the cardiac part of the stomach with the imposition of intrapleural esophagogastroanastomosis. However, due to the fact that a significant part of such 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 cardiac part of the stomach and a small sagittal diaphragmotomy top part The cardiac part of the stomach is transformed into a tube with collecting sutures, forming a continuation of the esophagus. 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.

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 hernia in children. M., I960.
2. Multi-volume 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 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 do not have 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. With plain fluoroscopy chest a rounded clearing is revealed 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, with bleeding, peptic structure of the esophagus and ulcers, which are treated differential diagnosis, 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, allow 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. Performance criterion conservative treatment are 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.

1. Anatomical cardia- area of ​​the esophagogastric junction.
2. Antiperistaltic position- such an arrangement of a fragment of the stomach or intestines (artificial esophagus), in which its own contractions are multidirectional with the natural passage of food through gastrointestinal tract.
3. Aspiration (in this context)- entry into the respiratory tract of stagnant contents of the esophagus.
4. Biopsy - diagnostic test, consisting of histological analysis tissue fragments taken from endoscopic examination.
5. Bougienage of the esophagus - medical procedure, in which the lumen of a narrowed section of the esophagus is expanded with hollow radiopaque plastic tubes, the so-called. bougies with a diameter of 5 to 20 mm (No. 12-40), drawn along the guide string.
6. Intraesophageal pH-metry- a study in which, using a special probe, the acidity of the stomach contents entering the esophagus, the height of the spread of reflux and the frequency of reflux are determined. It is a very reliable way to diagnose gastroesophageal reflux.
7. Gastrostomy (enterostomy)- surgical treatment for obstruction of the esophagus, which consists in removing the tube from the stomach (or small intestine) to the front abdominal wall for nutrition
8. Dysphagia- a symptom of many diseases of the esophagus, caused by a violation of the esophageal phase of the act of swallowing and consisting in a feeling of difficulty passing food through the esophagus. Dysphagia can be expressed in varying degrees - from difficulty swallowing solid food to complete obstruction of the esophagus.
9. Gastric tube- the most physiological type of graft (artificial esophagus), used to replace the affected esophagus. It is cut out from the greater curvature of the stomach in the isoperistaltic direction using special stapling devices with power supply to the right gastroepiploic artery.
10. Isoperistaltic position- such an arrangement of a fragment of the stomach or intestines in which its own contractions are unidirectional to the natural passage of food through the gastrointestinal tract.
11. Peptic stricture- a type of cicatricial narrowing of the esophagus that develops as a complication of severe reflux esophagitis as a result of direct damaging effects of hydrochloric acid and bile on the esophageal mucosa.
12. Esophageal fistula- is a pathological anastomosis between the esophagus and any organ or cavity.
13. Regurgitation- regurgitation, reflux of food from the esophagus into oral cavity.
14. X-ray of the esophagus- a type of special study of the esophagus, which involves taking pictures at the time of swallowing a thick contrast agent - an aqueous suspension of barium sulfate.
15. Selective proximal vagotomy (SPV)- cavitary surgical intervention, the essence of which is the selective intersection of multiple secretory branches of the vagus nerve innervating the fundus and body of the stomach.
16. Sideropenic syndrome (plummer-vinson)- dysphagia due to atrophy of the mucous membranes of the mouth, pharynx and esophagus in combination with seborrheic dermatitis and hypochromic anemia. Occurs only in women.
17. Esophageal stricture- narrowing of the lumen of the esophagus of various nature. There are cancerous (stenoses) and benign (scar, neuromuscular, etc.) strictures. According to their length, cicatricial (burn, peptic, traumatic) strictures of the esophagus are divided into short (up to 5.0 cm) and long. Among the extended ones, subtotal ones are distinguished, when only the thoracic esophagus is affected, and total ones, which involve the entire esophagus.
18. Thoracoabdominal lymph node dissection - surgical technique consisting in the removal of regional thoracic and abdominal lymph nodes for the esophagus.
19. Transhiatal (transdiaphragmatic, transmediastinal)- a type of surgical access to the esophagus, carried out from the abdominal cavity through an incision in the diaphragm.
20. Tracheobronchoscopy- intraluminal examination of the trachea and bronchi using flexible fiber endoscopes.
21. Angle of His- the angle formed by the abdominal segment of the esophagus and the fundus of the stomach.
22. Physiological cardia - collective concept, which includes a number of anatomical formations of the esophageal-gastric junction area (muscles of the lower segment of the esophagus, angle of His, gas bubble of the stomach, legs of the diaphragm, Gubarev's mucosal fold), providing the pectoral-valve function of the esophageal-gastric junction.
23. Fundoplication- a surgical technique for creating a special cuff from the fundus of the stomach that envelops the abdominal esophagus. A fundoplication cuff is an artificial valve that prevents the backflow of acidic contents from the stomach into the esophagus.
24. Esophageal shunt plasty- a variant of esophagoplasty, in which the continuity of the digestive tract is restored by passing a fragment of the colon behind the sternum, bypassing the own affected esophagus. In this case, the graft, like a "shunt", connects cervical region esophagus with stomach or small intestine.
25. Esophagogastroduodenoscopy (EGDS)- intraluminal examination of the esophagus (esophagoscopy), stomach and duodenum using flexible fiber endoscopes.
26. Esophagomanometry- a method for recording intracavitary pressure in the esophagus along its entire length, as well as in the cardia and stomach.
27. Esophagoplasty- surgical intervention to create an artificial esophagus from one’s own plastic material - stomach, large or small intestine, skin. In this case, the own esophagus can be completely removed (esophageal extirpation) or left in the posterior mediastinum (bypass surgery).

Other areas: reflux esophagitis, peptic strictures of the esophagus,