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Cardiospasm of the esophagus is a complex disease characterized by inflammation and spastic contraction of the walls of the organ. The condition is accompanied by unpleasant symptoms that reduce a person’s performance and worsen the general condition. Causes of cardiospasm of the esophagus may depend on various external and internal factors. The disease is difficult to treat, which often leads to complications.

What factors cause the development of the disease?

The disease is rare and is still under the special supervision of scientists. Cardiospasm of the esophagus can begin to develop against the background of neurogenic disorders, external and internal factors, as well as even at the time of intrauterine development of the embryo (congenital malformations).

The following internal factors for the development of the disease are distinguished:

• esophageal injury;
• bad habits and their toxic effects;
• development of neoplasms;
• prolonged muscle contractions of the cardia.

External factors

In addition, various types of esophageal stenosis also cause damage to the organ. External factors include various pathological processes that develop in the abdominal organs.

External causes include:

• gastritis;
• hematomegaly;
• pleurisy;
• sclerosis of the esophagus with adhesions;
• peritonitis;
• gastroporosis;
• aortitis;
• aortic aneurysm;
• aerophagy.

According to numerous studies, esophageal cardiospasm can develop in parallel with autoimmune diseases such as type 1 diabetes and hypothyroidism.

If we talk about neurogenic disorders, then this includes such diseases:

• typhus;
• polio;
• herpes;
• scarlet fever;
• flu;
• diphtheria;
• measles;
• meningoencephalitis.

These infectious neurotropic diseases violate the integrity of the nervous apparatus, which is located on the periphery of the organ.

By what signs can the disease be recognized?

At first, the disease develops imperceptibly, the symptoms increase gradually. This complicates timely diagnosis and treatment. The first thing that a patient may notice with the development of the disease is a few obvious signs that bring discomfort and become the first signal of negative changes in the upper digestive system.

First symptoms:

• during eating there is pain behind the sternum;
• there is an eructation with an unpleasant odor;
• the reflex process of swallowing is disturbed;
• there is a sensation of a lump in the throat.

It is worth paying a little more attention to the last symptom of esophageal cardiospasm described. The sensation of a lump in the throat appears after the passage of food from the esophagus to the stomach after a few seconds. A similar sensation is localized in the neck, and mainly when eating solid food. This is the first thing a person can feel when the disease develops.

Another characteristic symptom for this disease is regurgitation. In this condition, there is a reverse movement of food through the esophageal tube into the oral cavity, while without a gag reflex. This symptom most often occurs when eating large meals or during sleep (nocturnal regurgitation or "night cough").

Pain behind the sternum is distinguished by spastic and bursting character. The appearance of pain occurs due to the gradual stretching of the esophageal tube and, as a result, pressure on neighboring organs. In addition, pain can occur due to intense muscle contraction of the organ itself.

A patient suffering from cardiospasm of the esophagus often loses significant body weight. This happens due to the fact that while eating food, a sore throat is felt, so a person tries to eat less, and, as a result, loses weight.

Treatment Methods

If the disease can be detected at the initial stages of development, then the doctor will suggest conservative treatment. At a later stage, the treatment of cardiospasm of the esophagus is carried out with the help of surgery. The conservative method involves following a special diet, daily regimen and taking medications prescribed by a doctor.

Medicines that a doctor may prescribe:

• antispasmodics (No-shpa, Drotaverine, Dinitrate);
• antiemetics (Metamol, Latran, Perinorm, Senorm, Cerucal);
• sedatives or sedatives (motherwort tincture, Valerian, Belloid);
• enveloping agents for the mucosa of the esophagus (De-nol, Almagel, Gastal);
• painkillers (Novocain or Anestezin);
• prokinetics to improve digestion (Bromopride, Domperidone, Dimetramid);
• antagonists (Tiropamil, Nifedipine, Lacidipine);
• vitamin complexes (vitamins of groups B and C).

It is worth remembering that drugs should be prescribed only by the attending physician after a complete diagnosis and an accurate diagnosis. Self-medication often leads to complications.

Nutrition for cardiospasm of the esophagus

As for the diet, the patient needs to give up solid foods that will injure the esophagus, and give preference to warm and liquid foods.

From the diet you need to completely exclude:

• alcohol;
• vegetable oil;
• all semi-finished products;
• carbonated drinks;
• spices;
• kefir;
• potato;
• hard fruits.

Fried and spicy foods are under a particularly strict ban.

Surgery

In this case, balloon hydration is prescribed. During the procedure, a probe is inserted into the upper part of the digestive system, at the end of which there is a balloon. It is here that the correct pressure is created under the control of a manometer. During the operation, the surgeon uses small expanders with a gradual increase in their diameter. Complications during the intervention may develop at the very beginning of the therapy. In 85% of all cases, the results are positive.

Results

In order to get the desired results from the treatment, you need to pay attention to all the signals that the body sends. At the first manifestation of symptoms, you should seek professional help as soon as possible. When contacting a doctor in a timely manner, 86-87% of patients are cured. Later stages of the disease threaten the development of respiratory infections, dehydration and severe exhaustion.

The occurrence of a pathological condition, such as cardiospasm of the esophagus, brings the body into a reflex relaxed state of the lower sphincter during swallowing reflexes.

As a result, incoming food in lumps accumulates in the food duct, and expands its upper sections.

This pathology has no age restrictions and gender, so it affects all segments of society and gender equally.

With the manifestation of the first signs of the manifestation of this pathology, it is urgent to visit the doctor and undergo the diagnosis prescribed by him with the necessary treatment.

The main and first signs include:

• dysphagia;
• a sharp decrease in body weight;
• pain in the chest compartment (sternum).

In order to correctly establish the diagnosis of cardiospasm of the esophagus, the doctor uses instrumental and laboratory diagnostics of the patient's body.

Therapy for this type of disease is carried out by the method of surgical intervention or by the method of a conservative approach to treatment.

These methods are prescribed and selected by the doctor, depending on the course of the disease and the appearance of possible complications.

Cardiospasm of the esophagus - a characteristic of the disease

This pathology is expressed by the complete or partial absence of the swallowing reflex and contraction of the lower sphincter.

The cause of this condition is a complete failure in the motility of the esophagus.

The spasms resulting from this create stagnation of the food content in the esophagus, which leads to an increase in the upper part and the appearance of an inflammatory condition of the digestive organ.

The esophagus changes its shape due to the development of different stages of the pathological condition:

• the initial stage of the development of a pathological disease - no changes are observed;
• an increase in the esophagus by 3-4 cm occurs at the second stage of the development of the disease;
• expansion of the esophagus up to 6 cm and thickening of the walls - indicates the third stage of development;
• the fourth stage leads to an elongation of the esophagus and a change in its appearance to a peculiar shape in the form of the English letter S.

The main risk group for this pathology are people with obvious signs of mental disorders, but also different strata of society, regardless of status and age, as well as gender.

In some cases, children begin to suffer from this pathology, in whom this disease usually passes in a severe form due to a weak body.

Clinic of the esophagus

For the initial stage of the disease, certain symptoms of the disease are expressed, and as the pathology develops, they become more noticeable and pronounced. The main and obvious symptom is dysphagia.

This symptom and pathological deviation from the norm is expressed in a violation of the swallowing reflex, which leads to an abundant accumulation of food in the esophageal tube.

In addition, this symptom is characterized by two main features:

• belching with the smell of rotten and fermented food;
• severe arching pain in the chest caused by an increase in the esophagus.

These symptoms are complemented by common signs and troubles associated with this pathology:

• severe weakness of the whole body;
• lack of appetite;
• a sharp decrease in weight;
• chronic manifestations of diseases of the human cardiovascular system.

The lack of timely treatment of this pathology brings additional diseases to the patient's body:

• pneumonia of the lungs;
• abscesses of internal digestive organs and vessels;
• lung atelectasis.

When the first signs and causes characteristic of this pathology appear, it becomes the first wake-up call in which you need to act without delay.

Timely therapy will save the patient from severe and serious complications.

The course of treatment is prescribed by the attending doctor, according to the diagnostic measures taken. Self-medication in this situation is dangerous to life and health.

The occurrence and causes of this pathology

Even despite the development of science and medicine, scientific minds have not yet fully identified the cause of this pathology.

There are opinions that the development of this disease is preceded by such factors:

• mental disorders;
• stressful situations;
• structural changes in the tissues of the nerve endings that are responsible for the reflexes of the body and the esophagus itself.

The development of the above factors creates conditions for malfunction of nerve endings and untimely contraction of the smooth muscles of the esophagus.

The inconsistency in work interferes with the movement of food through the tube channel, which leads to its accumulation and inflammatory disease.

In addition, an increase in the tone of the muscular system plays an important role in the development of this pathology and the increased tone of the food tube.

Therapeutic measures of general importance

Therapy for cardiospasm of the esophagus is carried out in a conservative and surgical way and depends on the development and complexity of the pathology, the symptoms of the course of the disease.

Conservative treatment includes the use of drugs, dietary therapy and adherence to the regimen of the day and nutrition.

What medications are prescribed for cardiospasm of the esophagus (achalasia cardia):

• antispasmodics;
• sedatives;
• calcium antagonists;
• means having the ability to envelop;
• prokinetics.

At the beginning of treatment, dietary measures are prescribed, according to table No. 1 prescribed by the nutritionist.

Treatment with folk remedies is also allowed, which includes the use of tinctures, but only with the agreement of the attending physician, since, having a picture of the pathology in his hands, he will be able to correct this treatment.

In some cases, to normalize the general condition and improve reflex swallowing, doctors can use minimally invasive therapies, which involve the installation of a resorbable stent or balloon dilation.

In the absence of improvement in the patient's condition, surgical intervention is used.

Diet Therapy

With the pathology of this disease, dietary treatment is prescribed. Patients with cardiospasm are prescribed dietary nutrition with dietary table No. 1.

Food is consumed in liquid or grated form, in small portions 2-3 times a day.

It is completely forbidden to eat salty, sour, spicy, fatty, hot dishes.

You need to eat slowly, chewing food thoroughly. Types of foods that it is desirable not to eat or reduce in use:

• fresh bakery products;
• dairy products;
• apples of all kinds and varieties;
• peaches;
• boiled potatoes;
• meat of fatty varieties and breeds.

It is forbidden to eat before bedtime, as this will lead to stagnation in the esophagus and suppuration of food lumps.

Therapy with medicines for the pathology of cardiospasm of the esophagus

At the beginning of the disease, this pathology is amenable to drug treatment. Therapy in this situation is carried out in a complex, and drugs and tablets have a wide range of their action.

First of all, a certain group of medicines has a relaxing effect on the muscles and muscles in the lower part of the esophagus.

The group of these drugs include:

• dinitrate;
• Nitroglycerine;
• Isosorbite.

Cardiospasm of the esophagus, treatment requires complete relaxation of smooth muscles, for the free passage of food through the tube.

For this, myotropic antispasmodics are used. This group includes such drugs:

• Halidor;
• Papaverine;
• Drotaverine tablets.

These drugs relieve muscle spasms and reduce the pain of the patient. Doses of use are prescribed by the doctor, according to the picture of the course of this pathology.

It all depends on the stage of development of the disease, the severity of the course of the disease, the individual characteristics of each organism separately.

To speed up the healing process, general strengthening therapy is additionally carried out.

It improves the state of the immune system and the general condition of the patient's body. What is included in the general health course of treatment of this pathology:

• vitamin groups B;
• vitamin C;
• the use of glucose as a substitute and maintenance of the body.

The therapy takes place in full compliance with dietary nutrition and a sparing diet regimen.

Medicines are selected so that when they get stuck in the labor of the duct, they do not cause irritation of the walls of the esophageal mucosa.

In other cases, with the development of a serious pathology of cardiospasm of the esophagus, drugs are used by injection. Balloon dilation helps a lot.

What is balloon dilatation

Balloon dilatation is recognized as the most effective way to treat cardiospasm of the esophagus.

This procedure is performed under general anesthesia. The principle of therapy is to introduce a balloon dilator into the body of a sick person, which is a specially invented device with a balloon at the end of a medical tube.

This action has the ability to stretch the lower alimentary canal of the esophagus. After this event, the process of reflex swallowing improves.

By carrying out several of these procedures, there is a significant improvement in the effect of swallowing. This procedure is carried out in a course and after a certain period of time.

This procedure is not safe for humans. The main danger is the possibility of damage and rupture of the walls of the esophagus.

If the walls of the mucous membrane of the esophagus are ruptured, urgent surgical intervention will be required to eliminate the consequences of this rupture.

In some cases, this procedure, with inept measures, can cause death and is 2-4% of the total dilatation rates.

In addition to this unpleasant moment, mechanical damage to the esophagus can also occur, which will cause internal bleeding into the stomach and duodenum.

Therefore, in order to avoid side effects and processes, this procedure must be carried out only by specialists of high medical rank.

Surgical treatment of this pathology of cardiospasm

What is this surgical intervention? The sequence of actions during this operation:

• between the seventh and eighth rib, the thoracic region of the patient is opened;
• the distal esophagus is separated from the tissues of other organs;
• dissect muscles up to 10-11 centimeters long.

This operation passes at the last stage of the disease and brings positive results for the health of the sick person. Sometimes treatment is prescribed with the help of traditional medicine.

Therapy with traditional medicine

With the help of folk therapies, you can try to relax the muscle tissue of the larynx. For this, sedatives are used.

The following organics have a sedative property:

• valerian;
• herb motherwort;
• peony grass.

Medicinal decoctions are created from this vegetation. True, non-compliance with the rules for preparing tinctures can not only help with this pathology, but also cause serious harm to the body of a sick person, therefore it is better to purchase these drugs at pharmacy kiosks.

Moreover, they do not cost a lot of money and are sold in the public domain. These methods are used for treatment only in conjunction with drug treatment, according to the courses prescribed by the doctor.

Inflammatory processes associated with cardiospasm of the esophagus are also removed with the help of tinctures of such plants:

• chamomile;
• oregano herbs;
• alder leaves;
• althea root crop;
• quince seed.

To increase the tone of the muscles of the lower part of the esophagus, the following tinctures are used:

• Chinese lemongrass;
• ginseng root;
• Eleutherococcus leaves.

Therapy by folk methods is widely used only at an early stage of the disease.

In other cases, only as an aid, with drug treatment.

Preventive measures for this pathology of the esophagus

To prevent this disease or stop the progression of the pathology of the esophagus, it is necessary to organize proper and healthy nutrition.

To do this, you need to revise the food menu and turn off coarse foods from it, refuse fast food in public catering, exclude overeating and follow the daily routine.

It should be remembered that early access to doctors will prevent serious consequences for the health of the victim from this pathology of the disease.

Strict observance of the rules and daily routine, sports and physical therapy, completely eliminate the possibility of developing this human disease.

Forecast of the pathology of cardiospasm

For this pathology, the prognosis becomes positive only with early contact with a medical institution, and timely diagnostic measures are the best way to identify the disease at an early stage of its development.

Useful video

Damage to the upper gastrointestinal tract caused by a malfunction of the parasympathetic nervous system is called esophageal cardiospasm. The disease is accompanied by unpleasant symptoms that negatively affect the general condition and performance of a person. Cardiospasm is an inflammatory disease of the esophagus, it leads to a violation of the swallowing function. The disease must be treated in time to prevent complications.

Characteristics of the disease

Cardiospasm is manifested by the absence of reflex contraction of the lower esophageal sphincter during swallowing. The cause of the spasm is a violation of the motility of the esophagus. Spasms lead to stagnation of food in the esophagus, for this reason it begins to gradually increase in size, inflammatory processes appear.

Changes in the shape of the esophagus depend on the stage of the disease:

1. At the initial stage, no changes are observed.
2. The second stage is characterized by a narrowing of the cardia, the esophagus increases by 2-3 cm.
3. In the third stage, the esophagus expands to 5 cm, its walls become thicker.
4. During the fourth stage, the lengthening of the esophagus continues, it takes an S-shape.

People who are prone to psycho-emotional disorders are susceptible to the disease. The disease can develop at different ages, both men and women are susceptible to it. In some cases, the disease affects children.

The causes of the disease in most cases are associated with dysfunction of the central and autonomic nervous system. Also, the reason for the development of cardiospasm can be a psychological trauma, a strong emotional shock, a viral infection.

Clinical picture

The initial stage is characterized by episodic manifestation of individual symptoms of the disease. As the disease progresses, the symptoms of the disease become more frequent and more pronounced.

The main symptom is dysphagia. This pathological phenomenon is a violation of swallowing, which is accompanied by stagnation of food in the esophageal tube. In addition, the disease is characterized by two more main features:

• bursting chest pain caused by pressure inside the esophagus;
• belching with a rotten smell.

The main symptoms are complemented by concomitant ailments:

• general weakness;
• loss of appetite;
• weight loss
• problems with the cardiovascular system.

Lack of treatment or improper therapy leads to pneumonia, abscesses, atelectasis of the lungs.

The appearance of the first symptoms should be a wake-up call. You need to act immediately. Timely treatment will save you from irreversible processes and complications. The course of therapy should be prescribed only by a doctor. In no case should you prescribe medications for yourself without consulting a specialist.

How to treat the disease

At the initial stage, treatment is carried out in a conservative way. The therapeutic course includes:

• dieting;
• taking medication.

At the next stage, the procedure of forced expansion of the cardiac section is connected. This procedure is called dilatation. The advanced stage of the disease is treated by surgical intervention.

With cardiospasm of the esophagus, treatment should be started as early as possible.

Diet for cardiospasm

The disease requires a mandatory diet. Patients are recommended dietary table number 1 (a and b).

Food is recommended to be consumed in a pureed and semi-liquid state. Food should not be plentiful. Fractional meals are recommended, in small volumes several times a day. Spicy and fatty foods should be excluded from the diet. You can't eat hot food. You need to eat slowly, chewing food thoroughly.

Reception of some products is better to reduce. This applies to the following products:

• fresh white bread;
• kefir:
• apples;
• peaches;
• boiled potatoes;
• fat meat.

To improve the passage of food through the esophagus, immediately after eating, drink a glass of warm boiled water in one gulp. It is strictly forbidden to eat before going to bed, in this case, stagnation of food cannot be avoided.

Medical treatment

At an early stage, the disease is amenable to drug treatment. The treatment is carried out in a complex manner, it includes several groups of drugs with different spectrum of action.

The first group of medicines is aimed at relaxing the muscles in the lower esophagus. The group of these medicines includes:

• Isosorbite;
• dinitrate;
• Nitroglycerine.

Relaxing the muscles will ease the spasm and make it easier for food to pass through.

The group of myotropic spasmolytics includes:

• Papaverine;
• Halidor;
• Drotaverin.

These drugs reduce pain caused by muscle spasm.

The dosage regimen and dosage is developed by the attending physician. The planning of the therapeutic course is made taking into account the stage of the disease, its severity and the individual characteristics of the patient.

In order to speed up recovery, general strengthening therapy is needed. In order to strengthen the body and the immune system, you should include in the course of treatment:

• B vitamins;
• vitamin C;
• glucose solution.

Treatment should be accompanied by a sparing diet. Tablets are selected in such a way that, stuck in the esophagus, they do not irritate the mucous tissues. In some cases, the drug is administered into the body by injection.

Balloon dilatation

One of the effective methods of treating cardiospasm is balloon dilatation. The procedure is performed under anesthesia. The essence of the treatment is the introduction into the body of a balloon dilator - a special probe with a balloon at the end, which is a special device for stretching the lower esophageal canal.

After such treatment, the process of swallowing is greatly facilitated. To achieve the best effect, several procedures are required. You may need to repeat the course of treatment after a certain period of time.

Dilatation is an unsafe procedure, it is associated with the risk of rupture of the esophagus. In this case, an emergency operation to eliminate the consequences will have to be carried out. There is a certain risk of death during a procedure of this kind. As a percentage, the share of risk is 3% of the total number of procedures performed. Dilatation can cause mechanical damage to the esophagus, severe hemorrhage into the stomach. In this regard, it is better to entrust such a procedure to high-level specialists.

Surgical intervention

The most popular operation for diagnosing cardiospasm of the esophagus is the Heller operation. The course of treatment consists of the following steps:

• opening of the chest between the seventh and eighth ribs;
• separation of the distal esophagus from other tissues;
• dissection of muscles up to 10 cm long.

The operation is prescribed at the last, third stage of the disease.

ethnoscience

Traditional medicine offers several effective ways to relax the muscles of the larynx. Have a sedative effect:

• motherwort;
• valerian;
• peony.

Decoctions are made from these medicinal herbs. But it is better to purchase ready-made extracts that are sold ready-made in a pharmacy. Traditional medicine methods should complement the main course of treatment.

Inflammatory phenomena are removed with the help of infusions:

• chamomile;
• marshmallow root;
• oregano;
• alder;
• quince seeds.

You can increase the tone of the lower esophageal canal with tinctures:

• Schisandra chinensis;
• ginseng;
• eleutorococcus.

Treatment with folk methods is effective at the initial stage of the disease. Before starting treatment, a consultation with the attending physician is required.

Prevention

To avoid further development of the disease or prevent the disease, it is important to properly organize nutrition. It is necessary to reconsider the diet, exclude coarse food, do not eat at fast food restaurants. It is not recommended to overeat, meals should be carried out in six doses. An early visit to the doctor is a guarantee of complications of the disease.

Attention should be paid to the organization of the daily routine. Physiotherapy exercises, walks in the fresh air, swimming lessons will help stop the disease or prevent it.

The prognosis of the disease is favorable with early therapy. Timely diagnosis and compliance with preventive measures is the best way to cope with the disease.

Cardiospasm

It is believed that cardiospasm and esophageal achalasia are synonymous with one disease, but there is another point of view. Currently, a number of authors consider cardiospasm and achalasia as two different diseases.

Cardiospasm is a persistent spastic narrowing of the terminal part of the esophagus, manifested by dysphagia and, in advanced stages, accompanied by organic changes in its overlying parts.

With achalasia cardia, there is a lack of relaxation of the lower esophageal sphincter (LES) during the act of swallowing. The absence of this reflex leads to a violation of the tone and motility of the esophagus, which causes a delay in the passage of the food bolus.

Etiology and pathogenesis

The causes and mechanisms of cardiospasm have not been fully elucidated. There is a theory of congenital spasm, infectious, reflex, psychogenic and others. Currently, it is generally accepted that damage to the intermuscular nerve plexus of the esophagus plays a key role in the pathogenesis of cardiospasm. Histological and immunohistochemical studies of the removed preparations showed that with cardiospasm in the wall of the esophagus, a significant decrease and even disappearance of ganglion cells is determined; there are signs of chronic inflammation. The death of postganglionic inhibitory neurons innervating the LES area leads to the predominance of stimulating impulses that are carried by the fibers of the vagus nerve. As a result, the tone of the LES increases sharply, and its relaxation during swallowing is difficult.

It should be noted that the biochemical aspects of LES motility have not yet been fully deciphered. Recent studies point to the important role of nitric oxide and possibly vasoactive intestinal peptide (VIP) as mediators of neuromuscular transmission.

Unfortunately, the cause of damage to the intramural nerve plexus (the etiological factor of cardiospasm) remains unclear. In the past, great importance was attached to this aspect of severe mental trauma. Modern authors are actively discussing the role of a viral infection (in particular, herpetic) in the genesis of damage to the nerve structures of the esophageal wall.

In South America, especially in Brazil, the so-called "secondary" achalasia of the cardia occurs. Unlike the “primary”, idiopathic, etiology of this form of the disease is known - it is caused by Cruz trypanosoma and is one of the manifestations of Chagas disease (American trypanosomiasis). The death of ganglion cells localized in the cells of hollow organs leads to the development of their pathological expansion (megacolon, megaureter, megaesophagus) and dysfunction. The clinical symptoms of primary and secondary achalasia are very similar, as are the approaches to diagnosis and treatment.

Some authors attach great importance to a decrease in the content of nitric oxide, which leads to impaired calcium metabolism and transmission of the neuromuscular impulse. With cardiospasm, there is an increased pressure in the LES zone, the gradient of the esophagogastric pressure can reach 200 mm Hg. Art. and more, at a rate of 10 + 3 mm Hg. Art. The initial stages of cardiospasm are characterized by increased non-propulsive motility of the esophagus. Morphologically, degenerative-dystrophic changes are found in the preganglionic neurons of the dorsal nuclei of the vagus nerves and, to a lesser extent, in the postganglionic neurons of the Auerbach plexus of the esophagus. In connection with the violation of the central innervation during cardiospasm, the smooth muscles of the LES become more sensitive to its physiological regulator - endogenous gastrin, as a result of which a true spasm of the cardia is observed.

With achalasia of the cardia, on the contrary, predominantly postganglionic neurons are affected, as a result, the reflex of opening the cardia to the sip falls out. Manometrically, a normal or even reduced gradient of the esophageal-gastric pressure is found, a significant weakening of the motility of the esophagus is observed. With achalasia, there are no conditions for the occurrence of increased sensitivity of the smooth muscles of the LES to gastrin - the central innervation is preserved.

But, as a rule, a violation of the opening reflex of the cardia and esophageal motility are two parallel processes going on simultaneously, and many authors consider the terms "cardiospasm" and "achalasia of the cardia" to be synonymous.

Classification

In Russia, the most common classification of cardiospasm by stages, proposed by academician B.V. Petrovsky back in 1957. In accordance with this classification, four stages of the disease are distinguished: I - functional spasm of a non-permanent nature without expansion of the esophagus; II - stable spasm of the cardia with a mild expansion of the esophagus (up to 4–5 cm); III - cicatricial changes in the muscle layers of the cardia with a pronounced expansion of the esophagus (up to 6-8 cm); IV - pronounced stenosis of the cardia with significant dilatation of the esophagus (more than 8 cm, sometimes up to 15-18 cm), often its S-shaped curvature and esophagitis. Schematically, these changes are shown in Figure 17.

Some authors distinguish 2 types of the disease according to the nature of the expansion of the esophagus. In the first type, in addition to a persistent violation of the patency of the terminal esophagus, its moderate expansion above the narrowed area is observed, and the esophagus has a cylindrical or fusiform shape. In the second type, there is a significant elongation and saccular expansion of the esophagus, often with its S-shaped curvature (Fig. 18).

Some researchers refer to these two types of disease as cardiospasm and achalasia, respectively.

Clinical picture and objective examination data

Cardiospasm is characterized by a triad of symptoms: dysphagia, pain and regurgitation. The main symptom of the disease is dysphagia, that is, difficulty in passing food through the esophagus during swallowing.

Rice. 17. Scheme of macroscopic changes in I–IV stages of cardiospasm.

X-ray picture of cardiospasm:

A - with type I disease; B - in type II disease. (Cited according to: V.Kh. Vasilenko et al. Achalasia of the cardia. M., 1976)

More often it develops gradually, but in a number of patients it debuts acutely, among complete health. In such cases, the “triggering factor” of the disease is a negative psycho-emotional background or sudden stress. And in the future, the emotional state of the patient significantly affects the severity of dysphagia: excitement, negative emotions increase the difficulty of swallowing. Hurry, fatigue, swallowing poorly chewed pieces of food, drinking cold water also cause an increase in dysphagia. Washing down with warm water and taking warm semi-liquid food leads to easier swallowing. However, some patients experience paradoxical dysphagia - dense food passes into the stomach better than liquid.

There are 4 degrees of dysphagia: I - difficulties that arise when dense food (bread, meat) passes through the esophagus; II - difficulties that arise when taking semi-liquid food (porridge, mashed potatoes); III - difficulty in taking liquids; IV - complete obstruction of the esophagus, when patients are unable to swallow even a sip of water, even saliva does not pass.

Pain with cardiospasm usually occurs when swallowing and is localized behind the sternum. They are associated with stretching of the walls of the esophagus with unopened LES and disappear after regurgitation or passage of food into the stomach. Sometimes pain, on the contrary, appears on an empty stomach or after vomiting. In these cases, they are caused by esophagitis and decrease after eating. In some patients, pain can be quite intense, not associated with the act of swallowing, occur during excitement, physical exertion, or even at rest, at night, due to uncoordinated, spastic contractions of the esophageal muscles.

Regurgitation occurs at the height of difficult swallowing after several sips. In this case, at first there is a feeling of a “lump” in the upper part of the esophagus, and then the food masses involuntarily enter the oral cavity or out. With severe dilatation of the esophagus, regurgitation is less common, but more abundant. Sometimes it is provoked by a change in body position, more often when the patient lies down or leans forward. Most patients have nocturnal regurgitation, which is manifested by leakage of the contents of the esophagus onto the pillow (“wet pillow symptom”). In more severe cases, there is profuse regurgitation with choking and bouts of severe coughing due to the flow of food masses into the respiratory tract, which can lead to aspiration pneumonia.

Weight loss at the onset of the disease is not pronounced and is observed in about half of the patients. With the progression of dysphagia and regurgitation, there is a noticeable weight loss. A small proportion of patients develop malnutrition.

The data of an objective study in cardiospasm are uninformative due to their nonspecificity. The general condition in I-II stages of cardiospasm is good. At III–IV stages, a more pronounced decrease in nutrition is observed. Patients with significant dilatation of the esophagus may have bad breath due to rotting and fermentation of stagnant food masses. Old authors described the expansion of the boundaries of median dullness during percussion (due to the expansion of the esophagus and its displacement to the right) and changes in auscultatory data (splash noise in the presence of a pronounced expansion of the esophagus).

Laboratory and instrumental diagnostics

Laboratory methods for cardiospasm are uninformative, since there are no specific pathological changes in this disease. With the development of complications (for example, aspiration pneumonia, grade III-IV dysphagia), there may be leukocytosis, electrolyte disturbances, etc. Diagnosis of cardiospasm is primarily based on x-ray and endoscopic studies.

The main radiological symptom of cardiospasm is the detection of a conical narrowing of the distal esophagus, which is described as a symptom of "mouse tail", "bird's beak", etc. The overlying esophagus is usually dilated according to the stage of the disease. Dilatation of the esophagus can be very pronounced. X-ray reveals undisclosed cardia during the act of swallowing, impaired peristalsis of the esophagus. Quite often find absence of a gas bubble of a stomach and radiological signs of aspiration pulmonary complications of a cardiospasm (fig. 19).

Endoscopic examination of the esophagus reveals the degree of expansion of its proximal segments, the nature and severity of esophagitis and metaplastic changes. Almost always, with cardiospasm, it is possible to pass the endoscope into the stomach, in contrast to cardia cancer and organic cicatricial stenosis (Melzer's symptom).

Esophageal manometry can confirm the diagnosis of cardiospasm and differentiate it from other neuromuscular diseases. The main manometric sign of cardiospasm is complete or partial non-relaxation of the LES during swallowing. Often there is an increase in the “resting pressure” of the LES and a weakening of the peristalsis of the smooth muscles of the esophagus.

Abroad, to study the emptying of the esophagus in case of suspected cardiospasm, a radionuclide study (scintigraphy) is widely used. To do this, patients are given to drink a special solution containing a radiopharmaceutical, and then the intensity of the gamma radiation caused by it is recorded in the dynamics in a gamma camera. This allows you to specify the time of partial or complete emptying of the esophagus, which is usually significantly slowed down during cardiospasm.

Rice. nineteen. Radiological symptoms of cardiospasm: A - the esophagus is significantly expanded, elongated and shifted to the right; its distal segment is sharply narrowed, the gas bubble of the stomach is absent; B - on the right in the upper lobe of the lung phenomenon of pneumosclerosis as a result of multiple aspiration pneumonias. (Quoted according to: E.M. Kagan. X-ray diagnostics of diseases of the esophagus. M., 1968)

Differential Diagnosis

Cardiospasm is differentiated from tumors of the esophagus and the cardia of the stomach, cicatricial stenosis and diverticula of the esophagus, hiatal hernia (HH). All these diseases have similar clinical symptoms, and dysphagia is the leading symptom.

Malignant tumors the esophagus and cardia are much more common than cardiospasm. Usually people over 50-60 years old get sick, while younger patients suffer from achalasia. Cancer develops over several months and is accompanied by progressive dysphagia, a parallel deterioration in the general condition (increase in weakness, weight loss, up to exhaustion, anemia), while cardiospasm is a long-term disease with a slow course and a good general condition of patients that persists for years.

Narrowing of the cardia in cancer may be accompanied by suprastenotic expansion of the esophagus, which also happens with cardiospasm. However, cancer is characterized by a violation of the integrity of the contour of the wall of the esophagus and stomach with the formation of a filling defect. In this case, the stenotic area is uneven, fuzzy, as if corroded. The evacuation of barium into the stomach occurs in a continuous narrowed stream. The gas bubble of the stomach in cancer, unlike cardiospasm, is well detected (Fig. 20).

Rice. 20. Narrowing of the esophagogastric junction in cancer of the cardia of the stomach. The gas bubble of the stomach is clearly visible. (Quoted from: B. E. Peterson. Cancer of the proximal stomach. 1972)

At HHH the pain syndrome is more pronounced, burning pains are localized behind the sternum and in the epigastrium. Dysphagia is rarely severe, and regurgitation is usually absent. In the x-ray picture, there may be similarities with stage I cardiospasm. For differential diagnosis, it is necessary to conduct a study in a horizontal position, in which one can easily see a sliding HH. Some patients have symptoms diverticulum esophagus are similar to those in cardiospasm. An accurate diagnosis can be made on the basis of X-ray examination.

In complex and diagnostically unclear cases, CT of the chest and abdominal cavity, as well as endosonography of the esophagus, is indicated to clarify the diagnosis.

At I-II stages of cardiospasm, conservative treatment is carried out. The leading place in the treatment of stage III–IV of the disease belongs to surgical methods.

Conservative treatment. For the treatment of cardiospasm used a variety of drugs from a variety of pharmacological groups. However, only two of them have been more or less clinically successful: nitrates and calcium channel blockers. These drugs reduce the tone of the LES and make it easier to swallow. It is believed that nitrates are more effective, but have an intolerable side effect - a severe headache. Calcium channel blockers (nifedipine, diltiazem) are much better tolerated by patients. The latest research proves the promise of using sildenafil (Viagra) in the treatment of neuromuscular diseases of the esophagus.

Drug treatment of cardiospasm is best used in the early stages and in the so-called first type of disease, when the peristalsis of the smooth muscles of the esophagus is still preserved.

In practice, when drug treatment does not give the desired clinical effect (and this happens often), the "starting" method of treatment is most often cardiodilatation (CD). Its essence lies in the forced stretching and partial rupture of the muscles of the distal segment of the esophagus.

In the past, the Stark metal cardiodilator was widely used, which has 4 expanding jaws attached to a metal rod. At the opposite end, a handle with a ratchet is fixed, which provides a dosed opening of the jaws (Fig. 21).

Modern cardiodilators consist of a rubber or PVC probe with a balloon attached to its end (Fig. 22).

The dilator is inserted under X-ray or endoscopic control. The balloon is filled with air or water; while reaching a certain pressure level. The technical details of the intervention (type of anesthesia, duration of exposure to the dilator, repeated KD regimen) vary widely in different clinics. So, in our clinic, for many years, KD was successfully used with a rubber hydrodilator under a pressure of 300 mm Hg. Art. with 1 hour exposure. The intervention was performed under general anesthesia.

Rice. 21. Stark cardiodilator.(Quoted according to: 0. D. Fedorova. Cardiospasm. M., 1973)

In most cases, after KD, there is an improvement in the form of easier swallowing and regression of other symptoms of the disease. In the late stages of cardiospasm (III-IV), there are often indications for surgery, since KD is ineffective or dangerous due to the high risk of rupture of the esophagus.

The most common operations for cardiospasm are esophagocardiomyotomy (Geller operation) and its numerous modifications. Dissection of the muscular membrane of the distal segment of the esophagus eliminates non-relaxation of the LES during swallowing. The modern version of the Heller operation involves the dissection of the muscular membrane with a vertical incision on the anterior wall of the esophagus with a small (1–2 cm) approach to the cardia (Fig. 23).

Rice. 22. Balloon pneumocardiodilator worn on the distal part of the endoscope.(Cited according to: Yu.I. Gallinger, E.A. Godzhello. Operative endoscopy of the esophagus. M., 1999)

Many surgeons excise a strip of the esophageal wall to achieve a more reliable result. Esophagocardiomyotomy can be performed both abdominally and thoracically.

Rice. 23. Esophagocardiomyotomy according to Heller. The stage of separation of the mucous membrane from the muscular layer of the esophagus and cardia.

However, a technically flawless production of the Geller operation is far from always possible. With significant sclerotic changes in the wall of the esophagus, a full-fledged myotomy is difficult to perform. There is a high risk of accidental damage to the mucosa, which leads to the development of mediastinitis and / or peritonitis after surgery. In the remote period, an epiphrenic diverticulum of the esophagus may form due to prolapse of the mucosa through the myotomy opening. Often there is retraction of the dissected tissues with further scarring, which leads to a relapse of dysphagia. Excessive myotomy entails the development of severe reflux esophagitis. To eliminate the shortcomings of the original operation, its modifications were proposed, which provided for the shelter of the myotomy opening: with the method of B.V. Petrovsky - with a flap cut from the diaphragm, V.I. Kolesov - with an omentum on the leg (Fig. 24 and 25).

Rice. 24. Esophagocardioplasty with a diaphragmatic flap according to B.V. Petrovsky: A - a section of the muscular layer of the esophagus was excised, a diaphragmatic flap was formed, the latter was sutured to the muscular edges of the esophagus; B – the flap is fixed, the defect in the diaphragm is sutured. (Quoted according to: O. D. Fedorova. Cardiospasm. M., 1973)

However, the long-term outcomes of such operations were not very good, primarily due to rough scarring of the displaced flaps. A much better way was to cover the incision line with the anterior wall of the fundus of the stomach, which is rotated 180? (Fig. 26).

Rice. 25. Esophagocardiomyotomy with omentoplasty according to V. I. Kolesov: A - suturing of the omentum to the edges of the dissected muscles of the esophagus; B - the final form of the operation. (Cited according to: A.A. Shalimov et al. Surgery of the esophagus. M., 1975)

This operation makes it possible to make the angle of His more acute and thereby reduce the risk of developing cardial insufficiency and peptic esophagitis in the postoperative period.

Rice. 26. Esophagocardiomyotomy with partial fundoplication according to the method of T. A. Suvorova: A - suturing the fundus of the stomach to the edges of the dissected muscles of the esophagus; B - the final form of the operation. (Cited according to: A. A. Shalimov et al. Surgery of the esophagus. M., 1975)

A very serious achievement of recent decades has been the development of a technique for performing such an operation using endovideosurgical techniques. In many foreign clinics, laparoscopic esophagocardiomyotomy with partial fundoplication is currently the "gold standard" of surgical intervention for cardiospasm.

However, in the later stages of the disease (III-IV), esophagomyotomy should not be performed, since in such patients the entire esophagus is pathologically changed, and its peristalsis is sharply weakened or absent. Then a pathogenetically justified method of treatment is subtotal resection or extirpation of the esophagus with its one-stage plasty, as a rule, with a gastric graft. Resection intervention is also indicated after ineffective myotomy and with the development of peptic stricture of the esophagus (as a complication of reflux esophagitis). The experience of our clinic has shown good immediate and long-term results of such operations.

Thus, as already mentioned, in the most general terms, it is possible to formulate the dependence of the method of treating cardiospasm on the stage of the disease: in stage I, drug treatment is used, in II-III - KD, in III-IV - surgical intervention. This text is an introductory piece.

CARDIOSPASM(Greek, kardia heart, gastric inlet + spasmos spasm) - a disease accompanied by a violation of the normal contractility of the esophagus and reflex opening of the cardia.

The first clinical description of K. was given by T. Willisius (1674), and the anatomical description was given by Purton (Purton, 1821). In domestic literature, the wedge, the picture of the disease was first described by N. V. Eck in 1852. S. P. Botkin (1884) detailed the symptoms, differential diagnosis and treatment of "spastic or paralytic" narrowing of the esophagus.

There are various names for the disease. In Russian and German. literature use the term "cardiospasm", in English-Amer. literature "achalasia cardia" (implies the absence of reflex opening of the cardia); in French literature, you can often find the name "dolichoesophagus", "megaesophagus", "cardiostenosis", etc. The disease is also described under other names: idiopathic esophageal dilatation, S-shaped esophagus, esophageal dyssynergia, etc. Despite the abundance of terms, none of they do not fully reflect the essence of the disease.

According to Maingot (R. Maingot, 1944), I. T. Tishchenko (1949), the frequency of K. in relation to other diseases of the esophagus ranges from 3 to 20%; To. meets at any age, almost equally often at men and women. The disease has a different course. In some, a typical wedge, the picture develops in a few months, in others - for several years.

Etiology and pathogenesis

The etiology and pathogenesis have not been fully elucidated, so there are many different theories. Bard (K. Bard, 1919) and others consider K. a congenital pathology; they argue their theory by the fact that the disease occurs in newborns and young children. This theory is also supported by cases of familial K.

According to the organic theory put forward by Mosher (N. Mosher), K. develops as a result of a mechanical obstacle in the area of ​​the cardia. Here, as well as in the zone of the esophageal opening of the diaphragm, fibro-sclerotic changes are found. Expansion of the lumen of the esophagus occurs a second time.

The theory of essential spasm of the cardia, proposed by I. Mikulich (1904), explains K. by the predominance of sympathetic innervation over parasympathetic. The reduction of circular muscle fibers in the area of ​​the cardia creates an obstacle to the passage of food, which causes an increase in peristalsis of the esophagus, the lumen of which subsequently expands due to decompensation of contractility.

K.'s beginning is often associated with mental trauma. An esophageal motility disorder was obtained experimentally by the knocking method in dogs, and more pronounced changes were noted in animals with a weak type of nervous activity. In patients with K., disturbances in the normal interaction of the cortex, subcortex, and internal organs are revealed. Neuropsychiatric disorders are found in 70% of patients with K. It has been established that with K. the bulbodiencephalic sections are affected, in which the centers of swallowing are located, therefore, excitation simultaneously covers all the neurons involved in the conduction of impulses.

The theory of defeat of the vagus nerves has won many followers. In experimental studies and a wedge, observations found that inflammatory, degenerative processes in the vagus nerves, their compression by tumors, scars, enlarged limf, nodes can lead to changes described in K. However, with severe cicatricial-sclerotic and inflammatory processes in the tissue of the mediastinum, extending to the vagus nerves, as well as injuries with the intersection of the nerve trunks rife always develops K. At the same time, it is often observed in the absence of signs of damage to the vagus nerves. N. K. Bogolepov et al. (1960) and others showed that. at To. not only wandering, but also sympathetic nerves and ganglia are damaged.

According to the theory of achalasia proposed by Eingorn (M. E inhorn, 1888), the basis of K. is not a spasm of the cardia, but the absence of its reflex opening. Hurst (A. Hurst, 1914) and others drew attention to patol, changes in the intermuscular nerve plexus, which, in their opinion, are the cause of the disappearance of the reflex opening of the cardia.

According to Trounce et al. (1957) and others, the cells of the nerve plexus in the region of the cardia are not damaged during K. and are in an active state, but due to damage to the overlying sections, they do not receive the appropriate impulses.

Some researchers find damage not to cholinergic, but to adrenergic receptors in the muscle layers of the cardial part of the stomach or in the muscle fibers of the esophageal wall. This theory is the most popular, because it is based on a reliable fact - the degeneration of ganglion cells of the intramural plexus observed in this disease, which is, apparently, the main cause of the development of K.

pathological anatomy

The pathoanatomical picture depends on the duration and stage of the process. Usually, four stages are distinguished (Fig. 1) during the course of the disease (BV Petrovsky). In stage I, there are no visible macroscopic changes. In stage II, the lumen of the esophagus expands to 2.5-3 cm, and the cardia narrows. Microscopically, hypertrophy and edema of muscle fibers are noted (Fig. 2), distinct changes in the intraparietal plexus. In the structure of most nerve trunks, one can see their sharp thickening with distinct swellings caused by vacuolar focal dystrophy (Fig. 3). Some trunks have a branched, spike-like appearance. In stage III, the lumen of the esophagus expands to 3-5 cm. All layers of the esophageal wall are thickened, the predominantly circular layer is hypertrophied in the muscular membrane, and the mucous membrane is plethoric. In the submucosa, focal lymphoid infiltrates are found. The walls of some arteries are sclerosed, their lumen is slightly narrowed. Further progression of vacuolar dystrophy of nerve fibers with loss of their structure is noted (Fig. 4). In the intermuscular layers - the proliferation of connective tissue (Fig. 5), which divides the muscle fibers into separate complexes. In the nerve plexus, disintegration and fragmentation of axial cylinders is observed, the number of ganglion cells is significantly reduced. In stage IV, the expansion of the lumen can be more than 5 cm. The esophagus lengthens and acquires an S-shaped, or serpentine, shape. Its mucous membrane becomes rough, devoid of folds. Microscopic changes become even more pronounced, complete agangliosis is found in the nervous network.

The mediastinal pleura in the last two stages, especially in IV, becomes dense, often adherent to the surface of the esophagus and is difficult to separate from it during the operation. The fiber of the mediastinum surrounding the esophagus, from loose in the initial stages, gradually turns into a dense one. In the diaphragm, in the immediate vicinity of the edges of the esophageal opening, changes in muscle fibers, their swelling, vacuolization, basophilia, loss of striation, and swelling of the connective tissue are detected.

Thus, anatomical and gistol, data testify that sclerotic processes in a mediastinum at To. are secondary and depend on intensity of an inflammation in the esophagus.

Clinical picture

The wedge, for K. is divided into four stages: I - non-permanent spasm of the cardia, II - stable spasm, III - cicatricial changes in the cardia and expansion of the esophagus, IV - sharp cicatricial changes in the cardia and pronounced expansion of the esophagus. Some authors divide K. into compensated, decompensated and complicated forms.

Usually, patients associate the appearance of the disease with some kind of mental trauma, nervous strain. At first, they experience awkwardness when swallowing, a feeling of slow passage of food through the esophagus, "causeless" retrosternal pain. Such phenomena of discomfort in some patients can last for months or even years. In other cases, there is a more rapid progression of the disease, and from the very beginning the patient goes to the doctor with the main complaint of dysphagia (see), a characteristic feature of the cut in the initial stage of K. is its intermittent character. Sometimes patients feel a delay only in the first sips of food, especially if it is cold. There are cases when dysphagia is caused only by products of a certain taste, smell, type. The feeling of dysphagia is aggravated by fast eating. It can last from several minutes to several days and then suddenly disappear. In some cases, dysphagia with K. can be paradoxical: dense food passes well, and liquid and semi-liquid is delayed. Over time, dysphagia intensifies, there are unpleasant sensations behind the sternum, a feeling of compression and fullness, retrosternal pain. To alleviate the condition, trying to help the passage of food, patients use various techniques that increase intraesophageal and intrathoracic pressure, often every sip of dense food is washed down with water.

With the further course of the disease and the violation of the contractility of the esophagus, the food in it lingers for a long time, undergoing fermentation and decay. In advanced cases, patients cause regurgitation to empty the esophagus. This symptom, according to various authors, is observed in 50-90% of patients. Regurgitation can also occur involuntarily, especially during sleep or in the horizontal position of the patient, with torso bending, etc.; P.

From 50 to 80% of patients with K. are concerned about pain in the epigastric region, behind the sternum, in the interscapular space. By nature, they can resemble angina pectoris. At the beginning of the disease (stages I - II), pain occurs simultaneously with a feeling of food delay, that is, it is associated with spastic contractions of the esophageal wall; it has a transient, episodic character. In advanced cases (III-IV stage), the pain is caused by stretching of the esophagus with food accumulating in it, therefore it is more constant and disappears after emptying the esophagus.

Sometimes in III-IV stages of the disease, when the capacity of the esophagus is significantly increased, the feeling of dysphagia decreases, which may be due to damage to the afferent part of the reflex arc and the death of sensitive nerve cells. Apparently, the absence of contractions of the esophagus also matters.

The general condition of patients at To., as a rule, suffers slightly, the expressed weight loss seldom develops. Exhaustion as the cause of deaths is casuistry and is possible only in the absence of treatment. Due to dysphagia, patients try to eat separately, avoid society, their psyche is fixed on painful sensations. The astheno-neurotic reactions which are available before the beginning of specific wedge, K.'s manifestations amplify in process of progressing of a disease, the general weakness, decrease in working capacity appears.

Complications, both general and local, develop in advanced cases. These include primarily congestive esophagitis (see), manifestations to-rogo vary from mild hyperemia of the mucous membrane of the esophagus to the formation of ulcers in the wall of the esophagus. The most formidable common complications K. - pneumonia, lung abscess, caused by aspiration of the contents of the esophagus.

These complications are especially common in children. Quite often at To. diverticula and cancer of a gullet meet. BV Petrovsky and OD Fedorova (1963) observed cancer of the esophagus in 2.8% of patients K., Santy et al. (1958) - in 3.2% of cases. If diverticula of the esophagus develop in K. due to a violation of the nervous trophism of the muscular membrane and an increase in intraesophageal pressure, then congestive esophagitis is most likely the cause of cancer.

Diagnosis

Timely diagnosis To. allows to begin the corresponding treatment early and by that to avoid possible complications.

The main objective methods of diagnosis To. are rentgenol. study, esophagoscopy (see) and esophagomanometry, the study of intraesophageal pressure (see Esophagoscopy).

X-ray examination with suspicion of K. begins with a thorough survey of the transillumination of the chest. With a sharp expansion of the esophagus and the presence of fluid in it, it is possible to see a homogeneous shadow of the dilated esophagus.

A contrast study of the esophagus is carried out by portioning 1-2 glasses of barium suspension of normal consistency. In a polypositional study (see), the contours and walls of the esophagus, the relief of the mucous membrane of the suprastenotic esophagus, as well as the degree of its displacement are determined. In order to possibly improve the patency of the cardiac esophagus, you can give the patient a glass of "effervescent mixture" to drink, with the help of a cut it is also possible to determine the shape, size and elasticity of the gas bubble of the stomach.

The main rentgenol, a sign of K. is the narrowing of the terminal esophagus with clear, even and elastic contours. The folds of the mucous membrane in the area of ​​narrowing are not destroyed. The gas bubble of a stomach is absent. Suprastenotic expansion is noted, sometimes with overhanging of the walls of the dilated esophagus over its narrowed section (Fig. 6). With K., the first two sips of barium can freely enter the stomach. However, then a pronounced spasm of the terminal part of the esophagus sets in, and the esophagus looks as if amputated due to the absence of a shadow of its contrasted abdominal part.

Disclosure of the cardia can occur with intense "empty" swallowing movements, i.e., when air is forced into the esophagus or when an additional amount of barium suspension is taken.

During fluoroscopy, pronounced segmental contractions of the esophagus can be observed, under the influence of which the contrast mass makes pendulum movements. The evacuation of barium suspension into the stomach occurs regardless of the intraesophageal pressure.

Esophagoscopy is performed to confirm the diagnosis of K., detect its complications and conduct a differential diagnosis. Examining the mucous membrane collected during K. in transverse folds in the form of 15-20 rings, the degree of esophagitis and expansion of the lumen of the esophagus, the severity of stagnation of food in it, are specified. In cases of sharp dilatation of the esophagus, the transverse folds of the mucous membrane disappear, and the walls look like a leathery flabby bag. With further conduction of the esophagoscope, the cardia is examined, which, with K., looks like a point or a slit located vertically or horizontally. As a rule, the end of the esophagoscope at K. manages to be carried out through the cardia, which confirms the data on the predominant function, the nature of the changes in the esophagus.

Esophagomanometry is a valuable method of early diagnosis To., since changes in the contractility of the esophagus and cardia appear much earlier than typical wedge symptoms. Research is made by means of a special multichannel probe with rubber cartridges or "open" catheters, on the Crimea fluctuations of intraluminal pressure are transferred to the registering device.

Normally, after swallowing (Fig. 7, 1 and 2), a peristaltic wave begins to propagate through the esophagus (Fig. 7, 3), while the cardia opens and the pressure drops (Fig. 7, 4). After the passage of peristaltic contraction, the cardia closes again. With achalasia of the cardia after swallowing (Fig. 8, 1 and 2), there is no reflex relaxation of the esophagocardial sphincter, and intraluminal pressure remains at the same numbers (Fig. 8, 4), the absolute values ​​of which differ little from those in healthy people. When K. after swallowing (Fig. 9, 1 and 2), instead of a drop in pressure, reflecting the opening of the cardia, an increase in pressure appears (Fig. 9, 4), i.e., a perverted reflex reaction is recorded. Between these typical conditions, depending on the stage of the disease, there are transitional forms. In some cases, after individual swallowing movements, relaxation of the cardia may occur, but it is not enough either in amplitude or in duration. With the course of the disease, the contractility of the esophagus also undergoes changes: at first, post-swallowing contractions increase (Fig. 8, 3), then segmental contractions join them. Both types of contractions in K. do not have a propulsive ability, so they are not enough to push food through a closed cardia. Gradually, decompensation of contractile activity sets in, and any contractions cease to be recorded in the esophagus (Fig. 9, 3).

Thus, the main difference between K. and achalasia of the cardia is the nature of the reflex reaction of the cardia in response to swallowing, as well as the contractility of the esophagus. The initial pressure in the cardia at rest is not much different from the level recorded in healthy people.

In doubtful cases, a special test is sometimes used to diagnose K., which consists in the intramuscular injection of cholinomimetic drugs. Selectively stimulates the motility of the esophagus meholil (carbocholil). Injections of these drugs in other diseases of the esophagus and cardia, accompanied by a violation of their patency, do not lead to increased contractions of the esophagus.

differential diagnosis. In the initial stages, with atypical development, the disease in a wedge, the picture may resemble angina pectoris, a hernia of the esophageal opening of the diaphragm, a diverticulum of the esophagus, the initial stage of cancer of the cardiac esophagus and stomach. At K. pains are usually connected with meal, coincide on time with feeling of a dysphagia that distinguishes To. from stenocardia (see) when pains are generally provoked by physical. load. At hernias of an esophageal opening of a diaphragm (see) patients are disturbed by heartburn, an eructation, regurgitations are possible, but, unlike To., the food digested in a stomach. Peptic strictures have an appropriate history and clinic of reflux esophagitis (see Esophagitis). An additional argument in favor of the diagnosis of K. is the duration of the course and the young age of the patients, its connection with mental trauma. It is much more difficult to differentiate the initial stages of K. from the disease known in the literature as "esophagospasm". With this disease, there is a violation of the motor function and patency of the esophagus outside its terminal segment; the mechanism of disclosure of the cardia is not violated, which is fundamentally different from K. Esophagospasm is characterized by the intermittent nature of dysphagia, which is accompanied by pain that occurs at the time of swallowing and passing food through the esophagus. Regurgitation, as a rule, is mild, while the contents of the esophagus are almost unchanged.

Rentgenol, the study reveals a narrowing of the esophagus more often in its lower thoracic section during esophagospasm. It is better detected with swallowing movements and usually has a wedge-shaped shape and a large length (3-6 cm). In the course of the study, one can observe a change in spasmodic contractions with a good patency of the esophagus. At the same time, patients note a feeling of delay in barium suspension. Suprastenotic expansion of the esophagus with esophagospasm is moderate, there is little liquid and mucus in the lumen, the gas bubble of the stomach is well expressed. It is also extremely important to keep in mind that K. may accompany the initial stage of cancer of the cardiac esophagus (see) and stomach (see).

Treatment and prognosis

Conservative therapy aims to normalize the disturbances inherent in K. and which are its cause. General strengthening measures are of great importance. Patients must be protected from unnecessary experiences, convinced of the good quality of the disease and that their condition will certainly improve. It is necessary to create such nutritional conditions for patients so that they do not feel embarrassed by others. Diet therapy has a certain value in conservative treatment. The food consumed should be mechanically and chemically gentle. Food should be fractional. The last meal should be 3-4 hours before bedtime.

Conservative treatment provides for mandatory intensive vitamin therapy, especially with a complex of B vitamins.

Some reduction in dysphagia in stages I and II of the disease can be achieved by taking antispasmodics before meals or during meals. The most effective antispasmodics include drugs of the nitro group - nitroglycerin, amyl nitrite. In the later stages, antispasmodics inhibit the motility of the esophagus, which can adversely affect the patency of the cardia. True, they have a short-term effect. To relax the cardia, other antispasmodics are also used (platifillin, no-shpu, halidor, papaverine, etc.). Hopes for a therapeutic effect with the introduction of anticholinesterase adrenolytic and adrenomimetic drugs, according to numerous literature data, did not materialize.

In advanced cases, with severe stagnation in the esophagus and esophagitis, washing the esophagus with a weak solution of antiseptics can be used. This procedure should be treated with caution in complicated forms of esophagitis (hemorrhagic, ulcerative). Given the pronounced violation of the patency of the esophagus in stages III and IV of the disease, it is not recommended to use medicinal substances per os in tablets, especially if they have a local irritant effect.

Sometimes the therapeutic effect occurs after various physiotherapy procedures.

Modern conservative therapy in an isolated form is used practically only in the initial stage of K., and in the vast majority of cases it is used in the preparation of patients for surgical treatment or as an addition to cardiodilatation, which is the main method of treatment of K.

Surgical treatment is aimed at removing the obstacle to the advancement of food in the area of ​​the cardia by expanding it using bloodless or surgical methods. For the first time, cardiodilatation was made in 1898 by J. G. Russel, who used the dilator he created for this purpose. However, only in the 20th century the method was recognized and began to be used in the USA, England, the USSR and other countries.

In the USSR in 1930, P. A. Herzen, and then A. I. Savitsky, used the Stark mechanical dilator.

All dilators for expanding the cardia are divided into pneumatic, hydrostatic and mechanical. Various combinations of devices are also available. The first two types of dilators include devices designed by Plummer (H. S. Plummer, 1906). V. Bryunings (1906) proposed a mechanical expander, and in 1924 H. Starck modified it.

The design of pneumatic and hydrostatic dilators is based on the principle of stretching an elastic balloon with air or liquid. In a mechanical cardiodilator, the expansion of the cardia is carried out by metal branches connected by means of hinges to a lever located on the handle of the dilator. When using the Stark expander, various complications often occur - tears and ruptures of the esophageal wall, bleeding, there are difficulties with inserting and removing the instrument. So, according to Wenzel (Wenzel, 1970), 6 complications, often life-threatening, were registered for 47 dilations by the Stark apparatus (short-term cardiac arrest - 1 case, esophageal rupture - 2). At the same time, in 1118 expansions, Stark himself had a rupture of the cardia in only one case.

In 1964, a pneumatic cardiodilator was created at the All-Russian Research Institute of Clinical and Experimental Surgery (O. D. Fedorova, G. K. Melnikova), which was used to treat more than 500 patients. The method of cardiodilatation has become the method of choice in the treatment of K. and is used in many clinics in the USSR. The dilator (Fig. 10) consists of a radiopaque rubber tube-probe 120 cm long and dia. 15 mm with rounded end. At a distance of 5-6 cm from the end, a dumbbell-shaped balloon 15 cm long and dia. 4 cm. The wall of the cylinder consists of three layers (shells): the inner and outer - rubber, and the middle - nylon. Rubber sheaths provide tightness, and nylon - a constant diameter and shape of the cylinder when air is injected into it. At the end of the probe, a channel opens, going in an oblique direction to the axis and intended for a thread, or a conductor string. Cardiodilators have different sizes: dia. 25, 30, 35, 40, 45 mm.

Cardiodilation can be carried out at any stage of K. Usually, patients do not need special preparation. The procedure is performed in the morning on an empty stomach, usually without anesthesia.

The success of cardia expansion largely depends on the correct location of the dilator. Its "waist", i.e. the center of the balloon, should be in the esophagocardial region, approximately at the level of the gastric bubble of the stomach (Fig. 11). The installation of the balloon is carried out under the control of the x-ray screen. When air is injected into the dilator balloon, it may shift towards the esophagus or stomach lumen.

Begin a course of dilations with smaller dilators; the pressure in them is also increased gradually - from 180-200 to 300-320 mm Hg. Art. The duration of the expansion procedure is approx. 1/2 - 1 min., the interval between sessions is 1-2 days. In some cases, if after dilatation there is severe pain behind the sternum or in the epigastric region, the temperature rises or traces of blood are found on the instrument, the interval between dilations is lengthened. Usually, during expansion, patients experience moderate pain behind the sternum and in the epigastric region. After 2-3 hours after the disappearance of pain, liquid food is allowed.

Contraindications to cardiodilatation are limited: portal hypertension with varicose veins of the esophagus, ulcerative and ulcerative hemorrhagic esophagitis, blood diseases accompanied by increased bleeding, etc.

Patients who have already been operated on for cardiospasm, dilatation) should be performed with extreme caution. The effectiveness of dilatation must be judged not only by the patient's feelings, but also by the data of objective research methods (X-ray and esophagomanometric control).

At rentgenol, a research find improvement of passability of a contrast agent on a gullet, return of relative propulsivity of motility of a gullet, approximation to the normal size of diameter of its gleam, formation of a gas bubble of a stomach (fig. 12).

Esophagomanometry in the case of effective dilatation reveals a decrease in pressure in the cardiac sphincter. The degree of this decrease depends on the state of esophageal motility, its propulsion, and the functional response of the cardia to swallowing.

If complications of cardiodilatation appear (gastric bleeding, perforation of the esophagus), urgent measures must be taken to treat them (see Gastrointestinal bleeding, Esophagus).

Cardiodilation is a highly effective treatment for K. Almost 94% of patients can achieve excellent and good results. Preference should be given to expansion of the cardia using pneumatic or hydrostatic dilators. Unsatisfactory results are most often due to insufficient or excessive dilatation. In the first case, dysphagia decreases slightly, and in the second, a clinic of reflux esophagitis develops.

Indications for surgical treatment: 1) the inability to produce cardiodilatation); 2) lack of therapeutic effect after multiple courses of cardiodilation; 3) early diagnosed ruptures of the esophagus that occurred during the expansion of the cardia; 4) pronounced peptic strictures that developed as a result of overstretching of the cardia and are not amenable to conservative therapy and bougienage.

Most of the surgical interventions proposed for the treatment of K. are only of historical interest. Among them: 1) operations on the dilated part of the esophagus, aimed at reducing the lumen of the esophagus by excision of part of its wall or esophagoplication; 2) operations on the nervous system (vagotomy, sympathectomy, excision of the phrenic nerve, interventions on the submucosal nerve plexus); 3) operations on the diaphragm (diaphragmotomy, crurotomy, esophagolysis); 4) surgery to turn off the cardia (subdiaphragmatic esophagogastroanastomosis, transthoracic esophagogastroanastomosis, resection of the cardia and part of the esophagus); 5) operations on the "physiological" cardia (transgastric expansion, cardioplasty). All these interventions are not used due to low efficiency, frequent relapses of the disease and the frequent development of cardia insufficiency and peptic reflux esophagitis.

Of the diverse arsenal of proposed surgical methods, only interventions on the “physiological” cardia are used, based on the idea of ​​extramucosal cardiomyotomy.

Gottstein (G. Gottstein, 1901) proposed to dissect longitudinally only the muscular membrane in the esophagocardial region. Geller took advantage of this proposal (E. Heller, 1913). Extramucosal cardioplasty according to Heller (Fig. 13) is performed from the abdominal approach and consists in a longitudinal dissection of the muscular membrane of the terminal esophagus along the anterior and posterior walls for 8–10 cm. part of the stomach where a group of oblique muscle fibers is dissected. The edges of the dissected muscular membrane are parted to the sides, and the intact mucous membrane begins to prolapse into the formed defect.

According to most authors, good results after this operation are observed in 70-95% of cases. However, V. V. Utkin (1966), O. D. Fedorova (1973) found unsatisfactory results in 20-50% of patients due to relapse of the disease, cardiac insufficiency, peptic esophagitis, etc.

According to summary data, mortality after Heller's operation is on average 1.5%, sometimes reaching 4%. The main cause of deaths are unnoticed damage to the mucous membrane of the esophagus, leading to mediastinitis, pleurisy, peritonitis. These injuries are observed in 6-12.8% of operations. In the place of dissection of the muscular membrane after the Heller operation, the development of diverticula, scars, deforming the cardia, is described.

To prevent relapses, Lortat-Jacob (J. L. Lortat-Jacob, 1951) proposed not to dissect, but to excise a strip of the muscular membrane.

If a mucosal injury is found, it should be sutured. It is more dangerous if this injury goes unnoticed. Therefore, various methods have been proposed to cover the mucous membrane: omentum, anterior wall of the stomach, etc. Methods for closing the defect of the muscular membrane with various synthetic materials are not recommended.

Rice. Fig. 15. Schematic representation of some stages of the operation of cardioplasty with a diaphragmatic flap according to Petrovsky: a - the dotted line shows the lines of future incisions for excision of a portion of the muscular layer of the esophagus and cardia and cutting out the flap from the diaphragm (1 - lung, 2 - diaphragm, 3 - esophagus); b - a section of the muscular layer of the esophagus and cardia is excised, at the bottom of the defect, an intact mucous membrane is visible (1), which exfoliates with a tupfer (2); a flap (4) was cut out of the diaphragm (3); c - the flap is sutured to the muscular edges of the esophageal defect; d - the diaphragmatic flap is completely sutured to the edges of the defect (1); the hole in the diaphragm is sewn up (2).

Cardioplasty with a diaphragmatic flap according to Petrovsky (Fig. 15), which is a type of esophagophrenoplasty, was developed experimentally; since 1956 its introduction into a wedge, practice is begun. Access - thoracotomy in the VII intercostal space on the left; the mediastinal pleura is dissected over the dilated lower thoracic esophagus and the latter is isolated from the mediastinum. Under the esophagus, a rubber or gauze ribbon is carried out and a T-shaped myotomy 8-10 cm long is performed. Using a sharp and blunt way, a strip of the muscular membrane of the esophagus and cardia 10 X 3.5 cm in size is methodically cut off and excised. This should be done especially carefully in a narrowed area, because here, as a result of inflammatory-sclerotic changes, the muscular membrane is not always easily separated from the submucosa and the mucous membrane can be damaged.

In the initial version of the operation, the integrity of the edges of the esophageal opening of the diaphragm was not given significant importance, and subsequently this led to a violation of the barrier function of the cardia, gastroesophageal reflux and esophagitis. In the final version, the muscle and connective tissue elements that form the esophageal opening are not damaged. The flap is formed from the diaphragm, retreating 2-3 cm from the edges of the esophageal opening. After cutting out the flap through the resulting defect in the diaphragm, an additional expansion of the cardia is performed with a finger through the invaginated wall of the stomach and the excision of the muscular membrane is completed. The diaphragm flap is first sutured along the inner edge of the myotomy area, starting from the bottom, and then along the outside. After that, the integrity of the diaphragm is restored.

The positive aspects of the last modification include the preservation of the obturator function of the cardia with good patency of the esophagus, as well as the possibility of reliable covering of the mucous membrane. In addition, the defect in the muscular membrane is covered with a tissue similar in structure and function to the muscles of the esophagus.

According to O. D. Fedorova (1973), when analyzing the long-term results of cardioplasty with a diaphragmatic flap, it turned out that out of 98 operated patients, excellent and good results were obtained in 84 patients, in 12 - satisfactory, and only in 2 - unsatisfactory.

According to summary statistics, there were 4 deaths for 296 operations. The success of the operation is ensured by effective myotomy, correct cutting and suturing of the diaphragm flap, as well as suturing the defect formed in it. It is very important that the blood supply of the flap is complete; when suturing, it is necessary that it does not bend over, otherwise its blood supply may become insufficient and subsequent scarring. A muscle flap from the esophagus and cardia must be excised from the area where the branches of the vagus nerves do not pass,

In 1960, T. A. Suvorova reported on the operation of esophagocardiogastroplasty (Fig. 16), which consists in the fact that after esophagocardiomyotomy, the anterior wall of the stomach is sutured to the edges of the defect in the muscular membrane and to the mediastinal pleura. This operation prevents gastroesophageal reflux to a lesser extent than the combination of esophagocardiomyotomy with esophagofundorrhaphy or Nissen fundoplication, so it has not found wide application.

Cardiospasm in children

Cardiospasm in children was first described by G. Gottstein in 1901. In the domestic literature, one of the first observations belongs to H. N. Petrov (1926). K. in childhood is a relatively rare disease (4-5% in relation to adult patients).

The main patol, phenomena at To. at children, as well as at adults, violation of passability of a cardia and expansion of overlying departments of a gullet with frustration of their tone and motility is. It is characteristic that children with K. do not have organic stenosis in the abdominal part of the esophagus and hypertrophy of the muscles of this area.

Gistol, studies have found that in the genesis of K. in children, a congenital deficit of neurons in the ganglia of the intermuscular plexus of the esophagus, both in the cardial and in the overlying sections (Fig. 17), with secondary dystrophic changes in smooth muscle fibers due to motor denervation, matters.

The wedge, K.'s picture at children is characterized by two main symptoms: regurgitation and a dysphagia. Regurgitation is noted not after each feeding, and its frequency varies from day to day, regurgitation can be during sleep. In the vomit, unchanged food is found without signs of gastric contents (esophageal vomiting). Dysphagia older children define as a feeling of stopping, delaying food after the act of swallowing. In infancy and toddler age, dysphagia is determined by a number of indirect signs and microsymptoms (refusal of the breast and periodic regurgitation, the child chews food for a long time, “chokes”, food intake is very slow). Children often resort to washing down food with water. Regurgitation often leads to aspiration and pulmonary complications (recurrent bronchitis and pneumonia). Hron, malnutrition leads to a lack of weight and lagging behind in physical. development, anemia of alimentary origin is possible. Complaints of pain in the chest or in the epigastric region are presented by some patients of school age.

The disease occurs at any age, including in infants, but the main group is children of preschool and school age. The onset of the disease is usually gradual, periods of deterioration alternate with “light intervals”, but hron is characteristic, its course with a tendency to stabilize or progress patol, symptoms.

Of decisive importance in the diagnosis is a contrast rentgenol, a study of the esophagus. In this case, barium either does not enter the stomach at all, filling the dilated esophagus, or is squeezed out of it in a narrow stream, and the narrowing in the cardial section has even contours. Suddenly, at various intervals of time, there is a rapid evacuation of barium from the esophagus in a wide jet of the type of failure. This phenomenon in children is easily reproduced when drinking barium with water. At children two types rentgenol, changes are observed. In the first type, the expansion of the esophagus is moderate (no more than 2 times), the tone of the walls is preserved, after swallowing, chaotic and lively contractions of the esophagus are noted, which seem to break against the closed cardia. In the second type, the esophagus is sharply dilated and atonic. Among additional researches the ezofagoskopiya is reasonable, at a cut expansion of a gleam to food of a hearth with excess folding comes to light; inflammatory changes in the mucosa are not observed. It is characteristic that the tube of the esophagoscope passes freely through the cardia into the stomach.

Differential diagnosis is carried out with congenital and acquired (post-burn and peptic) stenoses of the distal esophagus. Of great importance are the data of esophagoscopy, as well as the absence of a symptom of barium suspension failure with contrast rentgenol, a study in patients with organic stenoses.

In children, as in adults, cardiodilatation and surgical interventions are used for K.'s treatment. Of the latter, extramucosal cardiomyotomy according to Heller or iris cardioplasty according to Petrovsky are the most common.

Some surgeons prefer myotomy in combination with esophagocardiofundoplication, which can be performed both by transpleural and abdominal access. After a wide longitudinal extramucosal esophagocardiomyotomy, the resulting muscle defect is closed by suturing the wall of the fundus of the stomach to the edges of the defect. This technique reduces the possibility of cicatricial wrinkling of the cardia and increases the reliability of the operation. Immediate and long-term results of surgical treatment in children are good. As a rule, the symptoms of the disease are eliminated, however, with a pronounced atony and dilatation of the esophagus, the latter often remains enlarged.

Bibliography: Berezov Yu. E. and Grigoriev M. S. Surgery of the esophagus, p. 56, Moscow, 1965; Vantsian E. N. et al. Treatment of cardiospasm by cardiodilatation, Surgery, No. 2, p. 19, 1974, bibliogr.; Vasilenko V. X., Grebenev A. L. and Salman M. M. Diseases of the esophagus, p. 84, Moscow, 1971; Vasilenko V. X., Suvorova T. A. and Grebenev A. L. Achalasia of the cardia, M., 1976; Vilyavin G. D., Solovyov V. I. and Timofeeva T. A. Cardiospasm, M., 1971, bibliogr.; Vorokhobov L. A. and Geraskin V. I. Clinic and treatment of cardiospasm in children, Surgery, jvft "6, p. 54, 1967, bibliogr.; Geraskin V. I. and Lindenberg L. K. On the pathogenesis of cardiospasm (esophageal achalasia ) in children, Issues of protection of mat. and children, vol. 12, No. 12, p. 48, 1967, bibliogr.; Kagan E. M. X-ray diagnostics of diseases of the esophagus, M., 1968; Kevesh L. E. X-ray - a cinematographic study of the esophagus, M., 1970, bibliogr.; Multi-volume guide to surgery, edited by B. V. Petrovsky, v. 6, book 2, page 214, M., 1966; Morgenstern A. 3. Achalasia esophagus, M., 1968, bibliography; Petrovsky B. V., Kanshin N. N. and Nikolaev N. O. Diaphragm surgery, L., 1966, bibliography; Rabkin I. Kh., Arablinsky V. M. and Danielyan G. A. X-ray television cinematography of the esophagus, M., 1969, bibliogr.; Rusanov A. A. Cancer of the esophagus, L., 1974, bibliogr.; Modern methods of research in gastroenterology, under the editorship of V. X. Vasilenko, M., 1971; Utkin V. V. Cardiospasm, Riga, 1966; Fedorova O. D. Cardiospasm, M., 1973, bibliogr. ; Shalimov A. A., Saenko V. F. and Shalimov S. A. Surgery of the esophagus, p. 67, M., 1975, bibliogr.; E f f 1 e g D. B. a. o. Primary surgical treatment for esophageal achalasia, Surg. Gynec. Obstet., v. 132, p. 1057, 1971; E 1 1 i s F. H. a. o. Esophagomyotomy for esophageal achalasia, Ann. Surg., v. 166, p. 640, 1967; Rossetti M. Osophagocardiomyotomie und Fundoplicatio, Schweiz, med. Wschr., S. 925, 1963, Bibliogr.; Spiro H. M. Clinical gastroenterology, L., 1970; SteichenP. M., Heller E. a. Ravitch M. M. Achalasia of the esophagus, Surgery, v. 47, p. 846, 1960; Wenzel K. P. u. Sanider E. Zur Therapie der Achalasia oesophagi, Zbl. Chir., Bd 95, S. 945, 1970.

B. V. Petrovsky; V. I. Geraskin (det. hir.), I. X. Rabkin (rents.).