Open gastric ulcer with bleeding: danger and treatment.

Bleeding during peptic ulcer disease occurs in 18-25% of cases, accounting for 60-75% of all cases of gastrointestinal blood loss. Most often, the source of bleeding in peptic ulcers is arrozen arteries located in the area of ​​the ulcer, and less often veins and capillaries. It can be obvious (acute), occurring suddenly, or hidden, appearing gradually. In most cases, ulcers of the lesser curvature of the stomach bleed (bleeding occurs from the system of the left and right gastric arteries) and duodenum, penetrating into the head of the pancreas or into the hepatoduodenal ligament (bleeding from the gastroduodenal and superior duodenal-pancreatic arteries).
Pathogenesis of hemodynamic disorders during ulcer bleeding.

First of all, blood loss is accompanied by a decrease in blood volume and hypovolemic shock. Developing hypovolemia negatively affects blood supply, primarily to the brain and heart. Under such conditions, the vital activity of the body is ensured by the activation of autoregulatory neurohumoral mechanisms of adaptation and protection. Thus, a deficiency of ODC up to 10-15% does not lead to significant hemodynamic disturbances and is compensated by a decrease in the capacity of the vascular bed, spasm of blood vessels in the skin, abdominal organs, and opening of arteriovenous shunts.

With blood loss of more than 15% of blood volume, blood pressure decreases by 15-30%. Compensation of the missing volume of blood volume, an increase in cardiac output, and ultimately normalization of blood pressure and improvement of blood supply to organs and tissues in this category of patients occurs due to greater tension in adaptive and protective mechanisms. The deficiency of BCC is compensated by a generalized spasm of blood vessels, the penetration of part of the tissue fluid, blood from natural depots, and lymph from lymphatic vessels into the general bloodstream. At the same time, replenishment of blood volume is accompanied by its hemodilution. The heart rate also increases. At the same time, under the influence of corticosteroids, aldosterone, and antidiuretic hormone, reabsorption of water and sodium in the renal tubules increases and diuresis decreases.

However, replenishment of circulating blood volume has a negative effect on tissue perfusion. Cell hypoxia develops, which inevitably leads to a switch of metabolism to the anaerobic type. Metabolic acidosis gradually occurs. In case of depletion of protective mechanisms for the restoration of bcc, blood pressure decreases to a critical level - 50-60 mm Hg. Art. An irreversible microcirculatory disorder occurs. The function of the liver (liver failure), kidneys (renal failure), and heart (myocardial infarction) is sharply impaired. Patients often die in this foyer.

The deterioration of the condition of patients with bleeding due to peptic ulcer disease is facilitated by intoxication of the body with hydrolysis products of blood poured into the intestines. The leading role in the intoxication process belongs to ammonia. The latter, due to a decrease in the detoxification function of the liver due to systemic hypotension, is not captured by hepatocytes. In combination with a decrease in diuresis, this leads to a significant increase in the concentration of ammonia and other toxic substances in the blood.

Classification of bleeding in peptic ulcer disease. Gastroduodenal bleeding is divided: I) according to etiology - from a chronic ulcer, from an acute ulcer, from a symptomatic ulcer; 2) by localization - from a gastric ulcer: a) cardia, b) body of the stomach, c) antrum, d) pyloric canal (lesser curvature, anterior wall, posterior wall); from duodenal ulcers: a) bulbous, b) postbulbar, c) descending (walls: anterior, posterior, upper, lower, transitional and combined); 3) by nature: ongoing: a) jet (profuse), b) laminar, c) capillary, d) recurrent, e) unstable hemostasis; occurred: a) stable hemostasis, b) posthemorrhagic anemia; 4) according to the severity of bleeding or blood loss.

E. L. Berezov distinguishes three degrees of severity of gastrointestinal bleeding in peptic ulcer disease based on the frequency of bloody vomiting, tarry stools, blood pressure and pulse, and the general condition of patients:

Mild degree: single vomiting, tarry stools, blood pressure and pulse are normal, general condition is satisfactory.
Moderate degree, fainting, repeated bloody vomiting, weakness, decrease in systolic blood pressure to 90-80 mm Hg. Art., increased heart rate up to 100 beats.
Severe degree, excessive repeated vomiting, tarry stools, systolic blood pressure decreases to 60-50 mm Hg. Art. pulse 120 or more beats per minute, the patient's condition is critical.

Symptoms of bleeding in peptic ulcers. Typical signs of gastrointestinal bleeding are bloody vomiting, tarry stools, and general symptoms. Their severity primarily depends on the severity and duration of bleeding and the volume of blood loss.

Bloody vomiting occurs in most cases of gastrointestinal bleeding during peptic ulcer disease. It can be one-time or often repeated, insignificant and profuse, such as coffee grounds and, less often, scarlet blood with clots. Bloody vomiting is most typical for bleeding from gastric ulcers. In persons with duodenal ulcer, it is observed when blood is thrown into the stomach through the gaping Pylorus. However, with a slow accumulation of blood in the stomach, vomiting may be absent, since the spilled blood has time to be evacuated into the intestines. A similar situation occurs in patients with gastric bleeding due to rapid gastric emptying.

Vomiting of blood with clots is observed with massive bleeding due to peptic ulcer disease. The appearance of vomiting at short intervals is a sign of ongoing bleeding, and after a long period of time it indicates its resumption.

Common symptoms of blood loss include weakness, dizziness, pale skin and mucous membranes, cold sticky sweat, acrocyanosis, blurred vision, hearing and mental disorders (brain hypoxia), pain in the heart (myocardial hypoxia).

Diagnosis of bleeding in peptic ulcer disease. When examining patients with gastrointestinal bleeding, the task is to establish its presence, determine the cause, location of the source and severity. Confirmation of continuation or stopping of bleeding is of great importance for subsequent tactics.

First of all, attention is paid to the nature of the complaints, anamnesis, and the results of an objective examination and digital rectal examination are analyzed. The disappearance of abdominal pain after bleeding and local pain upon percussion in the pyloroduodenal area are often detected. It is extremely important to assess the state of hemodynamics (pulse, blood pressure, central venous pressure, ECG, diuresis), hematological indicators (red blood cells, hemoglobin, hematocrit number, etc.) in order to timely diagnose hemorrhagic shock.

Phpbroeophagogastroduodenoscopy is performed on an emergency basis, including patients in extremely critical condition, as this allows simultaneous implementation. If it is impossible to examine the stomach and duodenum due to the large amount of contents, they are washed with cold water through a probe, followed by fibrogastroduodenoscopy.

Gastroduodenal bleeding in peptic ulcer disease is characterized according to endoscopic signs formulated by G. P. Shorokh and V. V. Klimovich (1998). The authors highlight:

Endoscopic signs of ongoing bleeding in peptic ulcer disease: a) pulsating bleeding; b) the presence of blood in the lumen of the stomach or duodenum, accumulating despite constant aspiration; c) diffuse capillary bleeding from the bottom or edges of the ulcer; d) bleeding under a loose red clot in the area of ​​the ulcer; e) scarlet blood clots that fill the lumen of the stomach or duodenum and do not allow the ulcer to be seen;

Existing bleeding in peptic ulcer disease, which is divided into stable (stable) and unstable (unstable) hemostasis.

Endoscopic signs of bleeding in a peptic ulcer with unstable hemostasis are as follows: a) the ulcer is covered with a dark blood clot, there is “coffee grounds” in the stomach, there is no fresh blood; b) in the crater of the ulcer there is a vessel closed by a red blood clot; c) a pulsating vessel is visible in the crater of the ulcer; d) the ulcer is closed with a loose red clot.

Endoscopic signs of bleeding in peptic ulcer disease with stable hemostasis: a) the bottom of the ulcer is covered with fibrin; b) small thrombosed vessels on the ulcer; c) the bottom of the ulcer is covered with hemosiderin (black color of the bottom), there is no blood in the stomach.

If, based on instrumental diagnostic methods, it is impossible to find the source of bleeding in a peptic ulcer, and the patient’s condition progressively worsens, emergency treatment is indicated.

Differential diagnosis of bleeding in peptic ulcer disease. More than 70 diseases are known that are accompanied by gastroduodenal bleeding. Most often, differential diagnosis of bleeding of ulcerative etiology is carried out with gastrointestinal bleeding in disintegrating, Mallory-Weiss syndrome, hemorrhagic erosive gastritis, varicose veins of the esophagus and stomach, Randu-Weber-Osler disease, leukemia, hemophilia, Werlhoff disease, Dieulafoy syndrome.

With a disintegrating stomach cancer, the bleeding is rarely profuse. Usually it is small, like coffee grounds, and is not accompanied by pain. Bleeding is preceded by loss of appetite, body weight, progressive increase in weakness, fatigue, etc. The fecal reaction to occult blood after the disappearance of bloody vomiting and tarry stools remains positive for a long time. The diagnosis is clarified based on the results of fibrogastroscopy with a biopsy of tumor tissue and x-ray examination.

Mallory-Weiss syndrome is manifested by bleeding from a rupture of the mucous membrane of the cardioesophageal region. There may be several breaks. They are located longitudinally. The syndrome occurs mainly at a young age. Bleeding occurs suddenly with severe vomiting and is accompanied by chest pain. With fibrogastroscopy, linear breaks in the mucous membrane of varying lengths and depths are found in the esophageal-cardiac zone.

Hemorrhagic erosive gastritis is characterized by bleeding of varying degrees of intensity from single and multiple erosions of the gastric mucosa, representing superficial ulcers. Erosions are localized in any part of the stomach, but more often in the body and in the prepyloric part. The development of erosive gastritis is facilitated by burn disease, drug overdose, myocardial infarction, acute cerebrovascular accidents, and traumatic brain injury. The only method for diagnosing erosive gastritis is fibrogastroscopy.

Bleeding from varicose veins of the esophagus and stomach due to portal hypertension is facilitated by portal crises, a disorder in the blood coagulation system, and ulceration of the mucous membrane of the esophagus and stomach under the influence of the acid-peptic factor. Bleeding often occurs after a heavy meal, as well as during sleep, when the blood flow into the portal vein system increases significantly. When examining patients, they find an enlargement or, conversely, a decrease in the liver, splenomegaly, often combined with ascites, and dilation of the veins of the anterior abdominal wall.

In Randu-Weber-Osler disease, the source of bleeding is multiple telangiectasias and angiomas of the mucous membrane. The disease is hereditary and is transmitted in a dominant manner. Often, along with gastrointestinal bleeding, bleeding from telangiectasia and angiomas, localized on the mucous membranes of the nose, oral cavity, lips, tongue, wings of the nose, earlobes, bladder, trachea and bronchi, is observed.

Gastrointestinal bleeding in patients with leukemia occurs due to increased permeability of the vascular wall of the mucous membrane. Bleeding can be either minor or profuse. The diagnosis is made based on the results of a blood smear, biopsy and bone marrow puncture.

In patients with hemophilia, the occurrence of gastrointestinal bleeding is associated with a drop in the level of antihemophilic globulin in the blood below 30%. The disease is inherited and occurs predominantly in men. Anamnesis data indicate increased bleeding from soft tissue wounds, the presence of intra-articular, subcutaneous and intermuscular hematomas. Increased blood clotting time to 10-30 minutes.

Typical signs of Werlhof's disease, in addition to gastrointestinal bleeding, are increased bleeding of the gums, nasal mucosa, renal and uterine bleeding, subcutaneous bruising and hemorrhages in the submucosal membranes. Thrombocytopenia and a significant increase in clotting time are found in the blood.

Dieulafoy's syndrome was described in 1897. It occurs mainly in men under the age of 50 who do not have any history of ulcers. The syndrome is characterized by the development of massive arterial bleeding, prone to recurrence from single superficial erosions mainly of the gastric mucosa. In 70-80% of cases, the source of bleeding is located in the stomach along the posterior wall of its upper third, 4-6 cm from the esophagogastric junction. However, Dieulafoy's ulcerations (Dieulafoy's ulcers) can also be localized in the proximal esophagus, duodenum, and large intestine. The usual diameter of lesions is 0.5-0.8 cm. The basis of the disease is a violation of the formation of vessels of the submucosal layer during embryonic development, which, in combination with chronic inflammation of the mucous membrane, leads to thrombosis of the artery and necrosis of its walls. At the bottom of the erosion there is always an aneurysmically altered small artery of the submucosal layer. The development of bleeding is promoted by the acid-peptic factor, mechanical damage to the mucous membrane, endotoxemia, disruption of hormonal homeostasis, circulation of aggressive autoimmune complexes, atherosclerosis, and hypertension. During fibrogastroscopy in patients with Dieulafoy's syndrome, a large amount of blood is found in the stomach, often in the form of a cast.

More rare sources of gastrointestinal bleeding are diverticula of the digestive tract, hiatal hernia, liver ruptures and hepatic artery aneurysm (manifested by hemobilia).

Treatment of bleeding in peptic ulcers. Patients with gastrointestinal bleeding and compensated hemodynamics are hospitalized in the intensive care wards of the surgical department or in the intensive care unit. In case of life-threatening bleeding, accompanied by hemorrhagic collapse and (or) shock, they are taken to the operating room, where measures are taken to stabilize hemodynamics (catheterization of the central vein or several peripheral veins for intensive infusion-transfusion therapy and control of central venous pressure). Against the background of the treatment, an emergency procedure with endoscopic hemostasis is performed. If it is ineffective and if the patient tolerates surgical intervention, laparotomy is performed. Patients with a high degree of risk are not offered, and they are transferred for further treatment to the intensive care unit. Patients with stopped bleeding after normalization of hemodynamics are admitted to the intensive care unit or intensive care wards of the surgical department.

Conservative treatment of patients with gastrointestinal bleeding due to peptic ulcer disease involves hemostatic therapy and replenishment of blood volume in order to normalize central hemodynamics, microcirculation, transcapillary exchange and respiratory function of the blood.

Hemostatic therapy is divided into local and general. Methods of local hemostatic therapy include endoscopic hemostasis; the use of agents that reduce fibrinolytic activity; hypothermia of the stomach.

Several methods of endoscopic hemostasis have been developed. Among them, the most common are incision of the source of bleeding with drugs (), diatothermocoagulation, targeted irrigation of a bleeding ulcer with hemostatic drugs, clipping of arrosive vessels, cryotherapy on the source of bleeding, etc.

The method of instilling the source of bleeding with drugs is based on achieving hemostasis both due to mechanical compression of the vessels with a solution of the injected fluid (filtration vascular tamponade), and the local influence of medications that cause vasospasm, increase platelet aggregation with thrombus formation in the arrosive vessel, and inhibit increased local fibrinolysis . For puncturing ulcers, ethoxysclerol, MK-6 glue dissolved in 70-96° ethyl alcohol, MIRK-10, MIRK-15 glue, norepinephrine, adrenaline, oil preparations (iodolipol, mayodil, aevit, etc.) are used. The drugs are injected into the ulcer, under a vessel or under a clot from 2-3 points in a volume of 1-2 ml per point.

When using the method, it should be borne in mind that after injection of alcohol into the tissue of the wall of the stomach or duodenum, the size of the ulcer may increase due to superficial necrosis of the mucosa.

Treatment of a bleeding ulcer with a diathermic probe begins around the arrozen vessel, which leads to its gradual compression by sealing tissues. In patients with a hanging thrombus located in the area of ​​the source of bleeding or blood leaking from under it, diathermocoagulation begins from the upper edge of the thrombus in a downward direction. As a result, a white scab forms at the site of the bleeding ulcer,

As a rule, bipolar electrocoagulation is used to thermally stop gastroduodenal bleeding, which is accompanied by a smaller depth of tissue damage and is not complicated by perforation of the wall of the coagulated organs,

Laser photocoagulation (videoendoscopic laser photocoagulation) of bleeding ulcers refers to methods of non-contact exposure to the source of bleeding. It is more advisable to use high-intensity laser radiation (YAG - neodymium laser, argon laser), which is not absorbed by hemoglobin and water, and therefore penetrates deeply into the stomach and duodenum with the formation of a durable whitish scab on the surface of the ulcer.

The effectiveness of low-intensity laser radiation for bleeding ulcers is disputed, since it can increase hyperemia and vulnerability of surrounding tissues with the appearance in some cases of flat erosions on the mucous membrane. Their formation increases the likelihood of recurrent bleeding. Based on the available data on the effect of low-intensity laser radiation, a number of authors (P. M. Nazarenko et al., 1999, etc.) suggest prescribing it to patients with bleeding ulcers only when a hemostatic effect is achieved within 4-5 days.

The disadvantage of laser photocoagulation is the inability to stop ongoing intense bleeding in peptic ulcers. More often, quantum coagulation is used in combination with other methods of endoscopic hemostasis.

For targeted irrigation of a bleeding ulcer, caprofer, 10% calcium chloride solution, thrombin, fibrinogen, aminocaproic acid, norepinephrine, mesaton, etc. are used. Of the listed medications, only irrigation of the ulcer with caprofer leads to stopping intense bleeding. All other drugs are used for hemostasis in patients with minor, predominantly capillary bleeding. The composition of caprofer includes iron carbonyl complex and aminocaproic acid. The hemostatic effect of the drug occurs immediately after its application to the surface of a bleeding ulcer with the formation of a dense black clot, well fixed to the mucous membrane of the stomach and duodenum. The clot is well retained for 12-16 hours.

The method of endoscopic clipping of bleeding vessels in an ulcer is based on the application of metal clips using a special clipper to the base of the vessel or along its length on both sides of the bleeding site,

The use of agents that reduce fibrinolytic activity and open arteriovenous shunts. To reduce the fibrinolytic activity of the mucosa, a mixture has been proposed consisting of 10 g of epsilon-aminocaproic acid, 200 mg of thrombin and 100 ml of water, which the patient takes orally every 15 minutes for 2 hours, and then 3 times a day. The opening of arteriovenous shunts, which leads to bleeding of the mucous membrane, is facilitated by the introduction into the stomach (including through a nasogastric tube) of 4 ml of a 0.1% solution of norepinephrine in 150 ml of isotonic sodium chloride solution. In the absence of a hemostatic effect, norepinephrine is prescribed again, but in half the dose.

Gastric hypothermia (cold applied to the epigastric region) is used in a complex of local hemostatic therapy methods. Gastric lavage with cold (up to +4 °C) water is used if it is impossible to use more modern methods of local hemostasis in patients with ongoing bleeding due to peptic ulcer disease. The formation of blood clots during gastric lavage is accelerated by the addition of silver nitrate and thrombin to the water.

For the purpose of general hemostatic therapy, 10 ml of a 10% solution of calcium chloride (gluconate) is administered intravenously; every 4-6 hours - 5% solution of fibrinolysis inhibitor epsilon-aminocaproic acid - 100-200 ml and native fresh frozen plasma. A 1% solution of vikasol is prescribed intramuscularly up to 3 ml per day, dicinone, etamsylate - 1-2 ml every 6-8 hours, and in severe cases - intravenously trasylol (100 thousand units) or counterncal (25-30 thousand units) . A good hemostatic effect is provided by secretin, which is administered intravenously in a dose of 100 mg per 50 ml of isotonic sodium chloride solution.

If successful, achieving hemostasis from a bleeding ulcer allows for a set of measures to normalize the hemodynamics of patients and stabilize their general condition. This makes it possible to either achieve healing of the ulcer using therapeutic methods, or perform surgery in more favorable conditions for patients.

Elimination of volemic disorders consists primarily in replenishing the volume of blood volume. Since the most favorable conditions for ensuring adequate hemodynamics and gas exchange in tissues occur during hypervolemic hemodilution, the volume of administered transfusion media in patients with gastrointestinal bleeding due to peptic ulcer disease should be three times higher than the blood loss due to blood substitutes and blood in a rational combination. In patients with hypovolemia of 25-30% of the bcc, the ratio between colloid and crystalloid drugs is 1: 1.5, and a deficiency of bcc of 30% or more is 1:2. Indications for blood transfusion arise when the hemoglobin concentration decreases below 80 g/l and the hematocrit number to 0.25. Thus, for mild blood loss (up to 1000 ml), 1.5-2 liters of glucose-saline solutions are administered intravenously in combination with plasma substitutes (5-10% glucose solution, acesol, disol, chlosol, gelatinol, etc.). Moderate bleeding (up to 2000 ml) is an indication for transfusion of 4500 ml of infusion-transfusion media, of which 1500 ml (no more than 1/3 of the total infusion volume) consists of glucose-saline solutions (1:1), 1500 ml - colloids ( of which 50% is fresh frozen plasma) and 500 - 800 ml donor red blood cells.

Volume replacement is carried out under strict control of central venous pressure, heart rate, hourly diuresis, red blood cell counts, hemoglobin and hematocrit.

Replenishment of blood loss is considered relatively adequate when the number of red blood cells reaches 3.0 x 10i/l, hemoglobin 90 g/l, hematocrit number 0.30.

In parallel, modern complex therapy for peptic ulcer is carried out, including the use of histamine H2 receptor blockers, primarily intravenously, hydrogen pump inhibitors, drugs that destroy HP, antacids, enveloping and adsorbent agents, reparants, anabolic agents, biogenic stimulants, vitamins, etc.

After stopping bleeding from a peptic ulcer, the patient follows the Meulengracht diet for 10-12 days: taking easily digestible food with a daily energy capacity of at least 1000-1200 kcal every 2-3 hours, 100-150 ml. Having buffering properties, food in the stomach neutralizes hydrochloric acid and proteolytic enzymes, reduces hungry peristalsis of the stomach and stimulates the regeneration process. If bleeding in this group of patients has not resumed, then, if indicated, they undergo a planned operation after 10-12 days of preoperative preparation. The remaining patients are treated conservatively for peptic ulcer disease.

Operations used in the treatment of patients with bleeding from peptic ulcers are divided according to indications into urgent, urgent and delayed.

According to G.P. Shorokh and V.V. Klimovich (1998), emergency operations should be performed; a) with ongoing bleeding due to peptic ulcer, which could not be stopped endoscopically; b) recurrent bleeding in the hospital. Operations of this group are performed: a) in the first 2 hours after the patient’s admission with ongoing bleeding from a peptic ulcer and a failed attempt at endoscopic hemostasis; b) in the first 2-5 hours after admission, when there is massive blood loss with unstable endoscopic hemostasis or massive blood loss with endoscopically achieved temporary hemostasis due to arterial bleeding; c) in case of recurrent bleeding due to peptic ulcer pain in the hospital, regardless of the time of previous bleeding.

Urgent operations are indicated in patients with a high risk of recurrent bleeding due to peptic ulcer disease and are prophylactic in nature in order to prevent possible recurrent bleeding. Surgical intervention in this group is performed within 6-36 hours after admission.

Delayed operations are performed 12-14 days after stopping bleeding from a peptic ulcer in patients who have undergone a full examination and comprehensive preoperative preparation for surgery (their ulcer defect has not healed during treatment).

The extent of the operation performed in patients with bleeding due to peptic ulcer disease depends on the timing of its implementation, the location of the ulcer and the general condition of the patients. In persons operated on for emergency and urgent indications and without severe concomitant diseases, with relatively stable hemodynamic parameters, radical surgery is performed. At the same time, in patients with unstable hemodynamics and severe concomitant pathology, palliative surgery is performed with the sole purpose of stopping bleeding.

During surgery, after revision of the abdominal organs, the location of the ulcer is clarified. In difficult situations, a wide longitudinal gastrotomy or duodenotomy is performed, followed by a visual examination of the mucous membrane of the stomach and duodenum. After identifying the source, they resort to a temporary stop of bleeding (stitching, ligation of the bleeding vessel) and perform the main operation. As radical operations for bleeding mediogastric ulcers (type I according to Johnson), resection of 2/3 of the stomach according to Billroth-2, Billroth-1, pylorus-preserving gastric resection, and ladder (stepped) gastric resection are used.

In patients with a bleeding ulcer of type II, the operation of choice is resection of 2/3 of the stomach according to Billroth-2, Billroth-1. Less commonly, they perform pyloroantrum-preserving gastrectomy and vagotomy.

When bleeding from type III ulcers, gastric resection is performed according to Billroth-1, Billroth-2, pylorus-preserving, antrumectomy with selective vagotomy.

The following are used as palliative operations in patients with bleeding gastric ulcers: a) gastrotomy and suturing of a vessel in the ulcer; b) sectoral excision of the ulcer, pyloroplasty and vagotomy; c) excision of the ulcer, removal of its crater outside the stomach with ligation of the bleeding vessel and suturing of the wall defect.

In patients with bleeding ulcers of the duodenum and pylorus of the stomach, the following types of operations are performed:

When the ulcer is localized on the anterior wall: a) hemipyloroduodenoresection according to Bely; b) excision of the ulcer and pyloroplasty according to Judd-Horsley; c) excision of the ulcer and duodenoplasty with vagotomy (usually truncal vagotomy as the most quickly feasible). Duodenoplasty is performed when the upper edge of the ulcer is removed to a distance of at least 0.8 cm from the pylorus;

For ulcers of the posterior wall with a diameter of 0.8-1 cm, the following is indicated: a) suturing the arrozed vessel at the bottom of the ulcer with suturing the defect of the mucous membrane above it, performing a stomach drainage operation and vagotomy; b) suturing of the arrozed vessel with tamponade of the bottom of the ulcer with the posterior lip of duodenoplasty (Finney type), Finney pyloroplasty and vagotomy; c) in patients who have a bleeding penetrating ulcer of the posterior wall of the duodenum, which is sutured with difficulty and often produces recurrent bleeding, it is more advisable to remove it outside the intestine with suturing of the resulting wall defect (extraduodenization of the ulcer), perform a stomach drainage operation and vagotomy.

For bleeding from large (more than 1 cm in diameter) penetrating ulcers of the pyloric stomach and duodenum, distal gastrectomy is performed.

In patients with unremovable bleeding ulcers of the posterior wall of the duodenum (low, postbulbar), gastric resection is performed to switch off, suturing of the bleeding vessel with gastric drainage surgery and vagotomy.

Mortality after gastric resections performed for bleeding ulcers is 4-8%, and at the height of bleeding - 10-28%. After vagotomy, deaths are observed 5-10 times less often.

The article was prepared and edited by: surgeon

According to statistics, 10% of people with peptic ulcers experience gastric bleeding, the intensity of which is influenced by the size of the affected vessels. This condition is characterized by suddenness, and experts do not note a connection with the severity of the disease. Bleeding from a stomach ulcer is often the first sign of a disease of this digestive organ. Sometimes it is the result of ineffective treatment. In both cases, a bleeding stomach ulcer is a dangerous condition that requires medical attention.

An ulcer in the stomach may be complicated by bleeding

Ulcerative bleeding can have both obvious and hidden forms. In the first situation, the cause of the condition is the damaged integrity of the artery, in the second - a small vessel. Venous involvement is much less common.

A bleeding ulcer due to stomach disease has the following symptoms associated with the severity of blood loss:

• dizziness;
• muscle weakness;
• darkening of the eyes;
• hypotension;
• pallor of the face;
• vomiting dark masses;
• blood clots in stool;
• oliguria.

When bleeding occurs, a change in heartbeat is observed

A stomach ulcer with duodenal bleeding is characterized by the appearance of tarry stools and the manifestation of an anemic state. In this case, painful sensations may cease against the background of increased leukocytosis. A little later, hyperthermia develops.

An open gastric ulcer poses a great danger to the elderly, who, due to hardening of the vessels, lack their ability to contract, which makes hemostasis impossible.

In the presence of callous disease, when the ulcer has opened, the bleeding does not stop on its own, since the affected mucous membranes containing scar tissue do not have the ability to regenerate. In such cases, blood is released from the ulcer until surgery is performed.

Against the background of bleeding, an increase in body temperature occurs

The acute form of peptic ulcer is characterized by intermittent bleeding, but even in this case, a referral to a specialist is required, since in case of serious blood loss only resuscitation measures can save the patient.

The danger of an open ulcer

In the case when a stomach ulcer opens, acute pain begins after eating, which leads to the person completely refusing to eat. The result is serious exhaustion, blood loss in which leads to severe weakness and dystrophy.

In a situation where a person has an ulcer and profuse bleeding begins, blood loss occurs very rapidly. In this case, symptoms develop:

• hypovolemic shock;
• swelling of the meninges;
• acute dysfunction of the liver and heart;
• intoxication.

The opening of bleeding may be accompanied by symptoms of cerebral edema

In this condition, when the functions of many organs are impaired, the risk of death is quite high.

Therapy for ulcer bleeding

Treatment of a bleeding stomach ulcer is usually carried out conservatively. Even with an independent process of hemostasis, professional help should not be neglected, since in the absence of therapy, relapses almost always occur. A bleeding stomach ulcer requires hospitalization, which includes bed rest and a ban on eating and drinking water.

First of all, the attending physician prescribes the patient the drug Vikasol in the form of injections, a course of drips with epsilon-aminocaproic acid. This therapy is aimed at stopping bleeding.

Inpatient treatment is necessary in case of bleeding

If the ulcer is accompanied by massive blood loss, a transfusion with red blood cells is performed. When the patient’s condition has stabilized, the patient is monitored to determine signs of ongoing bleeding.

Before treating a bleeding ulcer, its location is determined. If the lower part of the esophagus is affected, a special catheter with a balloon is inserted into it through the patient’s mouth. The balloon then begins to inflate to create pressure at the site of the damaged vessel. There is another therapeutic method that involves acting on damaged tissue with special means.

The endoscopic method, in which the vessel is cauterized using an electric current, can also help cure bleeding. A medication that enhances blood clotting is also injected into a vein.

The operation is necessary in particularly difficult cases

What to do if none of the above methods gave the desired effect? In this situation, specialists resort to surgical intervention.

Diet for an open ulcer

One of the components of effective therapy is nutrition, which involves the strictest restrictions. A diet for a bleeding stomach ulcer involves an absolute refusal of liquid and food on the first day. If there is severe thirst, the patient is given water (several teaspoons) or ice to suck. Subsequent meals include raw eggs, milk, jelly, and liquid jelly.

Experts have come to the conclusion that if there is an open process with bleeding, prolonged hunger is contraindicated, since the secreted gastric juice worsens the condition of the mucous membrane. The body must receive the required number of calories, mineral salts, vitamins, and proteins. In this case, the food should be liquid.

Therapy for peptic ulcer disease includes following a diet

What diet should you follow in the following days? A little later, you can add a soufflé of cottage cheese, meat, vegetable purees, crushed cereals, steamed cutlets, and butter to your diet. When a patient has an ulcer and starts bleeding, all spicy foods, alcoholic drinks, smoked foods, and fried foods are completely prohibited.

First aid

If a person shows signs of internal bleeding, help is necessary. First of all, you need to call a medical team. The patient should lie on his back and try not to move. If possible, experts advise applying ice to the abdomen to reduce the effects of blood loss. At this time, it is forbidden to drink, eat, take medications, or rinse the stomach.

If possible, the patient should be kept conscious; ammonia is used for this. It is also not recommended to get to the hospital on your own; this can lead to increased bleeding.

If bleeding occurs, you should call an ambulance and apply a cold compress or ice to the stomach

It is forbidden to treat an open ulcer at home; this can be extremely dangerous. It is important to know that even if you feel better and stop bleeding, the disease should be treated under the supervision of doctors. It is necessary to call emergency help if bloody vomiting, feces with bloody components, acute pain in the stomach, development of shortness of breath, tachycardia, or a sharp decrease in blood pressure occur.

The symptoms and treatment of stomach ulcers will be discussed in the video:

Acute gastric ulcer with bleeding is the main complication of gastric ulcers (GU) of any etiology.
Acute ulcers by etiology are usually symptomatic and stress ulcers.

Under acute stomach ulcer(AJ) should be understood as a PU of any etiology that has the morphology of an acute ulcer. PG should be distinguished from erosion and chronic gastric ulcer. Some authors also understand by this term the newly diagnosed ulcer or the stage of the course of peptic ulcer of the stomach and duodenum (including Helicobacter pylori etiology).

Erosion- shallow defect, damage to the mucous membrane within the boundaries of the epithelium. The formation of erosion is associated with necrosis of the mucous membrane. As a rule, erosions are multiple and are localized mainly along the lesser curvature of the body and the pyloric part of the stomach, less often in the duodenum. Erosion can have different shapes, ranging in size from 1-2 mm to several centimeters. The bottom of the defect is covered with fibrinous plaque, the edges are soft, smooth and do not differ in appearance from the surrounding mucous membrane.
Healing of erosion occurs in 3-4 days through epithelization (complete regeneration) without scar formation. If the course is unfavorable, it may develop into an acute ulcer.

Acute ulcer is a deep defect of the mucous membrane, which penetrates to the muscular plate of the mucous membrane and deeper. The reasons for the formation of acute ulcers are similar to those for erosions. Acute ulcers are often solitary; have a round or oval shape; in cross-section they look like a pyramid. The size of acute ulcers ranges from several mm to several cm. They are localized on the lesser curvature. The bottom of the ulcer is covered with fibrinous plaque, it has smooth edges, does not rise above the surrounding mucous membrane and does not differ from it in color. Often the bottom of the ulcer has a dirty gray or black color due to the admixture of hematin hydrochloride.

Microscopically: mild or moderate inflammatory process at the edges of the ulcer; after rejection of necrotic masses at the bottom of the ulcer - thrombosed or gaping vessels. When an acute ulcer heals within 7-14 days, a scar forms (incomplete regeneration). In rare cases, an unfavorable outcome may lead to a chronic ulcer.

Chronic ulcer- characterized by severe inflammation and proliferation of scar (connective) tissue in the area of ​​the bottom, walls and edges of the ulcer. The ulcer has a round or oval (less often linear, slit-like or irregular) shape. Its size and depth may vary. The edges of the ulcer are dense (callous ulcer), smooth; undermined in its proximal part and flat in its distal part.
Morphology of a chronic ulcer during an exacerbation: the size and depth of the ulcer increases.
There are three layers at the bottom of the ulcer:
- upper layer- purulent-necrotic zone;
- middle layer- granulation tissue;
- bottom layer- scar tissue penetrating into the muscle membrane.
The purulent-necrotic zone decreases during the period of remission. Granulation tissue, growing, matures and turns into coarse fibrous connective (scar) tissue. In the area of ​​the bottom and edges of the ulcer, the processes of sclerosis intensify; the bottom of the ulcer is epithelialized.
Scarring an ulcer does not lead to a cure for peptic ulcer disease, since an exacerbation of the disease can occur at any time.

An acute ulcer is usually understood as a symptomatic, stress-induced ulcer with a characteristic morphology that is not prone to chronicity (Cushing's ulcer Cushing's ulcer - an ulcer of the stomach or duodenum, sometimes developing when the central nervous system is damaged, for example after a traumatic brain injury
, Curling's ulcer Curling's ulcer is an ulcer of the stomach or duodenum that occurs as a result of serious injury or extensive burn of these organs
).
Sometimes an acute gastric ulcer can be understood as a newly diagnosed gastric ulcer without taking into account its morphology. This approach does not seem entirely correct and is permissible only if it is impossible to reliably (visually, histologically, etiologically) determine or assume the morphology or etiology of the identified ulcer.

An acute gastric ulcer is distinguished from a chronic Helicobacter-associated ulcer, in addition to morphological features, by the fact that it is almost always possible to identify a provoking factor, with the exception of which ulcer healing and recovery occurs quite quickly.

Term peptic ulcer, used in foreign literature, allows for a fairly broad interpretation of the etiology of stomach ulcers, including stomach ulcers, for example, with Zollinger-Ellison syndrome, taking NSAIDs, etc., which domestic medicine traditionally classifies as symptomatic ulcers.

Bleeding from an acute gastric ulcer defined as at least one episode of coffee grounds or melena detected during gastric lavage or after an enema (regardless of whether the hematocrit decreased or not). It should be noted that the criteria used to define bleeding in published clinical studies vary widely (eg, positive stool guaiac test or presence of blood in nasogastric aspirate, hematemesis, melena, or need for blood transfusion). Thus, different authors use different criteria for diagnosing this condition.

Examples of diagnoses:
1. Acute calculous cholecystitis, cholecystectomy (date); acute stress multiple erosions and small acute ulcers of the antrum of the stomach, complicated by moderate bleeding.
2. Rheumatoid arthritis; three large acute drug-induced ulcers of the anterior wall of the stomach (taking NSAIDs Non-steroidal anti-inflammatory drugs (non-steroidal anti-inflammatory drugs/agents, NSAIDs, NSAIDs, NSAIDs, NSAIDs) are a group of drugs that have analgesic, antipyretic and anti-inflammatory effects that reduce pain, fever and inflammation.
- indomethacin).

Classification

Forrest classification:

Type F I- active bleeding:
-I a- pulsating jet;
- I b- flow.

Type F II- signs of recent bleeding:
- II a- visible (non-bleeding) vessel;
-II b- fixed thrombus clot;
- II s- flat black spot (black bottom of the ulcer).

Type F III- an ulcer with a clean (white) bottom.

Etiology and pathogenesis

General information

All symptomatic gastric ulcers are united by such a common feature as the formation of an ulcerative defect of the gastric mucosa in response to the influence of ulcerogenic factors (factors leading to the formation of ulcers).

1. Symptomatic stomach ulcers(usually stressful)

Stress gastric ulcers are one of the types of diseases of the mucous membrane of the gastrointestinal tract (GIT) associated with stress (the so-called stress-related mucosal disease, SRMD).

SRMD in the gastrointestinal tract manifests itself in two types of mucosal lesions:
- stress-related hypoxic injury, which manifests itself as diffuse superficial damage to the mucous membrane (non-bloody erosions, petechial hemorrhages into the mucosa);
- discrete stress ulcers, which are characterized by deep focal lesions, penetrating into the submucosa, most often in the fundus of the stomach.
Stress-induced mucosal lesions ultimately affect many areas of the upper gastrointestinal tract.

The occurrence of symptomatic ulcers has previously been associated with activation of the hypothalamic-pituitary-adrenal axis with a subsequent increase in the production of corticosteroid hormones. The action of the latter causes damage to the protective mucosal barrier, acute ischemia of the mucous membrane of the stomach and duodenum, increased tone of the vagus nerve, and disturbances of gastroduodenal motility.
Modern approaches to the pathophysiology of the process do not exclude this mechanism, but they appear to be multifactorial and are associated primarily with hypoxia of the gastrointestinal mucosa.

The main SRMD factors recognized today are:
- decreased blood flow;
- damage associated with ischemia, hypoperfusion and reperfusion.

Under normal conditions, the integrity of the gastric mucosa is maintained by several mechanisms, including normal microcirculation in the mucosa. Good microcirculation nourishes the mucous membrane, eliminates hydrogen ions, free radicals and other potentially toxic substances formed in the intestinal lumen. Secreted mucosal “traps” in the form of bicarbonate ions can neutralize hydrogen ions.
If the barrier formed by the mucous membrane is unable to block the harmful effects of hydrogen ions and oxygen radicals, mucosal damage develops. An increase in the synthesis of nitric oxide, apoptosis and the release of cytokines from damaged cells play a certain role. In addition, there is a slowdown in peristalsis in the upper gastrointestinal tract. Decreased rate of gastric emptying results in prolonged exposure of the mucosa to acid, thereby increasing the risk of ulceration.

An acceptable level of SaO 2 does not indicate adequacy of mucosal perfusion. Most often, in critically ill patients on mechanical ventilation, peripheral saturation does not suffer or suffers moderately, which does not indicate the absence of ischemia of the gastric and duodenal mucosa.

Cushing's ulcers originally described in patients with brain tumors or cerebral trauma, that is, in a group of patients with high intracranial pressure. These are usually single deep ulcers that are prone to perforation and bleeding. They are associated with a high debit of hydrochloric acid in the stomach and are usually located in the duodenum or stomach.
Extensive burns are associated with the so-called " Curling's ulcers".
The factors listed above for the occurrence of stress ulcers are especially relevant in children and elderly patients.

Currently, the list of potential threats to the development of stress acute peptic ulcers (diseases, conditions, conditions) has been expanded.
Main antecedent conditions:
- sepsis;
- multiple organ failure syndrome;
- isolated positive blood culture (even without any clinic);
- endoscopically or radiologically confirmed peptic ulcer of the stomach and duodenum within 6 weeks before admission to the ICU;
- organ transplantation;
- a history of bleeding from the gastrointestinal tract within 48 days before admission to the ICU ICU - intensive care unit
;
- coagulopathy Coagulopathy - dysfunction of the blood coagulation system
(including due to the use of heparin, warfarin, aspirin and other anticoagulants);
- artificial ventilation lasting more than 48 hours;
- surgery on the aorta for aneurysm;
- elderly age;
- taking systemic corticosteroids GCS (glucocorticoids, glucocorticosteroids) are drugs whose main properties are to inhibit the early stages of synthesis of the main participants in the formation of inflammatory processes (prostaglandins) in various tissues and organs.
IV or orally more than 40 mg/day. (according to some authors, more than 250 mg in hydrocortisone equivalent);
- acute myocardial infarction;
- condition after extensive neurosurgical operations;
- any type of acute failure (liver, kidney, pulmonary, cardiovascular).

2.Dieulafoy's ulcer
The theory about Dieulafoy's disease as one of the causes of acute gastric ulcers with bleeding is controversial. A possible cause is an unusually tortuous and dilated artery of the submucosal layer of the stomach. However, even a targeted study, as a rule, does not reveal signs of vasculitis Vasculitis (syn. angiitis) - inflammation of the walls of blood vessels
, atherosclerosis or formed aneurysm Aneurysm - expansion of the lumen of a blood vessel or heart cavity due to pathological changes in their walls or developmental abnormalities
. Neighboring veins and medium-sized vessels resemble the picture of arteriovenous anomalies - angiodysplasia.

The cause of ulcerative bleeding is mainly a purely local ulcerative necrotic process during an exacerbation of the disease with damage to the vessel. In some cases, atherosclerotic vascular lesions acquire independent significance as a cause of ulcerative bleeding. In this case, vascular changes such as productive endarteritis are detected, apparently secondary. Endarteritis is an inflammation of the inner lining of an artery, manifested by its growth and narrowing of the lumen of the arteries, thrombosis and disturbances in the blood supply to the corresponding organs or parts of the body.
, endophlebitis Endophlebitis - inflammation of the inner lining of a vein
, sometimes with vascular thrombosis. The development of bleeding is favored by concomitant vitamin deficiency (vitamins C and K).

3.Acute ulcers associated with non-steroidal anti-inflammatory drugs (NSAIDs).
Taking NSAIDs more often leads to the formation of chronic stomach ulcers. Many authors use the term “NSAID-associated gastropathy” in relation to such ulcers and other processes associated with taking NSAIDs. However, in some cases, against the background of severe intercurrent pathology, taking NSAIDs directly provokes the development of stress ulcers and aggravates bleeding from them.

The following are considered as etiopathogenetic factors in the development of NSAID gastropathy:
- local irritation of the gastric mucosa (GMU) and subsequent formation of ulcers;
- inhibition of the synthesis of prostaglandins (PGE2, PGI2) and their metabolites prostacyclin and thromboxane A2 in the coolant, which perform the function of cytoprotection;
- disturbance of blood flow in the mucous membrane due to previous damage to the vascular endothelium after taking NSAIDs.

The topical damaging effect of NSAIDs is manifested by the fact that some time after the administration of these drugs, an increase in the penetration of hydrogen and sodium ions into the mucous membrane is observed. NSAIDs suppress the production of prostaglandins not only in areas of inflammation, but also at the systemic level, so the development of gastropathy is a kind of programmed pharmacological effect of these drugs.

It has been suggested that NSAIDs may induce apoptosis through proinflammatory cytokines. Apoptosis is the programmed death of a cell using internal mechanisms.
epithelial cells. When using these drugs, the hydrophobic layer on the surface of the coolant is affected, the composition of phospholipids is depleted and the secretion of gastric mucus components is reduced.
In the mechanism of the ulcerogenic effect of NSAIDs, changes in lipid peroxidation play an important role. The resulting products of free radical oxidation cause damage to the coolant and destruction of mucopolysaccharides.
In addition, NSAIDs have a certain effect on the synthesis of leukotrienes, a decrease in the number of which leads to a decrease in the amount of mucus, which has cytoprotective properties. A decrease in the synthesis of prostaglandins leads to a decrease in the synthesis of mucus and bicarbonates, which are the main protective barrier of the coolant against aggressive factors of gastric juice.

When taking NSAIDs, the level of prostacyclin and nitric oxide decreases, which adversely affects blood circulation in the submucosal layer of the gastrointestinal tract and creates an additional risk of damage to the coolant and duodenum. Changing the balance of protective and aggressive gastric environments leads to the formation of ulcers and the development of complications: bleeding, perforation, penetration.

4. Other mechanisms and conditions of occurrence.
Acute gastric ulcer, complicated by bleeding, occurs in patients with hypergastrinemia, hypercalcemia (isolated cases).

Epidemiology

Age: except younger children

Sign of prevalence: Rare

Sex ratio(m/f): 2

According to statistics, stress ulcers are the most common (about 80%). 10-30% of patients have symptomatic ulcers due to cardiovascular disease. The most rare are symptomatic ulcers due to endocrine diseases (Zollinger-Ellison syndrome Zollinger-Ellison syndrome (syn. gastrinoma) - a combination of peptic ulcers of the stomach and duodenum with adenoma of the pancreatic islets, developing from acidophilic insulocytes (alpha cells)
- no more than 4 per 1 million population per year).

Stress stomach ulcers
Stress lesions of the gastric mucosa (not only ulcers, but also submucosal petechiae Petechia is a spot on the skin or mucous membrane with a diameter of 1-2 mm caused by capillary hemorrhage
and non-bleeding erosions) are detected endoscopically in 75-100% of patients in the ICU ICU - intensive care unit
, in the first 24 hours after admission. Only 6-10% of identified lesions of the gastric mucosa (up to 30% of ulcers) are accompanied by bleeding, which is defined as at least one episode of coffee grounds or melena obtained during gastric lavage or after an enema (regardless of whether the hematocrit decreased or not). Only 2-5% of patients with mucosal stress lesions have bleeding requiring transfusion.

Symptomatic drug ulcers:
1. It has been established that about 50% of ulcers associated with taking NSAIDs are complicated by bleeding.
2. About 80% of ulcer bleeding stops spontaneously and about 20% continues or recurs after stopping.
3. About 80% of recurrent bleeding occurs in the first 3-4 days.
4. Up to 10% of recurrent bleedings lead to death (0.5% in people under 60 years of age, 20% in people over 80 years of age).

Symptomatic ulcers in other diseases
Frequency of development of hepatogenic gastropathy Gastropathy is the general name for stomach diseases.
with liver cirrhosis it is 50-60%, gastroduodenal ulcers - from 5.5 to 24%. This is 2.6 times higher than the prevalence of gastric and duodenal ulcers among the rest of the population.

Dieulafoy's disease is a relatively rare cause of upper gastrointestinal bleeding.

Ulcerations, as a source of massive gastrointestinal hemorrhages (bleeding), are observed in 0.3-5.8% of cases.
Bleeding recurs in 18-100% of patients - this is a hallmark of the disease. Severe bleeding is observed in more than a third of patients.

Risk factors and groups

I. For stress stomach ulcers and for stress-induced damage to the mucous membrane of the gastrointestinal tract (GIT), the following risk factors were formulated (according to the ASHP Commission on Therapeutics and approved by the ASHP Board of Directors, 1998, with additions and changes from 2012)

1. Independent risk factors:
- coagulopathy (including drug-induced) with the following indicators: platelet count<50 000 мм 3 , INR (INR International normalized ratio (INR) is a laboratory indicator determined to assess the extrinsic pathway of blood coagulation
) > 1.5 or PTT (partial thromboplastin time) > 2 normal values;
- respiratory failure: mechanical ventilation (MV) ≥ 48 hours.

2. Other risk factors:
- spinal cord damage;
- multiple injuries: injury to more than one area of ​​the body;
- liver failure: total bilirubin level > 5 mg/dL, AST > 150 U/L (or more than 3 times the upper limit of normal values) or ALT> 150 U/L (or more than 3 times the normal values along the upper border);

Thermal burns > 35% body surface area;
- partial resection Resection is a surgical operation to remove part of an organ or anatomical formation, usually with the joining of its preserved parts.
liver;
- traumatic brain injury with coma and a Glasgow scale score ≤10 or with the inability to follow simple commands;
- liver or kidney transplantation;
- history of gastric ulcer or bleeding within a year before admission to the ICU ICU - intensive care unit
;
- sepsis or septic shock, with hemodynamic support with vasopressors and/or positive blood culture or clinically suspected infection;
- stay in the ICU ICU - intensive care unit
more than 1 week;
- hidden or obvious bleeding lasting more than 6 days;
- therapy with corticosteroids, regardless of the route of administration.

Note. Some researchers from the USA indicate renal failure (serum creatinine level more than 4 mg/dL) among other risk factors.

II. Ulcers associated with NSAID use
According to the recommendations of the American College of Gastroenterology (2009) for the prevention of complications of gastropathy induced by NSAIDs, all patients can be divided into the following groups according to the degree of risk of toxic effects of NSAIDs on the digestive tract:

1. High risk:
- there is a history of a complicated ulcer, especially a recent one;
- multiple (more than 2) risk factors.

2. Moderate risk (1-2 risk factors):
- age over 65 years;
- high dose of NSAIDs;
- there is a history of an uncomplicated ulcer;
- simultaneous use of acetylsalicylic acid (including in low doses), corticosteroids or anticoagulants.

3. Low risk: no risk factors.

Taking NSAIDs increases the risk of bleeding by 2.74 times; at the age of more than 50 years - 5.57 times; with previous episodes of bleeding or while taking glucocorticoids - 4.76 times; when combining NSAIDs with anticoagulants - 12.7 times.

Clinical picture

Clinical diagnostic criteria

Hematemesis, melena, epigastric pain, tachycardia, weakness, dizziness, arterial hypotension, orthostatic collapse

Symptoms, course

Patients with acute gastrointestinal bleeding exhibit hematemesis Hematemesis - vomiting of blood or blood mixed with vomit; occurs when there is gastric bleeding.
, melena Melena - discharge of feces in the form of a sticky black mass; usually a sign of gastrointestinal bleeding.
, as well as additionally symptoms and signs of hypovolemia of varying degrees.

Signs of hypovolemia Hypovolemia (syn. oligemia) is a reduced total amount of blood.
:
- decrease in blood pressure (systolic or average) by more than 20 mmHg. Art., lying down, or more than 10 mm Hg. Art., sitting;
- increased heart rate by more than 20/min;
- decrease in hemoglobin by more than 20 g/l.

Coffee grounds, melena Melena - discharge of feces in the form of a sticky black mass; usually a sign of gastrointestinal bleeding.
, an admixture of blood in the aspirate from the stomach through a probe, positive tests for blood in the stool confirm the fact of bleeding from the upper gastrointestinal tract (GIT).

Hematemesis manifests itself in the form of vomiting of blood, either vomiting in an unchanged form, or vomiting in the form of a dark brown granular substance (“coffee grounds”) - formed as a result of prolonged presence of blood in the stomach and the conversion of hemoglobin into methemoglobin by hydrochloric acid.

Melena(the appearance of altered blood in the rectum) is recognized by black, loose stools, sometimes with a red tint (when the blood is fresh and has a characteristic pungent odor). This is due to heme oxidation by intestinal and bacterial enzymes and indicates that the source of bleeding is likely to be in the upper gastrointestinal tract and definitely proximal to the ileocecal Ileocecal - relating to the area where the ileum and cecum join.
anastomosis. It should be kept in mind that melena Melena - discharge of feces in the form of a sticky black mass; usually a sign of gastrointestinal bleeding.
may continue for several days after active bleeding has stopped. This fact can confuse doctors. In addition, it is necessary to distinguish melena from the results of ingestion of iron supplements, which cause the appearance of sticky, but relatively hard, gray-black stool.
With increased gastrointestinal motility (for example, stimulation with proserin) and a decrease in the acid-forming function of the stomach, melena Melena - discharge of feces in the form of a sticky black mass; usually a sign of gastrointestinal bleeding.
may contain an admixture of fresh, unchanged blood, which can also cause a diagnostic error.

Rectal bleeding of unchanged blood directly suggests that the source of bleeding is the colon, rectum or anus. However, it should be remembered that heavy bleeding from the upper gastrointestinal tract can manifest itself in the same way. Therefore, in a patient with massive rectal bleeding with unchanged blood, especially if there are signs of hypovolemia Hypovolemia (syn. oligemia) is a reduced total amount of blood.
, bleeding from the stomach or duodenum should be excluded.
If patients have previously undergone aortic surgery with a graft, the possibility of aortoenteric fistula should be considered with consultation with a vascular surgeon.

Diagnostics

Pre-insertion of a nasogastric tube to evacuate blood clots and improve the accuracy of endoscopy has not been universally accepted.

The main method is endoscopy (FGDS), which should be completed as early as possible (on the first day after admission). The endoscopic examination is performed under benzodiazepine sedation, but if the patient vomits a large amount of blood, then general anesthesia with endotracheal intubation with a cuffed tube may be used.

Endoscopic examination should begin with the patient positioned strictly on the left side, as this ensures the accumulation of blood in the area of ​​the fundus of the stomach, where ulcers rarely occur. If it is necessary to examine the fundus of the stomach, then the patient is turned over on his right side and the head end of the gurney is raised so that the blood moves to the antrum. Once the endoscope has passed through the esophagogastric junction, a seemingly obstructive collection of blood and clots is usually not detected. As long as the stomach is able to distend, a moderate amount of blood will rarely interfere with adequate visualization of the source of bleeding. Most likely, a clot covering the ulcer will be visible. It is important to try to wash it off to determine how tightly it is held in place - this affects prognosis and treatment, and careful washing rarely speeds up bleeding.

If there is too much blood in the stomach for an adequate examination, it is necessary lavage. The 40 Fr lavage tube is ideally inserted into the stomach, where suction is performed directly. This way, enough blood and clots are usually removed to allow inspection. If this does not help, then lavage Lavage - washing a body cavity (for example, the colon or stomach) with water or a medicinal solution
carried out with the introduction of a liter of water through the canal. Thanks to this, the clots will be broken up and can then be easily removed through a tube installed in the appropriate position.

FGDS FGDS - fibrogastroduodenoscopy (instrumental examination of the esophagus, stomach and duodenum using a fiber-optic endoscope)
should be performed urgently in all patients at risk who have bleeding from the upper gastrointestinal tract, an unexplained drop in hemoglobin (hematocrit in children) or positive tests for occult blood in the stool.

Laboratory diagnostics

Blood tests: hemoglobin, hematocrit, red blood cell count, platelet count, clotting time, coagulogram, blood group and Rh factor, acid-base balance ABC - acid-base state - balance of acids and bases, i.e. the ratio of hydrogen and hydroxyl ions in the biological media of the body (blood, intercellular and cerebrospinal fluids, etc.)
.

Stool analysis: determination of occult blood.

Differential Diagnosis

It should be differentiated from bleeding from other parts of the gastrointestinal tract (esophagus, duodenum, small intestine); with gastric bleeding of another etiology (acute erosive gastritis, varicose veins, vascular malformation, polyp, carcinoma, leiomyoma, lymphoma, etc.).

Complications

Possible complications:
- shock;
- anemia;
- consumption coagulopathy;
- recurrent bleeding.

According to modern concepts, the risk of recurrent bleeding and/or death is associated with the following endoscopic signs:
- detection of an exposed vessel at the bottom of the ulcer (risk 90%);
- exposed vessel at the bottom of the ulcer without visible bleeding (50% risk);
- a large unformed “red” thrombus that covers the defect and does not close when the ulcer is irrigated with isotonic sodium chloride solution (risk 25%).

According to the International Clinical Practice Guidelines for the Management of Patients with Nonvariceal Upper Gastrointestinal Bleeding (consensus meeting held in June 2002 under the auspices of the Canadian Association of Gastroenterologists), the risk of recurrent bleeding can be determined using the table below.

Statistically significant predictors of recurrent bleeding

Risk factors	Indicators of increased risk
Clinical factors
Age > 65 years	1,3
Age > 70 years	2,3
Shock (syst. BP< 100 мм рт.ст.)	1,2-3,65
General Status (ASA*)	1,94-7,63
Accompanying illnesses	1,6-7,63
Unstable level of consciousness	3,21 (1,53-6,74)
Continued bleeding	3,14 (2,4-4,12)
Previous blood transfusion	Indefined
Laboratory factors
Hemoglobin< 100 г/л или hematocrit< 0,3	0,8-2,99
Coagulopathy (prolonged aPTT)	1,96 (1,46-2,64)
Signs of bleeding
Melena	1,6 (1,1-2,4)
Scarlet blood on rectal examination	3,76 (2,26-6,26)
Blood in the stomach or tube	1,1-11,5
Hematemesis	1,2-5,7
Endoscopic factors
Active bleeding during endoscopy	2,5-6,48
Signs of high risk	1,91-4,81
Clot at the bottom of the ulcer	1,72-1,9
Ulcer size > 2 cm	2,29-3,54
Presence of peptic ulcer	2,7 (1,2-4,9)
Ulcer localization
Lesser curvature of the stomach	2,79
Top wall	13,9
Back wall	9,2

* ASA - American Society of Anesthesiologists

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Stomach ulcer(GD) is a multifactorial chronic disease accompanied by the formation of ulcers in the stomach with possible progression and development of complications.

Acute ulcer is a deep defect of the mucous membrane, which penetrates to the muscular plate of the mucous membrane and deeper. Acute ulcers are often solitary; have a round or oval shape; in cross-section they look like a pyramid. The size of acute ulcers ranges from several mm to several cm. They are localized on the lesser curvature. The bottom of the ulcer is covered with fibrinous plaque, it has smooth edges, does not rise above the surrounding mucous membrane and does not differ from it in color. Often the bottom of the ulcer has a dirty gray or black color due to the admixture of hematin hydrochloride.
Microscopically: mild or moderate inflammatory process at the edges of the ulcer; after rejection of necrotic masses at the bottom of the ulcer - thrombosed or gaping vessels. When an acute ulcer heals within 7-14 days, a scar forms (incomplete regeneration). In rare cases, an unfavorable outcome may lead to a chronic ulcer.

Perforation of the ulcer represents the occurrence of a through defect in the wall of the stomach at the location of the ulcer.

In the case of a combination of such severe complications, the clinical picture of a perforated ulcer is atypical. In particular, peritoneal symptoms and pain are less pronounced, and there may be no sharp tension in the abdominal muscles. This is especially noticeable when perforation of the ulcer occurs against the background of ongoing profuse Profuse - copious, strong (bleeding, diarrhea).
bleeding in a weakened, bleeding patient. Perforated ulcers in such patients are often diagnosed late, as a result of which the risk of surgery significantly increases and postoperative mortality increases several times (20-25% higher than with a perforated or only bleeding ulcer).
A rare case of a combination of bleeding and perforation is the perforation of an ulcer of the anterior wall of an organ and bleeding from a second ulcer located on the posterior wall (“kissing” ulcers) and penetrating into the underlying tissues and organs. Recognizing such a source of bleeding is difficult.

Period of occurrence

Minimum period of occurrence (days): 1

Maximum period of occurrence (days): not specified

Classification

There is no clear classification of gastric ulcers with bleeding and perforation. In this regard, it is advisable to use a classification of the predominant symptoms or morphological signs.

Bleeding
Classification Forrest(1974) plays an important role in assessing the risk of recurrent bleeding and death of the patient. Based on the endoscopic picture, it is possible to determine the volume of endoscopic manipulations to achieve hemostasis Hemostasis - 1) in surgery - stopping bleeding; 2) in pathology (syn. blood stasis) - stopping blood flow in the vessels of an organ or tissue.
or determine indications for surgery.

- F1A- jet bleeding from an ulcer;

- F1B- drip bleeding from the ulcer;

-FIIA- thrombosed vessels at the bottom of the ulcer;

-FIIВ- a blood clot covering the ulcer;

- FIIC- an ulcer without signs of bleeding or inclusion of hydrochloric acid hematin at the bottom of the ulcer;

- FIII- sources of bleeding are not detected or the ulcer has no signs of bleeding.

In terms of diagnosis and the significance of relapse prognosis, type IIA (visible vessel) causes the most debate. A visible vessel at the bottom of the ulcer may be represented by a “clock” thrombus or a “pearl” tubercle.

"Clock" thrombus is a thrombus that occludes a defect in an eroded vessel, and looks like a red or black bump protruding above the yellow bottom of the ulcer. In some cases, around the “clock” thrombus, part of the preserved vessel wall in the form of a pearl rim may be visible.

"Pearl" tubercle is an eroded vessel, the defect in the wall of which is closed due to its spasm, and not by a thrombus. The tubercle has a pearly-whitish color and rises above the bottom of the ulcer.

A number of researchers recommend indicating the presence or absence of a visible vessel in the protocol with the signs " v+" And" v-". Thus, the presence of a “pearl” tubercle or a “clock” thrombus with a pearl rim will be interpreted as a type FIIA v+(the risk of recurrent bleeding in this case is especially high). Type FIIA v- diagnosed in the presence of a “hourly” blood clot without a pearl rim.

A comparative study of the endoscopic picture and morphological studies has established that if EGDS reveals a pearl-colored tubercle or a red tubercle with a pearly rim (type FIIA v+) at the bottom of the ulcer, then during a morphological study the vascular wall protrudes above the bottom of the ulcer and more severe damage to the vascular wall is present, than in cases where EGD reveals a “hourly” thrombus without a pearly rim (type FIIA v-) (Chen et al., 1997).

In research by J.W. Law et al. (1998) showed that in most patients the eroded vessel is covered with a fixed thrombus-clot.

The risk of recurrent bleeding is considered low with an endoscopic appearance consistent with type FIIC (flat black spot).

During morphological examination, 20% of patients with a clean (white) bottom (type FIII) are found to have an eroded vessel at the bottom of the ulcer. Apparently, the white color of the vessel is not visible during endoscopic examination due to masking by fibrin. In this situation, the clinical picture and laboratory data are of particular importance for the endoscopist, since certain limitations of conventional visual assessment create the preconditions for erroneously determining the risk of recurrent bleeding as minimal. The use of a video endoscope and Doppler examination increases the possibility of detecting a vessel at the bottom of the ulcer.

The question of further management of the patient is decided after a visual assessment of the source of bleeding.

Perforation

According to the clinical course:

The typical form is the leakage of contents into the free abdominal cavity;

Atypical form - the defect is covered by the omentum or adjacent organ.

Etiology and pathogenesis

Etiology: acute gastric ulcer.
Pathogenesis is the erosion of all layers of the stomach wall by gastric juice in combination with an increase in intragastric pressure and processes leading to erosive bleeding from the ulcer.

Epidemiology

Age: Mostly older

Sign of prevalence: Extremely rare

Sex ratio(m/f): 5

It is extremely rare.

Clinical picture

Clinical diagnostic criteria

Sharp abdominal pain, abdominal muscle tension, nausea, hematemesis, vomiting coffee grounds, melena, pallor, tachycardia, dizziness

Symptoms, course

1. Pain syndrome - extremely intense, “dagger” pain in the epigastric region, which occurs suddenly, without “precursors” (sometimes after eating). The pain is initially localized in the pit of the stomach or in the right upper quadrant, but quickly becomes diffuse.
When pain occurs, the patient tries to move as little as possible and strives to take a comfortable body position, in which the pain is felt somewhat weaker.
Tension of the abdominal muscles quickly increases and moves from localized in the upper right quadrant to diffuse, and then the stomach becomes hard as a board. The respiratory movements of the abdominal muscles become superficial, weaken and gradually stop.

When diagnosing, the disappearance of hepatic dullness upon percussion is important. When the patient turns on his right side, he experiences pain in his left shoulder, and when he turns on his left, he experiences pain in his right shoulder.
The patient's condition quickly deteriorates and after 6-8 hours he develops signs of diffuse peritonitis Peritonitis is inflammation of the peritoneum.
, often - pneumoperitoneum Pneumoperitoneum - 1. The presence of gas in the peritoneal cavity. 2. Filling of the retroperitoneal space with gas
(disappearance of hepatic dullness during percussion, visualization of gas under the diaphragm during plain fluoroscopy). The patient also experiences increasing vascular collapse, dry tongue and fever.
A blood test reveals neutrophilic leukocytosis with a shift to the left and accelerated ESR.
Mortality from diffuse fibrinous-purulent peritonitis remains significant.

A limited, covered perforation, which occurs with the development of limited peritonitis, is characterized by less pronounced symptoms:
- gradual extinction of the inflammatory process;
- slight local pain;
- leukocytosis;
- low-grade fever;
- mild symptoms of peritoneal irritation.
However, even with such a course, there is always a risk of developing acute peritonitis and the formation of an abscess in the abdominal cavity, liver, and under the diaphragm.

2. Penetration Penetration is a complication of peptic ulcer in the form of spread of an infiltrative-destructive process (penetration with destruction) from the stomach or duodenum into the thickness of a neighboring organ - liver, pancreas, omentum
is a consequence of progressive destruction of the wall of the stomach or duodenum. It is accompanied by the formation of an adhesive process, which fixes the bottom of the ulcer to the adjacent organ, preventing the ulcer from breaking into the free abdominal cavity. Upon penetration, an inflammatory infiltrate, adhesions, and sometimes a delimited abscess develop.
Penetrating ulcers of the duodenum rather than the stomach are more common. The pancreas is most often penetrated, followed by the hepatoduodenal ligament, liver, lesser omentum, gall bladder and bile ducts, transverse colon, etc.

When diagnosing penetration, the following factors should be kept in mind:(Radbil O.S.):
1. Penetrations most often occur in obviously ulcerative patients with an old, sluggish process, in middle and elderly age groups.
2. Penetration is characterized by an exacerbation of pain sensations that become permanent; often this exacerbation is repeated at short intervals of time ("stepped" penetrations), and vomiting is often associated with the pain.
3. Penetration is characterized by local (symptoms of peritoneal irritation, inflammatory infiltrate) and general changes (inflammatory changes in the blood - leukocytosis, shift of the leukocyte formula to the left, increased ESR).
4. During penetration, symptoms develop that characterize the damage to the organ in which it occurs.
When an ulcer penetrates into the pancreas, the level of serum amylase and lipase increases markedly after stimulation of the pancreas with secretin. It should be borne in mind that an increase in enzyme activity is also possible with concomitant pancreatitis without penetration.

In case of penetration of ulcers into the bile ducts and gallbladder, internal fistulas appear, which cause severe cholangitis Cholangitis is inflammation of the bile ducts.
, and sometimes malignancy Malignization is the acquisition by cells of normal or pathologically altered tissue (for example, a benign tumor) of the properties of malignant tumor cells.
penetrated organ.
X-ray examination often reveals an infiltrative shaft and disturbances of peristalsis in the “niche” area.

Penetration may be combined with gastric bleeding.

3. Bleeding.
A patient with a peptic ulcer may experience two types of bleeding:
- sudden massive bleeding(is a sign of a new exacerbation);
- slight bleeding(most often occurs due to the use of excess amounts of contraindicated medications).

A small ulcer may bleed daily, causing the patient to lose blood in the stool (not black in color). In this case, the only manifestation of the condition may be unmotivated fatigue.

With massive ulcerative bleeding, a characteristic clinical picture is observed: black loose stools, nausea, chills, and sometimes fainting occurs during or after defecation.
Black stools are more often observed in patients with duodenal ulcers. In patients with stomach ulcers, bloody vomiting or vomiting of “coffee grounds” predominates.
Ulcerative bleeding can be either the first or an early sign of the disease. In some cases, the first sign is hypochromic, microcytic anemia.
If a patient loses more than 350 ml of blood, his blood volume noticeably decreases and the following symptoms occur: compensatory reactions:
- vascular spasm, manifested by pallor;
- progressive drop in blood pressure;
- decrease in the amount of circulating blood;
- electrocardiographic study records myocardial hypoxia.
With massive bleeding, patients develop low-grade fever and pain stops (possible anti-inflammatory effect of blood loss).

4. When combinations of perforation and bleeding from an ulcer One of these complications is most often not identified. This is due to the fact that in a patient weakened by bleeding, perforation of the ulcer proceeds atypically. When bleeding appears against the background of a strongly expressed clinical picture of perforation, it can also go unnoticed.

In some cases, against the background of profuse gastroduodenal bleeding in the epigastric region, the patient experiences a sharp “dagger” pain typical of perforation of an ulcer; Tension of the muscles of the anterior abdominal wall (“board-shaped abdomen”), lack of peristalsis, and pain on palpation of the abdomen are observed. These symptoms are not observed with gastroduodenal bleeding without simultaneous perforation.
Gastroduodenal bleeding, as a rule, is painless (pain that occurs before bleeding disappears).

The second place among gastrointestinal diseases in terms of frequency of diagnosis is gastric ulcer. Bleeding during this is a common complication. It arises due to non-compliance with diet or the use of incorrect therapy. Bleeding can be fatal, so the patient requires urgent medical attention. The complication is eliminated mainly by surgery.

A stomach ulcer is a defect in the mucous membrane of the organ, which is formed due to the aggressive effects of hydrochloric acid.

The disease is chronic and recurrent; as the ulcer heals, a scar forms on the surface of the mucosa.

According to statistics, bleeding from a stomach ulcer occurs in 10-15% of patients. It happens when a vessel bursts in the area of ​​damage to the mucous membrane. There are open and hidden bleeding. When hidden, there are no external manifestations. The complication can only be detected using the Gregersen reaction (stomach juice, urine or feces are treated with special reagents to detect traces of blood).

Open bleeding from a stomach ulcer manifests itself with the following symptoms:

• Vomiting containing blood. Vomit may be brown due to the blood being stained with hydrochloric acid. With massive bleeding, scarlet blood is released.
• The stool is tarry in consistency and dark in color.
• Signs of blood loss.

Depending on the degree of blood loss, there are 3 types of bleeding:

1. Minor blood loss (up to 10%). It manifests itself as mild symptoms: weakness, dry mouth, slight nausea and dizziness, a slight decrease in blood pressure.
2. Average blood loss (up to 20%). The patient develops stage 1 hemorrhagic shock, while the patient is conscious. The main symptoms of moderate bleeding with a stomach ulcer:

• nausea, dizziness;
• trembling of limbs;
• pale skin;
• increased heart rate up to 100 beats per minute;
• slight decrease in pressure.

Massive blood loss (more than 25%). Characterized by the development of decompensated hemorrhagic shock. Massive bleeding with a stomach ulcer manifests itself:

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Anna Poniaeva. She graduated from the Nizhny Novgorod Medical Academy (2007-2014) and Residency in Clinical Laboratory Diagnostics (2014-2016).

• tachycardia, shortness of breath;
• severe pallor of the skin and dry mucous membranes;
• thread-like pulse (up to 140 beats per minute);
• a sharp drop in blood pressure (below 90/50);
• loss of consciousness.

Causes

Ulcer bleeding opens for the following reasons:

• Infection. Viruses spread through an open stomach ulcer, affecting blood vessels.
• Injury to the surface of the ulcer during medical procedures (during FGDS).
• Strong physical activity. The pressure in the vessels increases, they burst, and ulcerative bleeding opens. It can be minor or severe if a large vessel is damaged.
• Poor diet, alcohol consumption. Spicy, fatty foods and alcohol irritate the already damaged mucous membrane. After eating, bloody vomiting may occur.
• Use of medications. Some medications are prohibited for use for ulcers because they irritate the mucous membrane. After taking such drugs, an exacerbation occurs, the open ulcer begins to bleed.