Bleeding of dilated veins of the esophagus emergency. The main signs of chronic bleeding. Bleeding from the esophagus of the stomach of the duodenum

Bleeding from varicose veins of the esophagus, the treatment of which should be timely, is life threatening condition, consequence of disease or damage to the vein by various factors.

Esophageal bleeding is a complication of extreme portal hypertension. It is characterized by increased pressure in the portal vein, splenomegaly, and ascites. Portal hypertension appears when there is a violation of the venous outflow of different localization.

In most patients, the cause is in the liver, which causes bleeding from the esophageal veins in cirrhosis. Without appropriate treatment, this condition is poor prognosis, the patient can live no more than two years. ICD-10 code - esophageal varicose veins with bleeding 185.0.

We got acquainted with the issue of bleeding from the veins of the esophagus ICD 10, we move on. Bleeding in the esophagus as a complication of varicose veins develops due to damage to the mucosa or the vein itself by foreign sharp objects, ulcer, toxic and poisonous substances. Less commonly, bleeding occurs due to aneurysm rupture, during and after surgery.

The reason directly for the VRV () is stagnant processes arising from cirrhosis or thrombosis of the liver. The disease of the upper part of the organ is associated with the formation of goiter and vascular pathology when ill Randu-Osler.

Bleeding from dilated veins of the esophagus and cardia develops suddenly under the influence of such factors:

• a sharp increase in blood pressure;
• exacerbation of pathologies of the gastrointestinal tract;
• straining and lifting weights.

precede this discomfort in the throat, vomiting blood, blurred vision and other symptoms of increasing blood loss.

Esophageal RVV bleeding is most commonly diagnosed in people with cirrhosis.

The development of varicose veins is due to the connection between the venous system of the digestive tract and the hepatobiliary system. Violation in any department can become a factor in the underlying disease and its subsequent complications, including bleeding.

Clinical signs and symptoms of bleeding from the esophagus

Clinical symptoms of bleeding from varicose veins of the esophagus include complaints in different period disease and at the time of blood loss, as well as external manifestations of the underlying pathology and related disorders. Patient complaints:

With such complaints, the doctor collects an anamnesis of the disease. It turns out which medicines the patient takes and what food he eats. In the anamnesis of patients with bleeding from the veins of the esophagus, there are often past liver diseases, the use of spicy, rough food, severe physical labor, previously carried out .

External signs when examining a patient:

• yellowness of the skin;
• cold sweat;
• increase in the volume of the abdomen;
• swelling of the legs;
• weak pulse and rapid breathing.

With severe blood loss, a person behaves restlessly, consciousness is inhibited and confused. Without timely assistance, a collapse is observed, which ends in a coma.

Diagnostics

Examination for such a phenomenon as bleeding from the esophagus includes:

If concomitant abnormalities are identified, an examination by a neurologist, oncologist, infectious disease specialist or cardiologist is prescribed.

Differential diagnosis is carried out with the disease Wilson-Konovalov, syndrome Mallory-Weiss, schistosomiasis.

First aid

At the pre-medical stage of care, when bleeding from varicose veins of the esophagus is observed, conditions must be created to limit blood loss. The patient is placed on his back horizontal position, the head turns to the side so that the blood can go out with the vomit and not fall into the peritoneum. It is necessary to ensure a comfortable temperature, cover or free from clothing.

Pulse and blood pressure are monitored. When the pressure drops to 80 there is a risk hemorrhagic shock, anti-shock measures will be required. Loss of consciousness indicates severe blood loss. To avoid this, the patient can be given cold water. Other liquids and food are strictly contraindicated. Upon arrival of the ambulance, the patient is transported on a stretcher.

Methods of treatment

The main goal of treatment is to monitor the source of bleeding and prevent secondary blood loss. After stopping the bleeding, the patient is prescribed diet No. 5.

First of all, the following methods are considered:

• Blackmore probe;
• vein sclerosis;
• dressing using gastrectomy or endovascular embolization.

Emergency treatment includes the administration of sodium hydrochloride. At the inpatient level, treatment differs depending on the degree of blood loss. A solution of glucose, sodium lactate, sodium acetate and gelatin is injected intravenously in different concentrations and quantities.

Follow-up activities include drug treatment, elimination of accompanying deviations. Vasoconstrictor therapy may be prescribed, endoscopic sclerotherapy and surgery when conservative methods fail.

Medical therapy

Medicines are used already at the stage of first aid. The patient is injected intravenously with sodium hydrochloride or dopamine. In the hospital, drugs are prescribed to normalize portal pressure. Fixed assets - Meropenem, vasoconstrictor, and its analogues - Vapreotil or Octreotide.

Medications to stop bleeding in the veins of the esophagus:

With concomitant bacterial peritonitis are prescribed antibacterial drugs in a week. For this purpose, cephalosporins are used - Ceftazidime, Cefotaxime and Cefoperazone. Alternative therapy is with fluoroquinolones, a drug Ciprofloxacin and Ofloxacin. When the condition of the kidneys worsens, it is prescribed intravenously sodium chloride, octreotide, albumen.

Non-drug methods

Treatment of bleeding from varicose veins of the esophagus is carried out by endoscopic sclerotherapy. A sclerosing drug is injected into the damaged vein. This method allows you to stop bleeding in 85% of cases. If carrying out two procedures does not give a result, they resort to other methods. A probe is inserted into the esophagus to compress the site of bleeding.

What other treatments are used? It:

• electrocoagulation;
• application of thrombin or adhesive film to the damaged vein
• endoscopic ligation.

Useful video

Why is bleeding from esophageal varices dangerous? The clinic of this phenomenon is already clear. Measures that should be taken by patients are announced in this video.

Operation

Options surgical treatment:

• operation TIPS;
• transverse subcardial gastrotomy;
• operation M.D. Patsiors.

Indications for surgery are inefficiency pharmacological treatment, prolonged bleeding when endoscopic hemostasis is impossible. Operation Tips ( transjugular intrahepatic portocaval shunting) indicated for portal hypertension asthenic syndrome and acute bleeding veins of the esophagus.

The effectiveness of surgical treatment is evaluated according to the following criteria:

• stop bleeding;
• no recurrence;
• improved prognosis;
• remission concomitant diseases GIT.

AT severe cases with cirrhosis, a decision is made on liver transplantation.

Prevention of secondary bleeding in VRV

After the main treatment, prevention of secondary blood loss is carried out. Combination therapy with the use of drugs to normalize portal pressure is prescribed. These are drugs Nadolol and propranolol. Sclerotherapy is performed if a different method was used at the stage of first aid.

Appointed ligation, with an interval of several weeks, rings are applied to the veins. The patient is constantly monitored regular examinations at the hepatologist and gastroenterologist.

Bleeding with varicose veins is the most dangerous complication that requires immediate hospitalization of the victim. On the causes of the disease and methods of helping the patient with bleeding from varicose veins in the lower extremities will be discussed in this article.

Possible causes of bleeding

Varicose veins most often affect women (in 75% of cases) older than 30 years of age. Very often, varicose veins occur in women during pregnancy and after childbirth. There are also varicose veins in men, especially those who are at risk (leading sedentary image life experiencing excessive load on legs with a genetic predisposition, etc.). It is extremely rare, but still there are varicose veins in children.

If varicose veins do not receive necessary treatment, they continue to thin out, and sooner or later there comes a critical moment when the vessel bursts under the influence of the blood that has stagnated in it. Most often, the rupture occurs in the lower leg. Bleeding is very profuse, and the loss of blood is so great that the consequence of this can be fatal.

Provoking factors for the occurrence of bleeding can be:

• mechanical impacts (impacts, cuts, bruises, punctures);
• weight lifting;
• significant physical activity;
• coughing;
• prolonged stay on the legs;
• constant squeezing of the veins with uncomfortable clothes or shoes;
• hypertensive crisis.

On the initial stage the disease very often proceeds secretly, however, with its exacerbation, the risk of bleeding increases sharply due to the weakness of the veins. Bleeding is localized in the lower third of the lower leg and in the ankle. Areas with pronounced venousness are especially vulnerable.

There is a classification of bleeding based on their causes and intensity:

1. Spontaneous. Arise as a result advanced varicose veins when the patient did not apply for qualified help. The veins in such patients are clearly expressed, their pattern is clearly visible under the skin. Venous nodes and trophic ulcers are often noted. Usually not only veins are torn, but also nearby tissues.
2. Traumatic. Occur as a result of mechanical action on the vein. Even with minor injuries (for example, a small cut) blood is coming a powerful stream, although the victim may not feel it right away. It will not be possible to stop the loss of blood in an upright position. As a rule, the patient loses a lot of blood.
3. Subcutaneous. They can be either spontaneous or resulting from trauma. Depending on the site on which the affected vein is located, blood loss may be mild or significant. Subcutaneous bleeding is visually indicated by hematomas. Most Potentially dangerous view bleeding - from a vein in the area of ​​​​the ulcerative bottom. The cause of such an outpouring can be purulent infectious process or autoimmunoaggression, leading to tissue and venous necrosis.
4. Outdoor. Bleeding begins as a result of damage to the surface of the skin. Due to a cut or puncture, the dermis is destroyed vascular walls, and blood begins to leave a nearby vein.

For all types of bleeding from the dilated veins of the legs, the absence of pain in the patient is characteristic, even when we are talking about traumatic injury. External blood loss is much more common than subcutaneous effusions.

Bleeding from the lower extremities is characterized by moderate or intense blood loss of dark blood from the damaged area. If a hematoma occurs, then pain syndrome leading to temporary disability.

Danger of bleeding

Since the victim most often does not experience pain at the time of bleeding, it is very likely that he will not notice the beginning of the process. As a result, patients often lose a lot of blood. In addition, when the patient becomes aware of blood loss, he may fall into a panic state, which excludes the adoption of reasonable decisions and only aggravates the situation. The result of panic is an increase blood pressure, acceleration of the heart rate and blood flow, which leads to even more intense blood loss.

It is impossible to predict the amount of blood loss in advance, but it is clear that the situation must be brought under control in order to prevent falling into a state of shock and lethal outcome. To prevent the dangerous consequences of rupture of the veins, the patient must receive first aid.

emergency measures

If a vein in your leg bursts, you need to force yourself to remain calm. If done correctly, the bleeding can be stopped.

You need to take the following actions:

1. Placed at the site of the ruptured vein hemostatic sponge. If a sponge is not available, you can use a clean piece of cloth folded several times.
2. A sterile gauze pad is placed on a sponge or piece of cloth. It must be folded several times.
3. An elastic bandage is applied on top.
4. When the bandage is applied, a very cold object (ice) should be applied to the affected area for 20-30 minutes.
5. Immediately after applying the bandage, you need to take a supine position with your legs raised up. If the bleeding started on the street, you don’t need to run around in search of a cold object yourself, but it’s better to ask the people around you about it.

1. The next step is to call an emergency medical care. If we are talking about an external rupture with varicose veins, doctors can apply finger pressure, applying a tight bandage. In cases with ruptures in ulcerated areas of the skin, a vein will need to be sutured to rule out septicopyemia and thromboembolism. If necessary and technically feasible, sclerotherapy with compression can be performed.
2. If the blood loss is large, antibiotics are given to prevent infection. In the case of internal ruptures, external ointment formulations, painkillers and non-steroidal anti-inflammatory drugs are used. Phlebotonics and phleboprotectors must be used.

Steps to take after bleeding has stopped

First of all, you need to make sure that the bleeding has stopped. This can be done as follows: we are located on a horizontal surface and lie with our leg raised for about half an hour, watching the bandage to see if the blood stain is increasing on it. If the spot does not change in size, it can be concluded that the bleeding has stopped. After that, you can lower the lower limb to the level of the body. For the rest of the day, strict bed rest should be observed. The bandage can not be removed until the morning.

During the day after the bleeding stops, you can not take drugs that thin the blood. You also need to pay special attention to the level of blood pressure.

In the morning you can not abruptly get out of bed. Too much activity can cause bleeding to resume.

So, getting out of bed should be done in several stages:

1. At first they sit on the bed, but the legs do not hang down - they are on the bed.
2. They sit on the bed for about 2-3 minutes, after which they lower their legs to the floor.
3. Again they wait a little and slowly rise to their feet.

The bandage during the time he was on the leg, firmly dries to the wound. It is categorically not recommended to tear it off by force, since in this case the bleeding will begin again. To avoid this, the bandage is moistened in a weak solution of potassium permanganate, furatsilina or plain water. lower limb dipped in a container with liquid for a few minutes. When the bandage gets wet, it is removed, and a bactericidal patch is applied to the wound, which is worn for 2-3 days.

Rules of behavior

With a sudden rupture of a vein, it is important to adhere to several rules:

1. In the presence of varicose veins, carry with you the simplest set of medical supplies for first aid.
2. Don't panic.
3. Do everything possible to stop or stop the bleeding until the doctors arrive.
4. Do not use a tourniquet to stop bleeding. This method of stopping bleeding can only be used experienced doctors. The fact is that stagnation in veins affected by varicose veins can cause bleeding from nearby vessels. If the blood loss is very intense, you can use finger compression of the vessels through a napkin.
5. When the bleeding is stopped, it is important to observe a calm mode of behavior during the day (or even more), avoiding physical exertion and stress.
6. In no case in the coming days, do not go to the bathhouse and do not take hot baths. As a result of a sharp expansion of blood vessels, blood loss can resume.

Prevention

Bleeding with varicose veins is a very dangerous complication of this disease. To prevent such a development of events, it is necessary to take a number of preventive measures:

1. Do not lift too heavy objects, avoid sports with jerky loads.
2. Support motor activity(by using therapeutic gymnastics, swimming).
3. Monitor body weight.
4. Avoid prolonged stay in an upright position.
5. Monitor blood pressure levels.
6. Avoid injury.
7. Wear comfortable, non-constricting clothing and shoes.
8. Do not delay with the treatment of varicose veins.

Thus, prevention is based on the prevention of those factors that can provoke bleeding. However, if nevertheless an unpleasant event has occurred, it is necessary to take all the measures described above to stop the bleeding and immediately call an ambulance.

The veins of the esophagus are very thin-walled vessels. With an increase in portal pressure, they stretch and change varicose.

Symptoms of bleeding from varicose veins of the esophagus

The clinical picture depends on the volume and rate of blood loss. In patients with prolonged (hidden) minor blood loss, the disease manifests itself as weakness and iron deficiency. Given the chronic nature of the process, with latent blood loss, the patient may experience a significant deterioration in the condition. On physical examination, the patient appears tired and pale. Arterial pressure, due to the absence of acute bleeding, remains normal. More often, manifestations of bleeding from varicose veins of the esophagus are more pronounced, accompanied by hematemesis, bloody stools, indicating massive bleeding.

With portal hypertension, the source of bleeding can be localized in almost any part of the gastrointestinal tract. However, more often the cause of massive blood loss is the rupture of the veins of the esophagus, stomach, or both of these organs. In case of blood loss caused by portal hypertension from sources of other localizations, similar resuscitation measures, assessment of severity and timely treatment should be carried out.

Patient examination

The first and foremost thing when examining a patient with suspected variceal bleeding is a comprehensive clinical evaluation. Pay attention to signs of ascites, encephalopathy and limb atrophy. The presence of any of the signs is indicative of severe cirrhosis and poor liver reserve. Often there are arachnids on the skin and palmar erythema, signs of increased cardiac output and low peripheral vascular resistance and other manifestations of severe progressive cirrhosis.

With a general examination, it is necessary to quickly assess the severity of the patient's condition. Severe hematemesis, melena with signs of hemorrhagic shock indicate severe bleeding and the need for appropriate treatment. Vital parameters, mental status and intensity of ongoing bleeding determine the conduct emergency care according to the ABC scheme (airway patency, bleeding control, hemodynamic maintenance). Protecting the airways and preventing aspiration of blood into the tracheobronchial tree is essential, especially in the presence of liver-related encephalopathy. Patients with low respiratory reserve or failure to protect the airway should be intubated prior to any intervention to avoid blood aspiration. Immediately after mechanical ventilation, it is necessary to replace intravascular volume and stop bleeding as soon as possible.

In patients with bleeding from esophageal varices, severe hematological abnormalities are often observed. Anemia can be the result of both acute and chronic blood loss. In the latter case, there may be Iron-deficiency anemia. Violations of hemostasis may occur due to ongoing blood loss, impaired synthetic ability of the liver, or. In patients with bleeding, it is imperative to correct clotting disorders with fresh frozen plasma and parenteral administration vitamin K. Sequestration of platelets in the spleen in patients with portal hypertension often leads to thrombocytopenia. At the same time, platelet transfusion is ineffective due to their quick removal from the bloodstream.

Numerous deviations of the results may also be observed. laboratory research. Electrolyte imbalance can be the result of taking diuretics, alcohol abuse, redistribution of fluid in the body, acute blood loss or resuscitation. Serum albumin, bilirubin and cholesterol levels, prothrombin time should be used to assess liver function and determine the need for replacement of clotting factors.

Evaluation of patients with bleeding from esophageal varices should include screening for hepatitis and HIV. Hepatitis screening can determine the cause of cirrhosis and also provide information for appropriate etiotropic therapy. Treatment of patients with severe viral load may differ from that of patients with long-term existing hepatitis in terminal stage cirrhosis without it. It is also necessary to look for signs of HIV infection. The choice of treatment for portal hypertension may depend on life expectancy with HIV infection and AIDS.

Allows you to establish the final diagnosis, possible etiology and morphological features of cirrhosis. Biopsy-determined degree of hepatitis activity may not match clinical picture hepatic reserve. AT emergency situations a biopsy is usually not performed due to its riskiness and duration of the study.

After completion of the physical examination and receipt of laboratory results, each patient should be assessed according to the Child and Child-Pugh classification, as well as taking into account the MLSP. In spite of known limitations these evaluation systems, they remain the best way determine the prognosis and help in the appointment of appropriate treatment.

Treatment of bleeding from varicose veins of the esophagus

Early Intensive Care

Once adequate respiration is achieved, intravascular volume replacement should begin. When planning resuscitation, it is important to assess the magnitude and severity of blood loss. At minor bleeding a transfusion of isotonic crystalloid solutions such as Ringer's lactate may be sufficient. With severe bleeding, early transfusion of red blood cells is necessary. Adequate hemoglobin levels should be maintained. The introduction of fresh frozen plasma reduces the initial coagulopathy and helps to stop bleeding.

Because successful resuscitation often requires transfusion of large volumes of fluid, catheterization is important. central vein and monitoring of central venous or intravenous pressure pulmonary artery. Usually, the internal jugular vein provides the best access, since in this area it is easier to control the formation of a hematoma than with a complication of the catheterization of the subclavian vein. It is also important not to exceed the volume of the transfused liquid. If a infusion therapy leads to an excessive increase in central venous pressure (for example, up to 20 mm Hg), there is a significant increase in portal venous pressure (for example, up to 40 mm Hg), leading to severe stretching of varicose veins and continued bleeding. The goal of resuscitation is to normalize blood pressure and intravascular volume with the restoration of adequate urine production.

Immediately after the patient's arrival at the hospital, treatment should be started to stop bleeding from esophageal varices even before a final diagnosis is established. Treatment prior to diagnosis is not entirely optimal, but in severe varicose bleeding it is carried out according to vital indications.

Pharmacotherapy

The initial treatment, with the exception of resuscitation, is pharmacotherapy. It usually starts before endoscopic methods, because it is readily available, relatively non-toxic and quite effective. Pharmacotherapy does not increase gastrointestinal bleeding unrelated to portal hypertension and may be beneficial.

The main drugs for pharmacotherapy are vasopressin and octreotide. Vasopressin has been the mainstay of treatment for bleeding patients with portal hypertension for several decades. Its intravenous administration should begin with a dosage of up to 1.0 U / min (do not inject more than 20 IU in 20 minutes), and then gradually reduce to 0.4 IU / min. Vasopressin has relative contraindications for lesions coronary arteries, because they reduce blood flow in the myocardium, causing spasm coronary vessels. In the treatment of elderly patients or patients with diagnosed coronary artery disease, treatment with vasopressin should be combined with intravenous administration nitroglycerin. In addition, vasopressin contributes to fluid retention in the body and an increase in ascites, so the duration of its administration should not exceed 72 hours.

AT recent times octreotide is increasingly being used instead of vasopressin. Octreotide does not adversely affect coronary blood flow and does not contribute to fluid retention with accumulation of ascites. In randomized trials comparing octreotide and vasopressin, they were found to be equivalent in the treatment of bleeding and in terms of 30-day mortality. Octreotide is administered as an intravenous bolus of 50 to 100 units followed by 50 to 100 units/hour. Treatment with these drugs is usually continued for 2 to 4 days, more specific treatment is planned and carried out.

Endoscopic and dressing

Emergency is of exceptional importance in the diagnosis and treatment of bleeding from varicose veins of the esophagus. In the management of these patients, it is indicated early holding endoscopic examination upper divisions GIT. It may also be required to exclude a source of bleeding in the lower gastrointestinal tract. Before endoscopic examination In such circumstances, there are three main challenges.

• - The first task is to determine the cause and localization of bleeding. To do this is sometimes simple, but sometimes almost impossible, for example, when filling the esophagus, stomach, duodenum with clotted blood, or when filling the colon with feces and blood clots. It is important to distinguish bleeding from portal hypertension from other etiologies (eg, peptic ulcers, Mallory-Weiss syndrome, esophagitis, or cancer).
• - The second task is to determine the size and localization of varicose vessels for treatment planning. For example, if the bleeding is associated with small varices located in the esophagus, without signs of gastric varices, the chances of success with endoscopic treatment exceed 90%.
• “The third task and ultimate goal of emergency endoscopy is treatment.

With the help of endoscopy, it is possible to directly control bleeding from varicose veins. The dilated veins of the esophagus, as well as, can be endoscopically ligated or sclerosed by injecting a special solution into them, without adversely affecting liver function. Large dilated veins are less amenable to endoscopic treatment and may be a source of rebleeding. Excessively enlarged varicose veins are very difficult to bandage, since the node can only consist of the anterior wall of the varicose vein. Ligation of the anterior wall does not lead to obliteration of the varicose vein. It can increase bleeding due to necrosis of the wall itself. Such patients are often prescribed sclerotherapy. In the US, the most commonly used sclerosing agents are sodium tetradecyl sulfate and sodium morrhuate. Sclerosing agents are usually injected directly into the varicose vein, although some endoscopists prefer to inject the sclerosing agent along the walls of the varicose vein (paravaricose injection). A number of studies failed to establish the advantage of either of these two methods. Gastric varices are not amenable to endoscopic treatment and usually require portal decompression. They are also not amenable to sclerotherapy or ligation because the thin wall of the stomach is easily perforated.

Endoscopic sclerotherapy and ligation has many potential complications, although serious complications meet infrequently. Severe bleeding from esophageal varices is a treatment complication that is characteristic of paravaricose sclerotherapy or inadequate ligation. Bleeding from an untreated site usually occurs as a result of refusing endoscopic treatment and is not considered a complication. With repeated bleeding from varicose veins of the esophagus, regardless of whether they arose after an unsuccessful treatment or due to refusal of it, endoscopic sclerotherapy or ligation is also used.

Esophageal perforation is a rare but serious complication of sclerotherapy. More often there is ulceration of the mucosa of the esophagus in the area of ​​​​injection of the sclerosing agent or the site of ligation of the nodes. Ulcers can occur within 1 week after treatment, sometimes being a source of significant rebleeding. Healing of severe ulceration may subsequently lead to the formation of strictures.

Endoscopic treatment of bleeding from varicose veins of the esophagus is accompanied by low mortality (l-2%). When dressing, there are fewer complications, strictures and ulcers are less likely to form. This treatment method is more effective in stopping bleeding from esophageal varices than sclerotherapy. In some circumstances, re-endoscopic intervention may be considered as the definitive treatment in patients with bleeding from esophageal varices. For the finality of the treatment, several sessions are required over a long period of time in order to obliterate varicose veins. However, repeat endoscopic procedures are not always applicable. Some patients are unable to tolerate the treatment regimen, while others live in rural areas remote from centers of care medical services. Patients with gastric or intestinal varicose veins are not suitable for long-term endoscopic therapy.

Balloon tamponade

In patients with ongoing bleeding who cannot be treated with endoscopic interventions (or with the ineffectiveness of such treatment), uncontrolled reception pharmaceuticals, the next stage of treatment should be balloon tamponade using a Sengstaken-Blakemore probe. In parallel, preparation for portal decompression or other types of radical treatment should be carried out.

A double-balloon probe is inserted through the mouth into the stomach. To prevent aspiration, an aspirator is attached to the probe proximal to the esophageal balloon. In this case, the secretion or blood is removed to prevent their aspiration into the tracheobronchial tree. After the introduction of the probe, the presence of its tip in the stomach is confirmed radiographically. Then the gastric balloon is filled with 250-300 ml of air, and the position of the probe tip is checked radiographically again. After confirming the position of the probe, a thrust of 0.5-1.0 kg is applied to it. It ensures the position of the balloon in the area of ​​the esophageal-gastric junction and compression of the fundic and cardiac varicose veins. If bleeding continues, air is pumped into the esophageal balloon, usually up to a pressure of 30 mm Hg. After correct placement of the Sengstaken-Blakemore probe, the channel of the gastric tube and the nasoesophageal tube are connected to a vacuum aspirator for periodic evacuation of the secret of the esophagus and stomach. You should carefully monitor the condition of the mucous lips of the patient in order to avoid the formation of bedsores.

The probe with inflated balloons should not be left for more than 48 hours. Within 48 hours, the patient's condition usually stabilizes and the coagulopathy is corrected. After 48 hours, the risk of ulcers or decubitus ulcers associated with inflated balloons is significantly increased.

INTRODUCTION

Bleeding in diseases of the esophagus, as one of the common causes of gastrointestinal bleeding (GIB), is a relatively small percentage of their total number, but it occupies one of the first places in terms of severity and poor prognosis. The share of bleeding from varicose veins of the esophagus accounts for 3.9-6.2% of the total number of gastrointestinal tract. The detection rate of VRVP in patients with liver cirrhosis (LC) ranges from 25 to 80%. Mortality in bleeding from esophageal varicose veins reaches 40%, causing half of all deaths in patients with cirrhosis In the literature, a discussion continues about the effectiveness and benefits of conservative and surgical methods for stopping and preventing bleeding from varicose veins of the esophagus and stomach, so the question of choosing a method of treatment and prevention of esophageal gastric bleeding is still relevant

High mortality in primary bleeding from varicose veins of the esophagus and stomach, early relapses and low survival rate with conservative management of these patients, indicates the need for surgical treatment, both at the height of bleeding and in order to prevent the development of this formidable complication.

etiology.pathogenesis

The following main etiological factors for the occurrence of bleeding from RVV have been identified:

1) an increase in the PG value due to an "internal portal crisis" in active hepatitis (normally, the pressure in the portal system is not more than 140-150 mm of water column, and at 250-600 mm of water column, there is a high probability of bleeding from RVV)

2) peptic factor (reflux esophagitis against the background of high acidity)

3) pronounced disorders of the blood coagulation system due to the initial liver disease (determine the duration and massiveness of bleeding) in combination with erosive esophagitis

4) Mallory-Weiss syndrome as a result of hiccups, vomiting of various origins (hiatal hernia, alcohol intoxication, "cerebral vomiting" in TBI and other brain pathologies, uremia in CRF, hypertensive crisis, acute respiratory infections with hyperthermia, poisoning with various organic and inorganic poisons taken accidentally or with the intent of suicide) - 5) constipation (intense defecation)

6) blows to the solar plexus

7) strong cough

8) serious emotional and physical overload, copious reception food

9) erosion of the mucosa due to prolonged use of glucocorticosteroids, NSAIDs (aspirin, indomethacin, etc.)

10) injury to the vein wall by a swallowed foreign body ( fish bone etc.) -

Moreover, in the vast majority of cases (81%) there was a combination of 2 or more factors. Of great importance in the genesis of this type of gastrointestinal tract is the development of a kind of "portal hypertensive crisis" Its occurrence is provoked by the activation of inflammatory changes in the liver during cirrhosis with increasing compression of intrahepatic vessels by regenerated nodes with the development of thrombosis of small hepatic veins and, as a result, a sharp increase in PG. The crisis can be triggered by alcohol intake, exacerbation of the course of chronic hepatitis, a manifest increase in the values ​​of bilirubin, ALT, AST, sedimentary samples, LDH, g-GTP, alkaline phosphatase). Portal hypertension is divided into 3 stages: initial (compensated PH), coinciding with the initial stage of liver cirrhosis, the stage of initial decompensation and the stage of decompensated (complicated) PH. and specialized centers for the treatment of gastrointestinal tract have to deal with patients who have developed the third (complicated) stage of PH: severe varicose veins of the esophagus, and sometimes the cardia of the stomach, cytopenia due to hypersplenism, hepatosplenomegaly, edematous-ascitic syndrome, porto-caval encephalopathy, jaundice.

Diagnostics. Inspection.

Diagnosis includes examination of the patient, careful history taking, fibroesophagogastroduodenoscopy (FEGDS), fluoroscopy of the esophagus and stomach, splenoportography, ultrasound of the liver, spleen and vessels (v. portae, v. lienalis), laboratory test data: sedimentary samples, ALT, ASAT, LDH , bilirubin, alkaline phosphatase, ESR, protein fractions, detailed coagulogram data.

1. Men with a history of alcohol or hepatitis are more likely to get sick. During an exacerbation, patients note a feeling of pressure and fullness in the epigastric region, nausea, weight loss, mood instability, pruritus, nosebleeds. 2. An objective examination reveals quite often a characteristic appearance: a red face and relatively pale, with a well-developed subcutaneous tissue trunk with gynecomastia and hairiness of the trunk and head along female type; erythema of the palms and soles, vascular "asterisks" on upper limbs, face, neck, back and other signs of estrogenization due to insufficient destruction of these hormones in the cirrhotic liver. icterus varying degrees. Signs of beriberi - atrophy of the papillae of the tongue, skin changes such as pellagra, disorders of the nervous system (paresis of the peroneal nerve - spanking foot, sensitive ataxia; paresthesia of various localization). Dupuytren's contracture, swelling of the parotid salivary glands. 3. When examining the abdomen - an enlarged and painful compacted liver and spleen, ascites, dilation of the veins of the abdominal wall. 4. Bleeding is usually manifested by massive regurgitation of scarlet or slightly changed blood, foaming, without pronounced vomiting. 5. A sharp increase in ESR, anemia, leukopenia, thrombocytopenia, hypoalbuminemia, hypergammaglobulinemia, moderate bilirubinemia, urobilinuria, a moderate increase in transaminases, alkaline phosphatase and isoenzymes. 6. Esophagogastroscopy: clusters of varicose veins, defects and erosion of the mucosa.

Some patients know their diagnosis or have a history of similar bleeding. FEGDS allows you to visualize the source even during ongoing bleeding. X-ray of the esophagus and stomach, ultrasound, and other methods are not always available and are possible only after the final stop of bleeding from RVV. From lab tests: general analysis blood (anemia, hypochromia, reticulocytes 2-10%, thrombocytopenia, increased ESR), coagulogram: normo - or hypocoagulation. Biochemical analyzes reveal hypoalbuminemia against the background of a decrease in total protein, an increase in globulins, an increase in bilirubin due to bound, an increase in alkaline phosphatase, GTP, LDH, and an increase in sedimentary samples. Research results and discussion . As a rule, bleeding from RVV begins acutely, is massive and is accompanied by hemorrhagic shock of varying severity. To correctly assess the volume of blood loss, the stage of hemorrhagic shock, the degree of hypovolemia and, in the future, to draw up an adequate treatment regimen, it is necessary to analyze a number of clinical symptoms and laboratory indicators tab. 1. Allgover shock index (1967) - the ratio of heart rate to systolic blood pressure. Normally, it is 0.6. With its help, you can approximately calculate the BCC deficit if the patient does not have concomitant cardiac pathology (paroxysmal tachycardia, AV blockade, etc.). The simplest calculation of the proper BCC can be made using the Light nomogram for body weight or height.

Table 1.

Determination of the severity of hemorrhagic shock and the volume of blood loss

Table 1 (continued).

ENDOSCOPY

With stable hemodynamic parameters and full consciousness of the patient, the study is performed in the endoscopy room. If a patient with acute esophageal-gastric bleeding, manifested by constant regurgitation of blood and unstable hemodynamic parameters, is delivered to the emergency department, the patient should be transported to the operating room, where FEGDS should be performed. Absolutely contraindicated is endoscopic examination in patients with acute esophageal and gastrointestinal bleeding under the following conditions:

1/ sharp deformity of the cervical spine;

2/ acute cerebrovascular accident;

3/ agonal state.

The endoscopist has the opportunity to examine the esophagus and duodenum, examination of the stomach is difficult due to the large number of blood clots. Having identified varicose veins with ongoing bleeding, the most effective is local exposure to the source of bleeding using a Blackmore-Sengstaken probe. The probe is left in the esophagus for up to 48-72 hours, while for hemostasis it is necessary to introduce 100-120 cm3 of air into the gastric balloon and up to 100 cm3 of air into the esophagus. The probe with inflated cuffs is left in the stomach for 4 hours, after which the air should be released from the esophageal cuff and the patient should be observed for 1.5-2 hours. The stomach at this time is washed through the probe-obturator until pure water and complex conservative hemostatic therapy is carried out. The endoscopist stops the examination, after which the obturator probe is inserted immediately using a laryngoscope. both balloons are inflated, the contents of the stomach are aspirated through the central channel, after which the stomach is washed "to clean water". The main idea of ​​washing is not to cleanse the stomach of blood clots, which in principle is not possible, but to assess the completeness of hemostasis. If there is no fresh blood flow through the probe, then hemostasis has been achieved.

Treatment

The main objectives of the treatment of this type of bleeding are: 1) the final stop of bleeding; 2) elimination of hypovolemia and complete replacement of blood loss, correction of the hemocoagulation system; 3) prevention of universal liver failure; 4) prevention of recurrent bleeding. The patient must comply with strict bed rest. Need to create local hypothermia(cold on stomach).

Conservative treatment

Drug hemostatic effect in patients with PH syndrome has the following main goals: 1) pressure reduction in the system portal vein ; 2) increase in coagulation potential, blocking pathological fibrinolysis. The solution of the first problem is facilitated by the use of drugs that reduce blood flow through the arterial link of the portal pool due to selective spasm of arterial vessels. The most widespread in this regard was pituitrin: 15-20 IU pituitrin in 200 ml of 5% glucose solution intravenously, then 5-10 IU intramuscularly every 3 hours. But the effect of this drug is short-lived - up to 40 minutes. At present, a new longer-acting drug has appeared - a synthetic polypeptide - remestip (terlipressin), 2-6 ml is administered, depending on the severity of bleeding, intravenously every 6-8 hours until the bleeding stops, gradually reducing the dosage. The duration of treatment is up to 7 days. The use of a synthetic polypeptide - stylamin (somatostatin) is also promising: 250 μg intravenously in a stream slowly (3-5 minutes), then continuous drip administration at a rate of 250 μg per hour (3.5 μg / kg / hour) for 5% glucose solution or 0.9% sodium chloride solution Glucocorticoids have anti-inflammatory, antiallergic effects, reduce the formation of fibrous tissue in the liver and intrahepatic cholestasis, which leads to a decrease in the manifestations of the internal portal crisis Prednisolone 30-60 mg / day (dexamethasone - 4 - 8 mg / day) - is administered intramuscularly for 7-12 days after bleeding has stopped with an existing clinic of active hepatitis. An increase in the coagulation potential is achieved by using dicynone (etamsylate) 12.5%, 2-4 ml intravenously or intramuscularly every 6 hours, vikasol 1% - 2 ml - 2 times a day, 10% calcium chloride solution (or calcium gluconate) - 10-20 ml per day intravenously bolus In order to stop pathological fibrinolysis, 5% aminocaproic acid is injected 100-200 ml up to 2 times a day. In case of severe thrombocytopenia, platelet mass is transfused intravenously, 1-2 vials of 50 ml each. 1-2 capsules per day or sorbifer - 1 tablet 2-3 times a day. A complex multivitamin preparation "multibionta", vitamin B12 is intramuscularly injected at a dose of 200-500 mcg per day - 14 days. The criteria for the effectiveness of treatment is the improvement of general well-being, the normalization of hemoglobin and serum iron. In the case of extrahepatic forms of PG, the above hemostatic measures, as a rule, are sufficient for the final stop of bleeding. If bleeding continues, especially in the hepatic form of PH, when the compensatory capacity of the liver is limited, it is necessary to immediately use an obturator probe with Blackmore-Sengstaken-type balloons. Hemostasis in most patients is achieved by inflating the cardiac cuff (balloon) with obturation of the esophagus by pulling the probe until elastic resistance is felt. This creates conditions for blocking the retrograde discharge of portal blood into the veins of the esophagus. If bleeding continues, then this means the presence of a source of bleeding above the upper third of the esophagus with involvement in the anastomoses of the superior vena cava system. In this case, there is a regurgitation of unchanged blood past the probe. To stop bleeding, it is necessary to carefully inflate the esophageal cuff, after prescribing analgesics and sedatives to the patient, since there are often complaints of shortness of breath, chest pain, and palpitations. If bleeding continues after the balloons are inflated, then this indicates the localization of the source of bleeding below the cardiac region, which indicates the need for additional hemostatic measures or emergency surgery. With continued bleeding, the probe may be in the esophagus for up to 3 days or more; balloons should be periodically dissolved every 3-4 hours in order to avoid the formation of bedsores in the wall of the esophagus as a result of trophic disorders. If the bleeding has stopped, after 6-8 hours the probe should be carefully removed, after giving the patient a sip of vaseline oil to drink. Infusion-transfusion therapy, carried out in parallel with hemostatic therapy, aims to eliminate hypovolemia as soon as possible while maintaining the necessary colloid osmotic pressure, sufficient oxygen capacity, rheological and hemocoagulative properties of blood. The liver with hypovolemia, especially in combination with anemia and hypotension, is in a state of severe hypoxia. This creates conditions for microcirculation disorders and severe metabolic disorders, which, if inadequate or late correction, lead to irreversible changes - universal liver failure, often resulting in death (Table 2). Timely correction of the acid-base state (ACH) and electrolyte balance is very important. In order to correct acid-base balance (acidosis), do not rush with the introduction alkaline solutions, since during blood transfusion from sodium citrate (a blood stabilizer), alkali is formed during metabolism, which can lead to metabolic alkalosis.

table 2

The program of transfusion-infusion therapy depending on blood loss

In severe cases of decompensated acidosis, a 4.2% solution of sodium bicarbonate or trisamine is injected intravenously. To correct the colloid-osmotic balance, albumin 10% is transfused intravenously, 200 ml per day - 1-2 times. The diet provides for absolute hunger for at least the first day after the final stopping bleeding, since at rest the esophagus practically does not peristaltize, which reduces the likelihood of rejection of a fresh thrombus at the site of damage to the esophageal mucosa and, accordingly, recurrence of bleeding. On the 2nd day - cold drink with the addition of aminocaproic acid, thrombin. By the end of 2 days the patient switches to a diet (table No. 1a), the food is chilled. To reduce the aggressiveness of the acid-peptic factor, it is advisable to use an H2 blocker: Rantak 150 mg intravenously 2 times a day or Kvamatel: 20 mg intravenously 2 times a day for 5 days; inside - taking antacids for at least 10 days (almagel, remagel, gastal, maalox, tisacid) 4 times a day 40-50 minutes before meals. To stop ongoing bleeding, as well as after its final stop, endoscopic phlebosclerosing therapy is possible: 2-6 ml of a 3% thrombovar solution is injected into the most affected veins through the endoscope channel. But the effect of therapy is unstable, associated with the risk of extensive damage to the vein wall, followed by profuse bleeding. In order to prevent recurrence of bleeding, it is necessary to follow a sparing diet, avoid physical and emotional overload. Of the medications, a good preventive effect is given by the use of: beta-blockers (anaprilin 40-160 mg per day - 3-4 months); it is necessary to achieve a decrease in heart rate by 25-26% (not lower than 58-60 beats per minute); the level of GHG decreases; The alpha-blocker prazosin has a systemic arterio-venodilating effect. Use with caution due to the possibility of orthostatic collapse; clonidine: 0.075 mg - 3 times a day; reduces total peripheral vascular resistance, cardiac output, blood pressure, including in the pulmonary artery and right ventricle; Corinfar (an antagonist of Ca channels) - reduces pressure in the portal system. During the period of remission, it is advisable to use hepatoprotectors (Heptral, Essentiale, Lipostabil, LIV-52, Carsil), complex vitamin preparations (? multibiont?, "Centrum?, etc.); the use of enterosorbents: enterosgel, polyphepan, polysorb in courses of 7-10 days for the purpose of detoxification.

SURGICAL TREATMENT

Superselective proximal vagotomy is performed from abdominal access, extramucosal myotomy of the esophageal-gastric junction is performed longitudinally, and after circular stitching of varicose veins throughout the myotomy zone, areflux cardia is restored.

The method is carried out as follows.

An upper median extended upward laparotomy is performed with bypassing the xiphoid process on the left with the intersection of the ligaments and sternocostal articulation, as well as correction of the access upwards with RSK-10 retractors with dislocation and compression of the left costal arch. They cross the outer part of the left triangular ligament of the liver, the upper segment of the left lobe of the liver is moved medially, thereby opening up access to esophagus diaphragm (OD) and the esophageal-gastric junction. At the base of the left crus of the diaphragm, the phrenic-esophageal ligaments are bluntly pierced with a clamp and enter the posterior mediastinum. The hole made is expanded by crossing ligamentous apparatus the esophagus and cardia along the edge of the POD, without damaging the aponeurotic case of the legs of the diaphragm. At the same time, as if skeletonizing the base right leg diaphragm, muscle loop and all left leg diaphragm (Fig. 1). The esophageal-gastric junction, together with fiber, remnants of ligaments and neurovascular inclusions, is reduced by 2.5-3 cm, i.e. removed from the posterior mediastinum, while the cardia and abdominal esophagus become clearly visible and accessible. To create optimal access to the posterior walls of the cardia and esophagus, the diaphragmatic fundus ligament and the proximal part of the splenogastric ligament are crossed with 1-2 short gastric vessels. The anterior and posterior trunks of the vagus nerves are taken on rubber bands for further control of their main branches. In the fiber surrounding the esophagus and cardia, dilated veins that enter the walls of the esophagus and cardia are determined. Devascularization and denervation of the esophageal-gastric junction using precision technology of superselective proximal vagotomy is started from behind. The bottom of the stomach is turned down and forward and the posterior walls of the stomach are gradually skeletonized, crossing the gastro-pancreatic ligament and the bundle of the first transverse gastric vessels and cardia, as well as the vascular bundles with dilated veins and cardiac nerves. The esophagus is skeletonized high, the stomach - along the lesser curvature - to the level of the first transverse gastric artery, including the last one. The anterior walls of the stomach, cardia and esophagus are skeletonized much easier - the main branches of the anterior trunk of the vagus nerve are well controlled here: esophageal, cardiac and main. The body of the stomach is skeletonized to the level of the first transverse gastric artery. The cardia and esophagus acquire significant mobility only after the intersection of the cardiac and esophageal branches. The ideal surgical technique is the intersection of the cardiac and preservation of the main gastric nerves with high external devascularization of the esophagus, complete external devascularization of the cardia and proximal sections of the bottom and body of the stomach.

Bleeding from these veins is usually insidious, difficult to control, and usually occurs in association with coagulopathy, thrombocytopenia, and sepsis.

Drugs that cause mucosal erosion, such as salicylates and other NSAIDs, can also cause bleeding. Varicose veins in other areas become a source of bleeding relatively rarely.

Bleeding from varicose veins of the esophagus: diagnosis

History taking and general examination suggest VRV as the cause of gastrointestinal bleeding. In 30% of patients with cirrhosis, another source of bleeding is identified. If a disease is suspected, it is necessary to perform fibrogastroduodenoscopy as soon as possible. Along with rupture of varicose veins of the stomach and esophagus, the cause of bleeding in rare cases is hypertensive gastropathy.

Bleeding from varicose veins of the esophagus: conservative therapy

Transfusion of blood, fresh frozen plasma and platelets, depending on hematological parameters. Vitamin K is administered at a dose of 10 mg intravenously once in order to exclude its deficiency. Avoid excess transfusion.

20 mg of metoclopramide is injected intravenously. This drug allows you to briefly increase the pressure in the lower esophagus and thereby reduce the blood flow in the system v. azy-gos.

Antibacterial therapy. Take a sample of blood, urine and ascitic fluid for culture and microscopy. Several studies have found an association of the disease with sepsis. Antibiotics are prescribed. Duration antibiotic therapy should be 5 days.

Terlipressin causes vasospasm in the basin of the celiac trunk, due to which it allows to stop bleeding from the esophagus esophagus (decrease in mortality by about 34%). Serious side effects occur in 4% of cases and include myocardial ischemia, spasm peripheral vessels, which may be accompanied by severe arterial hypertension, skin ischemia and circulatory disorders internal organs. Nitrates may reverse the peripheral effect of vasopressin but are not usually prescribed to treat the side effects of terlipressin. Octreotide is a synthetic analogue of somatostatin. It does not have a side effect on the heart, and therefore the appointment of nitrates with its introduction is not required. According to latest research from the Cochrane database, octreotide has no effect on disease mortality and minimal effect on the need for transfusion therapy.

Endoscopic injection of sclerosing agents into the VRV and surrounding tissues can stop acute bleeding. Side effects(severe - in 7%) include the occurrence of pain behind the sternum and fever immediately after injection, the formation of ulcers on the mucosa, late strictures of the esophagus. In the future, the introduction of sclerosing substances should be continued until complete obliteration of the veins. The greatest difficulties arise when injecting into the gastric this case thrombin should be used.

Varicose vein ligation is used frequently.

Balloon tamponade with a Sengstaken-Blakemore or Linton probe. Usually this alone is enough to stop the bleeding. The probe should not be used for more than 12 hours due to the risk of ischemia, the risk of which increases with the simultaneous administration of terlipressin.

Treatment of liver failure: for the prevention of encephalopathy, lactulose 10-15 ml every 8 hours should be administered orally or through a tube, as well as thiamine and multivitamin preparations. Patients with severe encephalopathy are prescribed enemas with magnesium sulfate and phosphates.

Of paramount importance in acute bleeding from esophageal varices is the correction of hemodynamic disorders (infusion of blood and plasma products), since in conditions of hemorrhagic shock, blood flow in the liver decreases, which causes a further deterioration in its functions. Even in patients with confirmed esophageal varices, localization of bleeding should be established using FEGDS, since other sources of bleeding are detected in 20% of patients.

Local treatment

To stop bleeding from varicose veins of the esophagus, endoscopic techniques, balloon tamponade, and open dissection of the esophagus are used.

Esophageal vein ligation and sclerotherapy

These are the most commonly used initial treatments. Ligation is a more complex procedure than sclerotherapy. In the presence of active bleeding, endoscopic procedures may be difficult. In such cases, balloon tamponade should be performed.

Balloon tamponade

Use a Sengstaken-Blakemore probe with 2 tamponade balloons. There are modified versions of the probe (for example, the Minnesota tube) that allow aspiration of the contents of the stomach and esophagus. The probe is inserted through the mouth, its penetration into the stomach is controlled by auscultation of the epigastric region during balloon inflation or radiographically. Light traction is needed to compress the varicose veins. The first step is to fill with air (200-250 ml) only the gastric balloon - this event is usually enough to stop the bleeding. The filling of the gastric balloon should be stopped if the patient experiences pain, because if the balloon is incorrectly placed in the esophagus, it may rupture during filling. If gastric tamponade is not enough to stop bleeding and esophageal tamponade has to be resorted to, the esophageal balloon should be lowered for 10 minutes every 3 hours. The pressure in the esophageal balloon is controlled using a sphygmomanometer. Special attention when setting the probe, attention should be paid to preventing aspiration of gastric contents (if necessary, the patient is intubated).

Dissection of the esophagus

Varicose vein ligation can be performed with a stapler, although there is a risk of developing esophageal stenosis in the future; The operation is usually combined with a splenectomy. This procedure is usually used if there is no effect from all the other therapies listed above and it is impossible to perform a transjugular intra-hepatic porto-caval bypass. Operations are associated with frequent complications and high mortality.

X-ray vascular methods of therapy

AT specialized centers transvenous intrahepatic portosystemic shunting is possible. Access through the jugular or femoral vein produces catheterization of the hepatic veins and between them (system low pressure) and portal venous system (high pressure) introduce an expanding stent. The pressure in the portal vein should decrease to 12 mm or less.

Surgery

Urgent porto-caval shunting allows to stop bleeding in more than 95% of cases, but is characterized by high (>50%) intraoperative mortality and does not affect long-term survival. This method of treatment is currently used only in isolated cases.

Prognosis for varicose veins of the esophagus

Mortality in general is 30%. It is higher in patients with severe liver disease.

The effectiveness of therapy aimed at stopping bleeding from the esophageal varicose veins

Injection of sclerosing drugs or vein ligation - 70-85%.

Balloon tamponade - 80%.

Terlipressin - 70%.

Octreotide - 70%.

Vasopressin and nitrates - 65%.

Bleeding from varicose veins (hereinafter VRV) of the esophagus. Long-term therapy

Injection of a sclerosing drug in a volume of 0.5-1 ml into the tissues around the VRV or 1-5 ml into varicose veins every week until the veins are completely obliterated; then at intervals of 3-6 months.

Ligation is carried out in the same mode as sclerosing therapy, while obliteration of varicose veins occurs faster (39 days versus 72 days).

The appointment of propranolol reduces the frequency of relapses. No decrease in mortality was noted.

Transvenous intrahepatic portosystemic shunting and other shunting procedures are considered to be more reliable in preventing rebleeding, which can only occur if the shunt is blocked. However, when they are carried out, the incidence of chronic hepatic encephalopathy increases.

Prevention of rebleeding

During endoscopic ligation, varicose veins are aspirated into the lumen of a special endoscopic instrument and tied with elastic bands. The ligated vein is subsequently obliterated. The procedure is repeated every 1-2 weeks until the obliteration of the veins. In the future, regular endoscopic monitoring is necessary for the timely treatment of recurrences of varicose veins. Endoscopic ligation is generally more effective than sclerotherapy. To prevent secondary bleeding due to ulceration induced by ligatures, antisecretory therapy with inhibitors of Na +, K + -ATPase (proton pump) is prescribed.

Sclerotherapy

Sclerotherapy is the introduction of sclerosing agents into varicose veins. After the introduction of endoscopic ligation this method used relatively rarely. Sclerosing therapy is not without drawbacks, as it may be accompanied by transient pain, fever, temporary dysphagia, and sometimes perforation of the esophagus. It is also possible to develop esophageal strictures.

Transjugular intrahepatic portocaval shunting

The operation consists in placing an intrahepatic stent between the portal and hepatic veins, which provides a porto-caval bypass and reduces pressure. The procedure is performed under x-ray control. Before surgery, it is necessary to confirm the patency of the portal vein using angiography and prescribe prophylactic antibiotic therapy. The occurrence of rebleeding is usually associated with narrowing or occlusion of the shunt (appropriate examination and treatment, such as angioplasty, is necessary). Transjugular intrahepatic porto-caval shunting can provoke the development of hepatic encephalopathy, for its relief it is necessary to reduce the diameter of the shunt.

Porto-caval shunt surgery

Portocaval bypass surgery can prevent rebleeding. The imposition of non-selective porto-caval shunts leads to an excessive decrease in the flow of portal blood to the liver. With this in mind, selective bypass surgery has been developed, in which the risk of developing postoperative hepatic encephalopathy is lower. However, over time, hepatic portal blood flow decreases.

Antagonists of p-adrenergic receptors (p-blockers)

Propranolol or nadolol lower blood pressure. They can be used to prevent recurrent bleeding. However, for secondary preventionβ-blockers are rarely used. Treatment compliance with these drugs may be low.

Mallory-Weiss syndrome

Rupture of the mucosa in the region of the esophageal-gastric anastomosis, resulting from strong vomiting movements and especially often observed with excessive alcohol consumption. Initially, the vomit is of a normal color, and then blood appears in them.

Treatment

• In most cases, bleeding stops spontaneously. Packing with a Sengstaken-Blakemore tube may be required.
• In some cases, surgery is required to suture the bleeding vessel or selective angiography with embolization of the feeding artery.
• The Child Score can effectively determine the severity of liver disease in a patient with cirrhosis of the liver. It should not be used in patients with primary biliary cirrhosis or sclerosing cholangitis.
• Group A<6 баллов.