What are the possible complications of gastric ulcer? Complications of gastric ulcer

During a peptic ulcer, complications may arise, the occurrence of which affects the symptoms of the disease, treatment tactics and the content of the treatment. The most common and typical complications of gastroduodenal ulcers are perforation of the ulcer and bleeding from the ulcer.

Perforation of gastric and duodenal ulcers.

In the structure of acute surgical diseases of the abdominal organs in the adult population, perforated gastric and duodenal ulcers account for 1.6-3.4%, and in relation to army and navy personnel this figure is 4.5-5.5%. In patients with peptic ulcers, perforation occurs in 5-15%, and in men it is 20 or more times more likely than in women.

Etiology

All the reasons that determine the occurrence of an ulcer and the activation of destructive processes during its chronic course ultimately contribute to the development of perforation, the immediate occurrence of which is often associated with physical stress, gastric overfilling due to heavy food, acute alcohol intoxication, and blunt trauma to the abdomen.

Pathogenesis

There is still no clear pathogenetic basis for the mechanisms of ulcer perforation.

Perforation of an ulcer is a special kind of process that, as a result of the influence of a number of factors, usually in conditions of exacerbation of peptic ulcer disease, causes the appearance of foci of destruction in the area of ​​the wall or bottom of the ulcer. The assumption of simultaneous destruction is confirmed by the nature of the morphological changes in the area of ​​the perforated ulcer (the perforation hole has the shape of a regular circle, resembling a defect knocked out with a punch), as well as by the fact that with the slow development of the process, as a rule, biological protective factors aimed at preventing development of peritonitis (fusion with neighboring organs, omentum), which do not work during perforation.

The further course of the complication is determined by the developing peritonitis, which at the beginning is aseptic (chemical) serous, and then turns into purulent. Depending on the location of the ulcer, the size of the defect and the conditions of perforation, diffuse or limited purulent peritonitis subsequently develops and in most cases, without urgent surgical intervention, the patient is doomed to death. With perforation into the retroperitoneal tissue, which is very rare, there may be no peritonitis, but retroperitoneal phlegmon develops.

If perforation occurs during empty stomach or a perforated hole of insignificant size, it can be independently closed by adjacent organs (the greater omentum, the lower surface of the liver, the gallbladder, etc.) or dense food particles, which helps to limit the inflammatory process and the formation of limited peritonitis, often in the form of an inflammatory infiltrate. If the perforation is located in the duodenum or distal stomach, and the contents pouring out of the lumen flow down the right lateral canal of the peritoneum into the ileocecal region with the subsequent development of limited or diffuse peritonitis in the right iliac region, then in some cases difficulties arise in differential diagnosis with acute appendicitis.

Pathological anatomy

Chronic ulcers of the stomach and 12 intestines, which are in the phase of exacerbation of the inflammatory process, perforate more often. Histological sections of small soft perforated ulcers show young granulation tissue with sequestration of areas of necrosis and an almost unchanged muscle layer, which ensures rapid healing of such ulcers after suturing. Perforation of an ulcer most often occurs when it is localized in the pyloroduodenal zone, especially on the anterior wall of the 12th intestine. In the stomach, ulcers of the lesser curvature often perforate, and much less often - in the cardiac region. The diameter of the perforation hole in most cases does not exceed 5 mm.

Classification

There are 3 types of perforations: open, covered and atypical. Open perforation is understood as one in which gastric or duodenal contents flow freely through the perforation into the free abdominal cavity. Covered perforation is indicated in cases where the perforation hole is immediately or shortly after its formation covered by a neighboring organ or food particles. With atypical perforation, the ulcer is usually localized on back wall stomach or duodenum and the duodenal (gastric) contents released during perforation enter the retroperitoneal tissue, the cavity of the lesser omentum, and the thickness of the ligamentous apparatus of the stomach (depending on the location of the ulcer).

Clinic

The clinical picture of perforation is very dynamic. It is customary to distinguish between the phase of shock, apparent remission (“imaginary well-being”) and peritonitis.

Perforation of a stomach ulcer (12-gut) occurs suddenly, often against the background of exacerbation of ulcer, because upon careful study of the anamnesis, more than 90% of patients note discomfort or pain in the epigastric region, often combined with heartburn, nausea, and vomiting during the last 4 to 5 days before perforation. Therefore, every exacerbation during a gastric or 12-gut ulcer should be regarded as a condition dangerous for the occurrence of perforation. Perforation so-called “silent ulcers” occur only in 8–10% of cases, and a retrospective analysis of them shows that more than 60% of these ulcers are chronic.

At the moment of perforation, a sharp, “dagger” pain occurs in the epigastric region, which can be so intense that a shock-like state develops, often with loss of consciousness, as a result of which the patient loses the ability to perform any activity. Pain sensations are localized first in the upper half of the abdomen, and then spread throughout the entire abdomen, sometimes moving to the right iliac region. Nausea and vomiting are not specific to perforated ulcers and do not occur consistently. Pallor of the visible mucous membranes and skin is often clearly manifested, and bradycardia is noted, which is apparently caused by irritation of the endings of the vagus nerves due to the influence of gastrointestinal contents and the reaction of the peritoneum.

When examining the patient, attention is drawn to the scaphoid abdomen, retracted in the upper half, sharp tension of the anterior abdominal wall (“board-shaped” abdomen), sometimes with a distinct relief of the intermuscular tendon bridges of the rectus muscles. Palpation of the abdomen causes sharp pain. Severe symptoms of peritoneal irritation. A pathognomonic sign of perforation of a hollow abdominal organ is the appearance of gas in the abdominal cavity, as a result of which the disappearance of hepatic dullness is often noted, which is caused by the accumulation of gas that has penetrated into the free abdominal cavity above the liver. Upon percussion in this area, tympanitis can be detected. The accumulation of a significant amount of fluid poured out from the perforation in sloping areas of the abdominal cavity causes a shortening of the percussion sound over these zones.

The pain shock phase lasts about 3–6 hours, after which the pain may decrease somewhat and a period of “imaginary well-being” or apparent remission begins. This period lasts from 4 to 6 hours, and sometimes more, and is dangerous because it can give the doctor examining the patient for the first time the impression that there is no acute surgical disease of the abdominal organs and entail a loss of time for surgical treatment in optimal timing, which significantly complicates the prognosis.

After a phase of apparent remission, as a rule, signs of developing purulent peritonitis appear and the patient’s condition progressively worsens.

The clinical picture of covered perforation has significant features that make it difficult to recognize this type of complication. A characteristic feature of covered perforation is the “break” of the pain syndrome – a sudden or rapid subsidence of pain. Covered perforation may end on its own, but most often purulent peritonitis develops or an abdominal abscess forms.

Atypical perforation is rare and occurs mainly when the ulcer is located on the extraperitoneal parts of the stomach wall (12-gut) - the cardial section of the stomach, the posterior wall of the stomach and the 12-gut. The moment of perforation in these cases is not very clearly expressed. Front tension is often absent abdominal wall and only slight rigidity of her muscles is determined.

Diagnostics

Diagnosis of perforated ulcers of the stomach and 12 intestines is based on clinical and anamnestic data, of which the following are of leading importance:

a history of ulcer, especially signs of its exacerbation in the previous days (but the absence of anamnestic data does not exclude the presence of a perforated ulcer);

sudden appearance of intense (“dagger-like”) pain in the upper abdomen or its right half: radiating to the right shoulder girdle;

immobility and sharp tension of the anterior abdominal wall (“board-shaped” inverted abdomen with a clearly visible relief of the rectus muscles);

positive symptoms of peritoneal irritation (from Shchetkin - Blumberg, from A.P. Krymov - pain when examining the navel or external opening of the inguinal canal with a fingertip, pain in the area of ​​the pouch of Douglas during digital examination of the rectum, etc.);

disappearance of hepatic dullness upon percussion of the anterior abdominal wall or in a position on the left side; zone of high tympanitis between xiphoid process and navel (sign of I.K. Spizharny);

retention of stool and gases.

In addition to the symptoms listed above, other signs are also of cumulative importance in the diagnosis of a perforated ulcer: strong, unquenchable thirst, dryness of the mucous membranes of the lips and oral cavity; shallow, intermittent and rapid breathing; forced, often motionless position of the patient on his back or side with his legs tucked to his stomach; location of the zone of audible heart sounds on the anterior abdominal wall to the level of the navel (Guiston), friction noise of the diaphragm under the costal arch (Brunner, etc.). At the same time, some patients may not have such a cardinal sign of a perforated ulcer as tension in the abdominal wall. This symptom may be absent or mild in exhausted or long-term starved patients, as was observed in blockaded Leningrad during the Second World War (E.S. Drachinskaya). This sm may also be absent in elderly patients with a very flabby abdominal wall and is very difficult to detect in very obese patients.

Changes in laboratory tests of blood and urine in perforated ulcers are nonspecific, but these data are necessary for differential diagnosis. On plain radiography of the abdominal cavity, a characteristic sign of perforation of a hollow organ is pneumoperitonium. To detect it, laterography is often preferred with the patient lying on his left side after a 15-minute stay in this position, when the gas has time to move to the highest parts of the abdominal cavity. If the possibility of a perforated ulcer is suspected and there are no signs of free gas in the abdominal cavity, pneumogastrography is used: a thick gastric tube is inserted into the stomach and after the maximum possible aspiration of gastric contents, up to 1000–1500 ml of air is introduced, and then radiography is performed. In the case of a perforated ulcer, pneumoperitoneum is detected. Contraindications to pneumogastrography are narrowing of the esophagus and cardia of the stomach, which prevent the passage of the probe, and the general serious condition of the patient.

In doubtful cases, the introduction of water-soluble X-ray contrast agents into the stomach and subsequent X-ray monitoring of their possible leakage through the perforation can help in diagnosis, which can also provide information about the localization of the ulcer. The use of barium suspension for this purpose is inappropriate, because its penetration into the free abdominal cavity causes the formation of dense, long-term non-absorbable infiltrates and conglomerates.

Of the instrumental research methods, the most information for diagnosing a perforated ulcer, especially with covered perforation of a gastric ulcer, 12-gut ulcer, can be obtained by fibrogastroscopy in combination with dynamic tonometry of the stomach. It has been established that the maximum intragastric pressure during endoscopy is 26 +/- 2 cm of water column, and with a cough or straining it almost doubles. With perforation of a gastric and 12-gut ulcer, intragastric pressure does not exceed 6–8 cm of water column and when coughing it only briefly reaches 10–12 cm of water column. Before and after endoscopy, a plain radiography of the abdominal cavity should be performed, and the appearance of pneumoperitoneum after FGDS is an absolute sign of perioration, because detection of a perforation during endoscopic examination is often unsuccessful.

In cases where, using non-invasive methods, it is not possible to reject the suspicion of the possibility of perforation of a gastroduodenal ulcer, the use of diagnostic laparocentesis and laparoscopy is justified. The release of gas from the abdominal cavity at the time of its opening indicates the presence of perforation. The nature of peritoneal exudate is of great diagnostic importance. In order to detect starch impurities in the exudate, which is typical for gastric contents, an iodine test is used: 2–3 drops of iodine solution are applied to a swab moistened with peritoneal exudate. Coloring the tampon dark blue indicates the presence of gastric contents in the exudate, and therefore the existence of perforation. Laparoscopy can detect signs of developing peritonitis, and sometimes a perforation.

Differential diagnosis

A perforated ulcer of the stomach and duodenum must be differentiated from all acute surgical diseases of the abdominal organs, acute myocardial infarction, lower lobe pneumonia, pleurisy, food intoxication, and acute gastritis. In the differential diagnosis of a perforated ulcer with acute myocardial infarction, it is of great importance to assess the history, nature and localization of pain, the absence of tension in the anterior abdominal wall during myocardial infarction and symptoms of peritoneal irritation. The results of the ECG study are decisive.

Pneumonia and pleurisy are characterized by increased body temperature, chills, tachycardia, shortness of breath, hyperemia (and not pallor, as with a perforated ulcer) of the face. In addition, there are corresponding pathological changes detected during physical examination of the respiratory organs. Chest X-ray examination can help in differential diagnosis in these cases.

The clinical picture of food intoxication is quite characteristic: an anamnestic connection with the intake of poor-quality food, stool upset, nausea, vomiting, tachycardia, and possibly increased body temperature. When carrying out differential diagnosis, it is necessary to carefully analyze the onset, duration and nature of the disease. A perforated ulcer begins with severe pain, accompanied by retention of stool and gases. Food intoxication is usually manifested by nausea, vomiting, and stool disorders, which are often its first clinical manifestations. Tension of the abdominal wall and the presence of other signs of irritation of the peritoneum are not characteristic of toxic infection. In addition, with food intoxication and toxic infection, pain does not occupy a leading position in the clinical picture of the disease.

The most difficult differential diagnosis is a perforated ulcer of the stomach and 12 intestines with acute appendicitis, because in both cases, pain may initially occur in the epigastric region with subsequent movement to the right iliac region. However, with a perforated ulcer, sharp pain appears suddenly, then after 4 to 6 hours it usually decreases somewhat. In acute appendicitis, pain intensifies gradually (excluding obstructive forms of acute appendicitis) and reaches a maximum after a few hours. With a perforated ulcer, a sharp tension of the anterior abdominal wall is noted in the upper abdomen (immobile, retracted “board-shaped” abdomen), and acute appendicitis is characterized by muscle deflation in the right iliac region. In addition, acute appendicitis is characterized by signs of an inflammatory process - increased body temperature, leukocytosis with shift leukocyte formula blood to the left, an increase in the leukocyte index of intoxication - are uncharacteristic of a perforated ulcer.

In difficult cases of differential diagnosis with acute surgical diseases of the abdominal organs, laparocentesis and examination of peritoneal exudate can help: the hemorrhagic nature of the exudate indicates acute pancreatitis, pancreatic necrosis or thrombosis of mesenteric vessels; an abundance of bile in the exudate indicates gangrenous perforated cholecystitis. In acute appendicitis, the exudate can be purulent, horous, and foul-smelling. A perforated ulcer is characterized by a cloudy, odorless exudate mixed with mucus, food, and sometimes bile with a positive iodine test (see above).

Treatment

At the pre-hospital stage, suspicion of perforation of a gastric and 12-gut ulcer is an absolute indication for immediate evacuation of the patient, lying down, by ambulance to the nearest surgical hospital. If indicated, cardiotonics, vascular and cardiac analeptics are administered before transportation. The use of painkillers is prohibited. It is also prohibited to leave a patient with suspected perforation of a gastroduodenal ulcer for dynamic observation at home or in an outpatient clinic, including for the purpose of clarifying the diagnosis.

In a surgical hospital, the diagnosis of a perforated ulcer of the stomach and 12 intestines is an absolute indication for surgery. In doubtful cases, when this diagnosis cannot be confidently rejected, an urgent diagnostic laparotomy is performed, which, when the diagnosis is confirmed, is transferred to a therapeutic one. Any delay in surgical intervention for a perforated ulcer significantly worsens the prognosis.

In the preoperative period, the stomach must be emptied using a thick gastric tube.

The most common operation for perforated gastric and duodenal ulcers is suturing the ulcer or plastic closure of the perforation hole (for example, with a strand of the greater omentum) with mandatory examination of the abdominal cavity and washing it with a large amount of sterile isotonic sodium chloride solution or furatsilin solution. If the ulcer is localized in the duodenum, anamnestic data indicate increased acid-forming function of the stomach, and with the appropriate qualifications of the surgeon, truncal vagotomy and one of the options for drainage surgery (pyloroplasty, gastroduodenostomy, gastroenterostomy) are usually performed. In some cases, according to appropriate indications, a typical gastrectomy or antruectomy in combination with vagotomy can be performed. In the presence of purulent peritonitis, surgical intervention is usually limited to suturing the ulcer, the abdominal cavity is sanitized and the whole range of measures for the treatment of peritonitis is carried out.

Conservative treatment

Conservative treatment for perforated gastric or duodenal ulcers is carried out extremely rarely, mainly due to the patient’s categorical refusal to undergo surgery. It is based on the following principles, the observance of which is mandatory:

bed rest;

under local anesthesia with 1% dicaine solution, a thick probe is inserted into the stomach to completely remove gastric contents, and then a thinner gastric probe is inserted for constant active aspiration for 5–6 days;

during this entire time, the patient should be placed in bed so that the intended location of the perforated ulcer occupies the highest position in relation to the rest of the stomach (12th section of the intestine);

correction of water and electrolyte status and complete parenteral nutrition for 7 – 10 days;

massive therapy with broad-spectrum antibiotics during infusion therapy (7–10 days).

Aspiration stops after the expiration of the above period and the disappearance of visible bile impurities in the aspirated gastric contents. Before removing the probe, a water-soluble X-ray contrast solution should be injected, an X-ray examination should be performed and make sure that there is no leakage of the X-ray contrast agent beyond the contours of the stomach or colon.

The outcomes of surgical treatment largely depend on the timing of the surgical procedure: for example, according to the academy’s clinics, among those operated on in the first 6 hours from the onset of the disease, the mortality rate is about 2%; for operations within 6 to 12 hours, this figure rises to 9%, and during operations within 12 to 24 hours after perforation, it is 14%, but if the operation is performed at a later date, then from 30 to 45% of patients die.

Acute gastrointestinal bleeding.

The leakage of blood into the gastrointestinal tract cavity is combined into the syndrome of gastrointestinal bleeding, which can be acute, occurring suddenly, and chronic, beginning unnoticed and often lasting for a long time. In addition, gastrointestinal bleeding can be obvious or hidden. In case of hidden bleeding, the admixture of blood in the contents of the gastrointestinal tract (vomit, feces) can only be detected using laboratory research methods (for example, Gregersen's reaction), and such bleeding is not included in the group of acute gastrointestinal bleeding. In case of obvious bleeding, blood is detected in a slightly changed or unchanged form along with the contents of the gastrointestinal tract and its presence is detected during a routine examination of vomit or feces. In the clinical course of gastric and duodenal ulcers, gastrointestinal bleeding can occur in any of the above options.

For stomach and 12-gut ulcers gastrointestinal bleeding occurs in every 4–5 patients with these diseases. In approximately half of those who died from gastric and duodenal ulcers, the immediate cause of death was gastrointestinal bleeding.

Etiology

Currently, more than 100 human diseases are known during which acute gastrointestinal bleeding can occur. Among the causes of such bleeding, about 60% are due to gastric and duodenal ulcers; the remaining 40% for other diseases: stomach tumors (15 - 17%), erosive and hemorrhagic gastritis (10 - 15%), Mallory-Weiss syndrome (8 - 10%), portal hypertension syndrome (7 - 8%), intestinal tumors , ulcerative colitis, diverticulosis and other diseases (7 – 10%).

Pathogenesis

The pathogenesis of acute gastrointestinal bleeding with gastric and 12-gut ulcers seems to be quite complex, because in some cases, bleeding occurs from arrozed large vessels in the area of ​​the ulcer, in others - from small arteries and veins of the walls and bottom of the ulcer, in others - there is parenchymal bleeding from the gastric mucosa outside the ulcer, where, along with increased permeability of the vascular wall, multiple small arrozia are often found , which are a source of profuse bleeding. Gastrointestinal bleeding in ulcers is provoked by a large meal of rough food, especially when it is difficult to evacuate it from the stomach, physical stress, blunt trauma to the abdomen, especially when the stomach is full.

When bleeding due to erosion of the wall of a large blood vessel in the area of ​​the ulcer, resulting from necrosis and subsequent exposure of gastric chyme to the wall of an exposed blood vessel (usually an artery), destruction of the vascular wall and the occurrence of bleeding usually occurs during the exacerbation phase of ulcerative disease and the lumen of the arrosion vessel often remains open , because destruction of tissue structures prevails over proliferative processes in the area of ​​the bleeding source. Local factors of hemostasis, including vessel retraction (very limited due to degenerative changes in the vascular wall and fibrosis of surrounding tissues), aggregation of blood cells, and blood clot formation are not enough to spontaneously stop bleeding and it often takes on a profuse nature.

With a slowly progressing ulcer outside the acute phase, productive inflammation of the vascular wall can prevent massive bleeding even with arrosion of a large vessel, the lumen of which is often narrowed due to proliferation of the intima and subendothelial structures, so thrombosis of such a vessel may be sufficient to spontaneously stop bleeding. However, focal degenerative changes may occur in the walls of chronic ulcers blood vessels with the formation of arterial aneurysms in the area of ​​the edges and bottom of the ulcer. Destruction of the thinned walls of these aneurysmal dilatations is accompanied by severe profuse bleeding.

The pathogenesis of bleeding in microscopic defects in the walls of small blood vessels, the bottom and edges of the ulcer has been less studied, but in these cases, progressive necrosis in the crater of the ulcer, characteristic of the exacerbation phase of the disease, appears to be of decisive importance in the pathogenesis of bleeding. The pathogenesis of bleeding from the gastric mucosa outside the ulcer is also not well understood. According to a number of studies, the main pathogenetic mechanisms of such bleeding may be:

permanent plethora of the entire vascular system of the stomach, especially superficial capillaries and veins, causing hypoxia and impaired vascular-tissue permeability, which leads to massive erythropedesis and hemorrhages;

severe dystrophy surface layers mucous membrane and decreased nucleic acid metabolism, promoting the formation of microerosions;

accumulation of neutral mucopolysaccharides as a consequence of the breakdown of tissue protein-carbohydrate compounds and increased vascular permeability;

disruption of the rhythms of polymerization, depolymerization of acidic mucopolysaccharides in the wall of blood vessels, changes in the permeability of hematoparenchymal structures;

hyperplastic and dystrophic processes, restructuring and pathological regeneration of glands of the entire gastric system, disrupting the secretory activity of the stomach, supporting vasodilation and tissue hypoxia (V.D. Bratus).

Disturbances in the hemostatic system also play a significant role in the pathogenesis of acute gastroduodenal bleeding in ulcerative disease. They boil down to a decrease and complete loss of the ability of an arrosive vessel to retract, which plays a very significant role in the mechanisms of local spontaneous hemostasis. In an acidic environment, thrombin is inactivated, which leads to a decrease in blood clotting ability, and the higher the acidity of gastric juice, the more the blood coagulation system in the intragastric bleeding site is inhibited. Simultaneously with a decrease in blood clotting, fibrinolytic activity increases directly in the area where the source of bleeding is located under the influence of the acidic environment of the gastric chyme and the chemically active proteolytic enzymes it contains. This is also facilitated by trypsins secreted by the pancreas tissue if a bleeding ulcer penetrates this organ.

As the severity of blood loss increases, signs of blood hypercoagulation appear, its fibrinolytic activity increases even more and rheological properties deteriorate due to the progressive aggregation of formed elements (V.V. Rumyantsev).

Deficiency of vitamins P, C, K, especially in the winter-spring period, when exacerbations of ulcers occur most often, also disrupts the mechanisms of hemostasis. For these reasons, despite the decrease in blood pressure in the bleeding vessels, due to hypovolemia and collapse, spontaneous spontaneous stopping of gastroduodenal bleeding with gastric and 12-gut ulcers is always problematic. As with any acute blood loss, the patient’s condition is characterized by the following changes: a decrease in the mass of circulating blood, centralization of blood circulation and impaired cardiac activity, which ultimately leads to oxygen starvation, primarily of the heart muscle, parenchymal organs and brain.

Pathological anatomy

Most often, morphological changes in acute gastroduodenal bleeding from an ulcer indicate rapidly progressing necrosis, reaching deep-lying blood vessels with necrosis of their walls with preserved lumen.

Classification

Acute gastroduodenal bleeding differs mainly according to two classification criteria: bleeding due to gastric and duodenal ulcers and bleeding of non-ulcer etiology are distinguished. Bleeding is also distinguished by the location of its source (stomach, colon and their anatomical sections). The classification of gastroduodenal bleeding according to the severity of blood loss is of very great practical importance (see table). Thus, the use of simple classification criteria involves establishing an etiological and topical diagnosis in conjunction with determining the severity of blood loss, which is necessary to determine therapeutic tactics and the content of transfusion therapy.

Clinic

Acute gastroduodenal bleeding usually occurs suddenly, against the background of a patient’s usual exacerbation of peptic ulcer or another of the diseases listed above. Often, after the onset of gastrointestinal bleeding in ulcer, the previously existing pain in the epigastric region disappears (Bergmann's symptom). At the same time or earlier, general symptoms of acute blood loss appear and initially come to the fore - pallor of visible mucous membranes and skin, dizziness, noise in the head, ears, often fainting, and then after 15 - 20 minutes or later, bloody vomiting appears and melena. Vomit in acute gastroduodenal bleeding can be in the form of “coffee grounds,” which usually indicates slow bleeding, and the spilled blood has time to react with the acidic gastric contents in the lumen of the stomach, as a result of which hemoglobin turns into hydrochloric acid hematin, which has a dark brown color. With heavy bleeding, especially if its source is located in the stomach, the spilled blood does not have time to react with the gastric chyme; it coagulates and forms blood clots that fill the lumen of the stomach. These bundles sometimes resemble raw liver in appearance, and patients often note vomiting “with pieces of liver.” With very intense bleeding, stomach fullness and vomiting occur before blood clots have time to form and vomiting of scarlet blood occurs, which is, like vomiting blood clots, a sign of heavy bleeding from upper sections Gastrointestinal tract. Vomiting repeated at short intervals indicates continued bleeding, and the appearance of vomiting after a long period indicates recurrent bleeding.

With slow and mild bleeding, especially if its source is located in the 12-gut, against the background of moderately severe symptoms of acute blood loss, dark stools may appear, the admixture of blood in which is easily detected by a pronounced positive Gregersen reaction. In cases of anamnestic bleeding manifested by melena, when examining the patient, it is necessary to conduct a digital examination of the rectum, which makes it possible to determine the nature of its contents and the presence of an admixture of blood that has undergone decomposition with the formation of iron sulfide, which gives such clots a dark color. With more intense bleeding, due to the excitation of the peristaltic activity of the intestine, liquid, tarry stool appears, and with very intense bleeding, stool, sometimes involuntary, may look like “cherry jam” or consist of slightly changed blood.

Acute gastrointestinal bleeding, manifested only by melena, has a more favorable prognosis compared with bleeding, manifested by hematemesis. The most unfavorable prognosis is for bleeding, manifested by hematemesis and melena.

With a mild degree of blood loss, its general signs are unstable, because they are not caused by hypovolemia, but by reflex reactions and pathological blood deposition. Creating conditions of physical and mental peace leads in some cases to the disappearance of these signs. Noticeable hemodynamic disturbances caused by bleeding usually appear with blood loss of more than 0.5 liters, because the bleeding rate, even with arrosion of a large vessel in the ulcer, does not exceed the rate of blood loss during exfusion of blood from the donor. In addition, approximately 15 minutes after blood loss, compensatory hydremia develops, often against the background of short-term reflex arterial hypertension, so in the early stages from the onset of bleeding, hemodynamic changes may be less pronounced than they should be for a given degree of blood loss. Subsequently, with significant blood loss, thirst appears, dry mucous membranes of the oral cavity, and diuresis decreases, which indicates dehydration due to blood loss. These symptoms usually occur against the background of hemodynamic changes - tachycardia, decreased blood pressure, compensatory tachypnea, etc.

Perforation of an ulcer - the formation of a through hole in the wall of the stomach or duodenum. In this case, their contents enter the abdominal cavity, and inflammation of the peritoneum develops - peritonitis.

Perforation is accompanied by sudden intense (“dagger”) pain in the abdomen. The patient cannot get out of bed - he lies quietly and motionless on his side with his legs drawn to his stomach (the “embryo” position), sweat appears on his forehead. Body temperature rises. The tongue becomes dry, the stomach becomes “board-shaped” (tense, flat). As peritonitis develops, the patient's condition worsens; In the absence of immediate surgical intervention, death occurs.

If you suspect a perforation of the ulcer, you should immediately call an ambulance. You should not take independent therapeutic actions; it is forbidden to apply a heating pad to your stomach.

Treatment of perforation is only an emergency operation. Most often, the rupture is sutured; in some cases, it is also necessary to remove part of the affected organ.

Ulcer penetration

This is also the formation of a hole in the wall of the stomach or duodenum. However, it does not open into the abdominal cavity, but into nearby organs: pancreas, large intestine, liver, lesser omentum, etc.

Manifestations depend on which organ the perforation occurred in.

General symptoms: pain intensifies and becomes constant. They do not go away after eating and using antacids (Almagel, Maalox). Body temperature rises.

Treatment is urgent, surgical.

Bleeding

Enlargement of the ulcer can lead to exposure of the vessel wall of the affected organ, and its “corrosion” by acid. Bleeding occurs. Symptoms depend on the amount of blood loss.

Signs of bleeding:

• sudden weakness
• fainting,
• drop in blood pressure,
• vomiting scarlet blood or “coffee grounds” (clotted blood),
• loose, tarry black stools (called melena).

Treatment of bleeding is carried out only in a surgical hospital.

To identify the source of bleeding, gastroscopy is performed. During this procedure, bleeding is stopped using special solutions or suturing the bleeding vessel with special staples. In addition, the patient is prescribed intravenous administration of drugs that reduce the production of hydrochloric acid.

If the bleeding has stopped, the patient is left in the hospital for observation for 3-5 days.

If it is not possible to stop the bleeding during endoscopy, surgical intervention is resorted to. The type of operation is chosen by the surgeon depending on the characteristics of the disease: from suturing a vessel to removing part of an organ.

Pyloric and duodenal stenosis

Otherwise called “obstruction of the pyloric part of the stomach”, i.e. difficulty passing food from the stomach to the intestines as a result of deformation or narrowing of the junction of the stomach and the duodenum. Occurs as a result of scarring of an ulcer located in the final part of the stomach or the initial part of the duodenum.

A slight degree of narrowing of the pylorus is manifested by heaviness in the upper abdomen for several hours after eating, sour belching, periodic vomiting of food eaten, which brings relief.

As this condition progresses, there is a constant retention of part of the food in the stomach and its overdistension, putrid smell from the mouth, rotten belching, patients complain of intense abdominal pain, constant vomiting food. Digestive disorders over time lead to exhaustion and dehydration of the patient.

Treatment is surgical.

Peptic ulcer is an acutely occurring disease, prone to a chronic relapsing course, which is based on deep ulceration of the mucous membrane of the stomach or duodenum against the background of various degenerative and inflammatory changes.

Healing ulcerative defect occurs with the formation of dense deforming scars. An exacerbation of peptic ulcer disease usually develops in spring and autumn.

This is one of the most common pathologies digestive organs. The disease occurs at any age, most often after 20 years. There is a predominance of male patients due to the high risk of exposure to harmful predisposing factors and genetic characteristics.

The classification of peptic ulcer distinguishes:

1. By localization ulcerative defect: gastric ulcer, duodenal ulcer, ulcer with double localization.
2. 4 stages of the ulcerative process:
   1. stage of ulcer healing while inflammation in surrounding tissues persists
   2. stage of complete remission.
   3. According to the presence of complications: uncomplicated and complicated (bleeding, perforation, penetration, cicatricial stenosis, etc.).
   4. Based on existing concomitant diseases.

Etiology and pathogenesis of peptic ulcer

The etiology and pathogenesis of peptic ulcer disease are constantly being studied by the global medical community due to the high costs of treating patients and high rates of disability. Currently, the leading causes of peptic ulcer disease are:

1. Exposure to Helicobacter pylori. This bacterium is capable of multiplying in the aggressive environment of the stomach and duodenum. A colony of microbes releases products that are toxic to the mucous membrane, leading to degeneration and cell death. As a result, an ulcerative defect is formed, which becomes deeper and deeper under the influence of the acid of the food bolus and gastric juice, bile. It has been proven that chronic peptic ulcer disease is formed precisely as a result of long-term persistence of Helicobacter in the lesion of the mucous membrane.
2. The predominance of aggressive factors over protective ones. In some patients, a genetically or endocrine-determined excess of hydrochloric acid or pepsin, especially in combination with duodenogastric reflux, cannot be completely neutralized by protective factors (mucus, bicarbonates and lysozyme). As a result, chemical ulcerations of the mucous membrane develop.
3. For other reasons, as a result of which a stomach and duodenal ulcer can develop include medications (cytostatics, non-steroidal anti-inflammatory drugs, hormonal drugs, diuretics), dietary errors (irregular, spicy, hot or cold food, alcoholic and fizzy drinks, excess carbohydrates), stressful situations. Among the diseases that can provoke the occurrence of ulcers are any toxic-allergic, severe pain and shock conditions, cardiac or pulmonary decompensation, strokes, thrombosis, tuberculosis, AIDS.

Ulcer: symptoms and treatment

Symptoms of peptic ulcer during exacerbation:

1. Abdominal pain. Its most common location is the epigastrium (upper abdominal cavity). Depending on individual pain tolerance, the size and location of the ulcer, the severity of the pathological process, the involvement of the muscular lining of the intestine and surrounding organs, it can be of varying intensity, acute or aching dull, dagger-like, burning, encircling. On examination, protective local tension in the muscles of the anterior abdominal wall is noted.
   Duodenal ulcer often causes pain to radiate to the area of ​​the right kidney or lumbar muscles, in the right arm and collarbone. It is characterized by their intensification at night and 3 hours after eating (the so-called “hunger” pains). Relief for the patient comes from taking antacids, milk drinks, mucous decoctions.
   For ulcers in the fundus of the stomach, pain during eating is typical, especially if the dishes, due to the abundance of fiber and seasonings or uncomfortable temperature, can increase irritation of the inflamed lesion. The further the ulcer is located from the esophagus, the more time passes before pain appears. For pyloric ulcers this is usually about 2 hours. Exacerbation of peptic ulcer disease is manifested primarily by increased pain.
2. Dyspeptic disorders associated with impaired motor skills and enzymatic activity intestines, delay in the movement of food masses from the stomach. Heartburn and belching, nausea and a feeling of fullness are observed, vomiting of eaten food brings relief, stomach cramps, constipation and, less often, diarrhea and weight loss. The consequences of a long-term disease are the appearance of signs of multivitamin deficiency, and in children there is a lag in physical development.
3. General symptoms. Patients report increased fatigue and irritability, sleep disturbances, and apathy. Gastric ulcer is often accompanied by asthenic syndrome. A biochemical blood test shows concomitant dysfunction of the liver and pancreas, an increase in inflammatory proteins. Temperatures may rise to subfebrile levels.

Therapy for peptic ulcer disease is carried out in a hospital and includes limiting physical and emotional stress, special diet, medicinal and eradication antibacterial therapy, physiotherapy, herbal medicine, physical therapy.

The interictal period, as well as a chronic ulcer in the scarring stage, require no less careful attention, active anti-relapse treatment and gentle nutrition. Only in this case is long-term, for many years, remission possible and a guarantee of the absence of life-threatening complications in the development of peptic ulcer disease.

symptoms .

Causes of peptic ulcer

Highlighted in separate form diseases many decades ago. Given its widespread prevalence, doctors carefully study all possible causes of stomach ulcers. After all, this is the only way to effectively prevent and effectively treat this disease. In parallel with the development of medicine, views on

Currently, the most common theories are:

1. Infectious. According to this theory, up to 80% of cases of peptic ulcer are bacterial in nature. A special type of spiral-shaped microorganisms called Helicobacter pylori has been isolated, which are able to neutralize acid and survive in the very aggressive environment of the duodenum and stomach. The waste products of these bacteria cause inflammation and death of cells in the protective layer of the mucous membrane. As a result, superficial erosions develop, which over time turn into deep ulcers. It was also revealed that only one out of four Helicobacter carriers gets sick. That is, at the same time there must be other predisposing causes of ulcers and exposure to external aggressive factors for the disease to develop.
2. Disequilibrium theory factors of protection and aggression against the mucous membrane of the duodenum and stomach. The first group includes congenital features immune and hormonal local protection and blood supply, as well as lysozyme produced by epithelial cells of the mucous membrane, bicarbonates to neutralize acid and mucus. The second group of factors includes a hereditarily determined tendency to increased production of hydrochloric acid in the stomach, duodeno-gastric reflux, and Helicobacter. The predominance of sympathetic innervation and, as a result, frequent vascular spasms, leading to the formation of areas of atrophy of the mucous membrane of the duodenum and stomach. According to this theory, aggressive causes of stomach ulcer must outweigh protective factors for the development of the pathological process.

Other causes of ulcers

1. Medicinal. Taking reserpine, non-steroidal anti-inflammatory, hormonal, cytostatic, and some diuretic drugs. Occurs more often stomach ulcer due to this reason.
2. Nutritional. Consumption of excessively hot or cold food, carbonated drinks, strong coffee, hot spices, smoked foods, an abundance of baked goods and sweets, lack of diet.
3. Toxic-allergic. Damaging factors include nicotine tar, drinks with a high alcohol content, poisoning, and severe allergic reactions.
4. Neurogenic. This group includes focal disorders of the blood supply to the mucous membrane during strokes, chronic and acute stressful situations, dystrophic diseases nervous system. Occurs more often duodenal ulcer due to these reasons.
5. Trophic. Multiple gastric ulcers often occur due to decompensation of heart or lung diseases due to decreased blood supply or thrombosis of small vessels of the gastric mucosa.
6. Shock. According to the mechanism of occurrence, they are close to the previous ones. Causes: severe burns, myocardial infarction, extensive injuries leading to a drop in blood pressure.
7. Chronic specific diseases. Duodenal or stomach ulcers may be a symptom tuberculosis , AIDS syphilis.

Symptoms of peptic ulcer

Prevention of peptic ulcers

Prevention of peptic ulcer disease is conventionally divided into primary (preventing the development of the disease), secondary (reducing the risk of relapses and exacerbations), and tertiary (reducing the likelihood of complications). The second and third groups have practically no fundamental differences. Therefore, a set of measures for secondary and primary prevention ulcers

Primary prevention of peptic ulcer

Primary prevention of gastric ulcer or duodenal ulcer involves:

1. Prevention of Helicobacter pylori infection. If there are patients with ulcers or carriers of this microbe in the family, it is recommended to strictly follow anti-epidemic measures. These include individual dishes and cutlery, personal towels, and sharp limitation of kissing to reduce the risk of transmitting the pathogen to healthy people, especially children.
2. Timely caries treatment teeth and maintaining oral hygiene.
3. Quitting strong alcoholic drinks and smoking.
4. Organization proper nutrition. The composition and regularity of food intake should correspond to the age and needs of the body. Gentle culinary processing with a sharp limitation of spicy, smoked and irritating foods is of no small importance. Do not consume extremely hot or very cold foods, caffeine-containing drinks, or carbonated drinks.
5. Prevention and active treatment of hormonal disorders, acute and chronic diseases especially relevant for the prevention of duodenal or gastric ulcers.
6. Elimination of frequent or unsystematic use of medications, causing the formation of ulcers.
7. Rational organization of work and rest, sports. Be sure to adhere to the daily routine and sleep at least 6 hours per day (and for children, adhere to the age norm).
8. Timely psychological assistance. Calm relationships in the family and school and quick resolution of conflict situations in adolescence are especially important.

Prevention of exacerbations of peptic ulcer disease

Secondary prevention of peptic ulcer or duodenal ulcer includes mandatory medical examination measures:

1. Regular courses of anti-relapse treatment, especially in the autumn and spring periods. They should consist of medications prescribed by a gastroenterologist, physiotherapeutic procedures, herbal medicine, and drinking mineral water.
2. Sanatorium-resort preventive treatment of ulcers in specialized institutions.
3. Sanitation of chronic foci of infection and any diseases that can provoke an exacerbation of the ulcer.
4. Long-term and strict adherence to an anti-ulcer diet.
5. Constant laboratory and instrumental monitoring ulcer conditions for early detection of symptoms of exacerbation and early initiation of active treatment.
6. Secondary prevention of ulcers also includes complete a set of measures for its primary prevention.

Complications of peptic ulcer

Common complications of duodenal and gastric ulcers:

1. Bleeding from an ulcer.
2. Penetration of ulcers (transition of the process to nearby organs and tissues).
3. Malignancy of the ulcer.
4. Vegetative-vascular dystonia.
5. Chronic cholecystitis And pancreatitis, hepatosis.
6. Clinic of intestinal obstruction.
7. Perforation (perforation) of an ulcerative defect.

Complications of gastric ulcer:

1. Stenosis or cicatricial deformation of the pyloric (outlet) part of the stomach.
2. Gastroesophageal reflux, chronic esophagitis.

Complications of duodenal ulcer:

1. Dyskinesia or spasm of the biliary tract.
2. Cholestasis.
3. Cicatricial deformation of the duodenum.
4. Recurrent duodeno-gastric reflux.

Characteristics of complications of peptic ulcer

Bleeding from a peptic ulcer may be mild (detected only by laboratory examination of stool for occult blood), moderate (leads to chronic anemia) or massive, which is one of the most serious complications. It develops when the walls of blood vessels of different sizes are damaged. There is black stool, vomit scarlet blood or “coffee grounds”, anemia. At massive blood loss There may be a drop in blood pressure, loss of consciousness, shock.

The consequence of the spread of ulcerative lesions to all layers of the stomach wall is its rupture with the leakage of the contents of the duodenum or stomach into the abdominal cavity. The patient feels a sudden (dagger) pain and a sharp deterioration in health. As a result, life-threatening diffuse peritonitis develops very quickly, requiring emergency surgical care.

Chronic ulcers of the duodenum and stomach have consequences in the form of extensive adhesive processes affecting nearby organs. As a result, it is possible that the ulcerative process at the site of adhesions can transfer to the tissue of the pancreas, greater or lesser omentum, intestinal loops, and in very rare cases even to the diaphragm or right ventricle of the heart. The patient feels a sharp increase in pain, which takes on a girdling character. Symptoms of indigestion quickly appear, and the general condition worsens. Without emergency treatment, this complication is fatal.

Obstruction of the duodenum or pylorus of the stomach develops due to persistent spasm of their muscle layer or due to severe cicatricial deformation that blocks the path for the movement of food masses. There are constant nausea, repeated vomiting, constipation, feeling of fullness in the stomach, weight loss.

Diet for peptic ulcers

Diet for gastric or duodenal ulcers is one of the most important therapeutic factors, which under no circumstances should be ignored. There are several types of dietary menus, designed taking into account the period of the disease and the presence of complications. They differ in the set of permitted food products and by the method of preparing dishes. the main objective diet for ulcers - maximum thermal, mechanical and chemical sparing of the mucous membrane of the digestive canal to quickly subside inflammatory manifestations and reduce reflex excitability of the duodenum and stomach. Wherein nutrition for peptic ulcers should completely replenish the body’s energy and nutrient expenditures, and also serve as a complete source of protective factors.

Diet No. 1A

Symptoms of duodenal ulcer

The symptoms of a duodenal ulcer are in many ways similar to the clinical manifestations of a gastric ulcer. Poor health, unmotivated fatigue, slight increase in body temperature, irritability, tendency to constipation, sudden change in food preferences, epigastric pain, heartburn , nausea bringing relief vomit, dry gray coating and pronounced papillae on the tongue, a tendency to caries teeth and periodontal disease appear with exacerbation of peptic ulcer disease. There is also a large percentage of painless, “silent” ulcers that clinically manifest only when complications develop

But duodenal ulcer It also has distinctive symptoms associated with the localization of the ulcer and the involvement of nearby organs in the pathological process. They help the doctor in a quick preliminary diagnosis of this disease and its complications. Here are the main ones:

1. Digestive disorders in the form of loose and frequent stools. They occur when the pancreas is involved in the process of inflammation. The intestinal ulcer has similar symptoms, but more pronounced. At the same time, there may be intolerance to products made from fresh milk and fruits, and girdling pain in the left hypochondrium and lower back.
2. Increased appetite. It is associated with the patient’s subconscious attempt to “eat” the pain and with a violation of the processes of enzymatic breakdown, as well as the absorption of nutrients. In this case, during exacerbation, weight loss is observed.
3. Tendency to stagnation of bile. Caused by inflammatory spasm of the bile ducts. It manifests itself as an icteric staining of the coating on the tongue, and in severe cases - on the skin, nagging pain in the right hypochondrium. With endoscopic diagnosis, one can see the reflux of bile into the pyloric part of the stomach. This is the so-called duodeno-gastric reflux, which causes heartburn.
4. Nausea and vomiting many hours after eating, gastroesophageal reflux. Duodenal ulcer has these symptoms in the case of a long course of the disease, leading to persistent spasm or gross cicatricial changes in the pyloric part of the stomach. This prevents the evacuation of food and leads to vomiting of stagnant stomach contents.
5. The special nature of the pain.

Pain due to duodenal ulcer

The main signs of a duodenal ulcer are pain - on an empty stomach (hungry) and at night. They can be constant, aching or paroxysmal and sharp. Their intensity increases approximately two hours after eating and decreases immediately after eating. Dairy products and slimy soups help especially quickly. To treat pain, patients apply a hot heating pad to the area of ​​the right hypochondrium, take antacid, antispasmodic and medications that reduce the secretion of gastric juice.

The epicenter of pain is usually located closer to the right hypochondrium in the epigastric region. The spread of pain is observed in the right arm, in the back. There are specific pain points on the right clavicle, in the lower thoracic and lumbar vertebral segments.

Duodenal ulcers are characterized by seasonal spring and autumn increases in the severity of pain.

You can find symptoms of all diseases on our website in the section

Peptic ulcer(peptic ulcer) – chronic cyclical

ongoing recurrent disease prone to progression,

characterized by a common morphological feature - a chronic ulcer

stomach or duodenum, which can cause certain dysfunctions in

digestive system, as well as shifts in homeostasis at the level of the holistic

body.

Peptic ulcer disease is characterized by a number of significant distinctive features

signs that allow one to have a certain clinical picture, course and

prognosis: 1) peptic ulcer is defined as a defect of the mucous membrane,

spreading through t.muscularis mucosae and healing by

epithelial and connective tissue proliferation with scar formation; 2)

peptic ulcer disease is chronic from the moment of its onset and often

has a relapsing course.

Numerous complications of peptic ulcer disease can be divided into two groups:

1. occurring suddenly and directly threatening the patient’s life (bleeding, perforation);
2. developing gradually and having a chronic course (penetration, stenosis of the pylorus and duodenum, malignancy, as well as perivisceritis, reactive hepatitis, reactive pancreatitis).

The course of gastric and duodenal ulcers with the development of these complications is significantly aggravated and in most cases there is a need to perform surgery due to the possible danger to the patient’s life. Refusal of further conservative treatment of peptic ulcer in the development of such conditions in some cases is also due to the fact that it does not have the necessary therapeutic effect, and unjustified continuation of therapy for a complicated peptic ulcer only contributes to the progression of the pathological process. Thus, subcompensated pyloric stenosis turns into a decompensated form, and failure to perform timely surgery for malignant ulcers leads to the appearance of distant metastases.

Perforated gastro duodenal ulcers

Perforation- breakthrough of an ulcer into the free abdominal cavity with the entry of gastric and duodenal contents into it. The frequency of this complication in patients with gastroduodenal ulcers ranges from 5-15%. More often, ulcers perforate when they are localized in the duodenum - up to 75% of patients, as well as ulcers of prepyloric and pyloric localization. Perforation of ulcers localized in the stomach occurs relatively rarely - up to 5%. The age of patients with perforation is usually 20-40 years, while their ulcer history is no more than 3 years, and in 25% it may be absent altogether. The ratio of men to women with this complication of peptic ulcer disease is 7-8:1. Seasonality is characteristic - an increase in the number of perforations of ulcers in the autumn-spring period. In 1-5% of patients, perforation of the ulcer can be combined with bleeding.

Etiology, pathogenesis, pathomorphology, classification

Perforation of gastroduodenal ulcers in most cases occurs as a result of the progression of an acute or chronic destructive inflammatory process in the ulcer. Perforation is usually preceded by a period of exacerbation of peptic ulcer disease with characteristic symptoms. However, in in some cases it can arise without any manifestations of the previous period in the midst of complete well-being. Such perforated ulcers are called “ dumb" It is believed that the cause of their occurrence is acute neurodystrophic changes in the wall of the stomach and duodenum.

Factors such as overfilling the stomach with rough food, drinking alcohol, physical stress, and negative emotions can contribute to perforation.

The perforation hole is always located in the center of the ulcer. Its dimensions vary widely - from microperforation to a defect several cm in size. The peri-process is expressed in the form of perigastritis or periduodenitis. The edges of the perforation are hyperemic, thickened, have a fibrinous coating, and are easily cut through during stitching. Histologically, the destruction of all layers of the wall of the stomach or intestine, abundant development of scar tissue, degenerative changes in the arteries surrounding the ulcer, abundant leukocyte infiltration fabrics. More often, perforated ulcers are single, but can also be double, on the anterior and posterior walls of the stomach or intestines - the so-called “ mirror" or " kissing“ulcers.

Gastroduodenal contents spilling into the abdominal cavity through the perforation cause the development of diffuse peritonitis. In the first 6 hours of the disease, due to the bactericidal effect of gastric juice, the inflammatory process in the abdominal cavity has the character of non-bacterial, chemical inflammation. Then an infection occurs with the development of bacterial peritonitis. Accordingly, in the first hours of perforation, the abdominal effusion is serous, then serous-fibrinous and fibrinous-purulent.

Classification of perforated gastroduodenal ulcers (according to V.S. Savelyev):

1. By etiology:

a) ulcerative; b) hormonal.

2. By localization:

a) stomach ulcers: lesser curvature, anterior wall, posterior wall;

b) duodenal ulcers: anterior wall, posterior wall .

3. Downstream:

a) perforation into the free abdominal cavity;

b) covered perforation;

c) atypical perforation.

Clinical picture of perforated gastroduodenal ulcers.

In the clinical picture of perforated gastroduodenal ulcers, three phases are distinguished:

1)abdominal shock- up to 6 hours from the moment of perforation;

2)period of imaginary prosperity- 6-12 hours;

3)period of diffuse peritonitis- after 12 o'clock.

The most typical clinical picture is perforation of an ulcer into the free abdominal cavity. Clinical manifestations in this case, they are associated with the body’s reaction to sudden irritation of the peritoneum by the effusion of gastroduodenal contents. 95% of patients experience acute “dagger” pain in the epigastric region and reflex vomiting, which does not bring relief, 1-2 times. The pain syndrome is so severe that patients develop a shock reaction. They are in a state of prostration, the expression is pained, the skin is cold to the touch, with an earthy tint, acrocyanosis is pronounced, shallow rapid breathing, the tongue is dry. In the initial phase of ulcer perforation, bradycardia is characteristic, as a reaction associated with the effect of acidic gastric contents on n. vagus, as well as a decrease in blood pressure. The patient's position is forced - on the right side or back with the legs brought to the stomach. The slightest movement leads to a sharp increase in abdominal pain. Gradually, the pain spreads throughout the abdomen, possibly radiating to the area of ​​the collarbone, shoulder blade, and neck.

A physical examination reveals hyperesthesia of the skin of the abdomen, tension in the muscles of the abdominal wall (“board-shaped” abdomen), the abdomen does not participate in the act of breathing, it is “scaphoid” retracted. The Shchetkin-Blumberg symptom immediately becomes positive, intestinal motility is sharply weakened or completely absent. Percussion reveals dullness in the lateral canals and small pelvis, which indicates the presence of free fluid in the abdomen, and hepatic dullness disappears. During digital examination of the rectum, severe pain occurs (Kullenkampf's symptom).

IN phase of imaginary well-being, after 5-6 hours from the moment of perforation, some relief of the patient’s condition occurs, pain and tension in the abdominal muscles decrease, and shock disappears. However, pain on palpation of the abdomen remains, symptoms of peritoneal irritation are positive, peristalsis is absent, hepatic dullness is smoothed out. After 6-12 hours, the clinic of diffuse peritonitis already develops. In this phase, the patient's condition progressively worsens, the symptoms of intoxication, paralytic intestinal obstruction with bloating and repeated uncontrollable vomiting increase.

In the peripheral blood, leukocytosis, neutrophilic shift to the left, and toxic granularity gradually increase. Protein, casts, and leukocytes appear in the urine.

During X-ray examination in vertical position between the dome of the diaphragm on the right and the upper surface of the liver, free gas is found in the form “crescent-shaped stripes”. This radiological sign is characteristic of perforation of any hollow organ of the abdominal cavity. If it is impossible to examine the patient in a standing position, conduct it in horizontal position(lateroscopy), in which free gas is detected under the anterior abdominal wall or under the edge of the costal arch. In 25% of patients this symptom may be negative. In this case, pneumogastrography is indicated. The contents are removed from the stomach through a tube, and then, while lying on the left side, 500-700 ml of air is introduced, which, if there is a hole in the stomach or intestine, enters the free abdominal cavity and is detected during repeated X-ray examination.

Currently, to clarify the presence of perforation, a combined X-ray and endoscopic examination using a fibrogastroduodenoscope is widely used, during which an ulcer with signs of perforation is visually detected.

At small sizes perforation, the hole in the wall of the stomach and duodenum can be covered by an adjacent organ (liver, gall bladder, omentum, etc.), fibrin, a lump of mucus or food masses. This is facilitated by the small diameter of the perforation, weak filling of the stomach at the time of perforation, and the proximity of the perforation site to the liver and other organs. Such perforations are called covered and make up 5-8% of the total.

Clinic of covered perforated ulcers manifests itself as an acute onset with the appearance of symptoms of perforation into the free abdominal cavity. After covering the perforation, clinical manifestations subside, the condition improves, and self-healing may occur in some patients. A characteristic clinical sign of covered perforation is long-term persistent tension of the abdominal wall muscles in the right upper half of the abdomen with a satisfactory general condition of the patient. In some patients, the disease may be remitting in nature, giving rise to new outbreaks of the acute process.

Diagnostics Covered perforations are difficult due to periodic improvement in the general condition of patients. Help in these cases can be provided by an X-ray examination, during which, in the presence of a perforation of a hollow organ, gas in the abdominal cavity is determined, fibrogastroduodenoscopy, as well as diagnostic laparoscopy. When diagnosing a covered perforation, the doctor’s tactics should be active. Patients are operated on mandatory even if a covered perforation is suspected.

Atypical forms of perforation occur in 3-4% of patients, usually elderly and senile or severely weakened. With this form, the main symptoms of a perforated ulcer are significantly smoothed out. Abdominal pain is insignificant, without clear localization, there is no pronounced defence. There may be moderate rigidity of the muscles of the anterior abdominal wall, determined in the upper half of the abdomen. The diagnosis of perforation in such cases is made by indirect signs, ulcer history, X-ray data, results of fibrogastroduodenoscopy, diagnostic laparoscopy.

A number of authors consider cases of extraperitoneal perforation of ulcers to be an atypical form. When ulcers of the posterior wall of the stomach and duodenum are perforated, their contents do not enter the free abdominal cavity, but into the retroperitoneal tissue, so there is no such sharp pain as is usually observed with classic perforation. Air enters the retroperitoneal tissue along with the contents of the hollow organs. which is detected by palpation in the form of subcutaneous emphysema. In this case, the disease can occur as a purulent-septic process in the retroperitoneal tissue.

Differential diagnosis

Differential diagnosis of a perforated ulcer is carried out with acute diseases of the abdominal organs, which are characterized by epigastric pain: acute cholecystitis and pancreatitis, appendicitis, as well as renal colic, gastralgic form of myocardial infarction, lower lobe pleuropneumonia.

Acute cholecystitis women get sick more often increased nutrition. Patients note attacks of pain in the right hypochondrium in the anamnesis and associate them with taking fatty, smoked and fried food. Repeated vomiting of bile is typical. Upon objective examination, muscle tension is localized in the right hypochondrium and is not diffuse. Here, a clearly palpable infiltrate, or the bottom of the gallbladder, is often determined. From the very beginning of the attack, tachycardia, high body temperature, and leukocytosis develop. Often the attack is accompanied by symptoms of obstructive jaundice. An ultrasound examination of patients with acute cholecystitis reveals stones.

Acute pancreatitis, just like perforation of an ulcer, it begins with acute pain in the epigastrium, but it is of a girdling nature and is accompanied by repeated vomiting. There is no board-like tension in the abdomen; on the contrary, at the beginning of the disease the abdomen may be soft. The Shchetkin-Blumberg symptom becomes positive at a later date with the development of pancreatogenic peritonitis. The presence of high blood amylase levels confirms the diagnosis of acute pancreatitis.

Acute appendicitis may begin with the occurrence of pain in the epigastrium (Kocher's symptom), but the clinical picture is never accompanied by muscle tension in this area, while at the same time there is a pronounced defence in the right iliac region. Sometimes, when the patient is examined 5-6 hours after the perforation, gastric contents along the right lateral canal can descend into the iliac fossa and cause severe pain here. In this case, an erroneous operation for acute appendicitis from the Volkovich-Dyakonov oblique approach is possible.

During intraoperative examination, the presence of a large amount of characteristic contents coming from the upper floor of the abdominal cavity and the absence of changes in vermiform appendix allows one to suspect ulcer perforation. In unclear cases, diagnostic laparoscopy is indicated.

In patients with myocardial infarction in the presence of pain in the epigastrium, it is decisive in the formulation correct diagnosis is an electrocardiographic study that reveals fresh focal lesions of the coronary circulation. Myocardial infarction often develops in elderly patients with a history of angina attacks. The abdomen is painful in the epigastrium, not distended, muscle tension is insignificant, active peristalsis remains, and there are no symptoms of peritoneal irritation.

At renal colic pain is paroxysmal in nature, localized in lumbar areas with irradiation to the genitals and groin areas. accompanied by dysuric disorders. Patients are extremely restless and constantly change body position. The abdomen may be somewhat tense and distended, but active peristalsis remains, the Shchetkin-Blumberg symptom is negative. The diagnosis is confirmed by X-ray examination, when shadows of stones are detected in the projection of the kidneys and ureters, by chromocystoscopy, and ultrasound examination.

Among other therapeutic diseases, the clinic of a perforated gastroduodenal ulcer can be simulated basal pneumonia And pleurisy. Suspecting this pathology in the presence of pain in the epigastrium allows a systematic examination of the patient, auscultation and x-ray examination of the lungs and pleura.

Treatment.

Patients with perforated ulcers should undergo immediate hospitalization to the surgical department and emergency surgery. If it is impossible to perform the operation, in exceptional cases (the patient’s categorical refusal of the operation, the absence of conditions for the operation), the Taylor method of conservative treatment can be used: the Fowler position, constant aspiration of gastric contents using a probe, cold on the stomach, antibiotic therapy, detoxification therapy.

The type and volume of intervention for a perforated ulcer is determined strictly individually. There are palliative operations - suturing the perforated hole and radical - gastric resection, vagotomy with pyloroplasty.

When choosing a surgical method, it should be taken into account that in young people (up to 25-30 years), ulcers in 80% of cases tend to heal after suturing, and gastric ulcers in the elderly often undergo malignancy after suturing. Not only the patient’s tolerance of the intervention should be taken into account, but also the technical capabilities of the operating team, resuscitation and anesthesiology services.

The operation is performed under endotracheal anesthesia. It is performed from the upper midline laparotomy approach. Recently, methods have been developed for the surgical treatment of perforated gastroduodenal ulcers using minimally invasive endovideosurgical technologies.

Indications for gastric resection are large callous gastric ulcers, suspicion of malignancy, malignancy, repeated perforation, combination of perforation with bleeding. For duodenal ulcers trunk or selective proximal vagotomy with drainage surgery in the form of pyloroplasty and excision of the ulcer is indicated.

In the absence of indications for radical surgery or there are no conditions for its implementation, the perforation hole is sutured. Suturing indicated when the period after perforation is more than 6 hours, the presence of symptoms of diffuse peritonitis, the presence of severe concomitant diseases.

Ulcers of the pyloroduodenal zone are preferable suturing according to Oppel-Polikarpov with tamponade of the perforated hole with a strand of the greater omentum on the pedicle. Ulcers of more proximal sections can be sutured with a double-row suture in the transverse direction with fixation of a free strand of the omentum to the suture line.

With retroperitoneal perforations, air and bile imbibition are detected in the paraduodenal tissue. Before suturing such an ulcer, preliminary mobilization of the duodenum according to Kocher is necessary. After suturing, it is advisable to drain the retroperitoneal tissue in the area of ​​the sutures placed on the perforated hole from the lumbar approach.

IN postoperative period Management of a patient with perforation is similar to the management of patients with peritonitis and after planned gastric surgery.

Penetration of gastroduodenal ulcers

Penetration– germination of a stomach or duodenal ulcer into surrounding organs or tissues. According to some authors, penetration is a variant of a covered perforated ulcer, characterized by a slow course. Thus, histologically, in the initial stage of this complication of peptic ulcer, as well as with perforation, destruction develops as a result of a destructive process of all layers of the wall of the stomach or duodenum - mucous, submucosal, muscular and serous. This stage of the pathological process is called intramural penetration. However, unlike perforation, in the next stage fibrinous adhesions develop with the organs or tissues subject to the ulcer without penetration of the contents of the stomach or intestines into the free abdominal cavity. The third stage is the stage of completed penetration, in which the bottom of the ulcer is the tissue of the organ into which it penetrates. In the circumference of the focus of penetration, tissue infiltration occurs, an extensive adhesive process is formed with the phenomena of perigastritis and periduodenitis.

More often, gastric ulcers penetrate into the lesser omentum, pancreas, liver, transverse colon and its mesentery. It is possible for a stomach ulcer to grow into the diaphragm, spleen, or anterior abdominal wall. Duodenal ulcers are characterized by penetration into the head of the pancreas, gallbladder and common bile duct, sometimes with the formation of an internal biliodigestive fistula.

Clinic.

Clinically, a penetrating ulcer is manifested by an exacerbation of the process with a pronounced inflammatory component that is difficult to treat conservative therapy.

Characterized by an increase in the intensity of pain, which becomes permanent. The pain quite often radiates to the back and often has a girdling character. In the presence of severe pain in the spine, there is usually penetration into the head of the pancreas.

Often there is severe pain and tension in the muscles of the anterior abdominal wall with symptoms of local peritonitis. In a number of patients, it is possible to palpate the inflammatory infiltrate in the projection of penetration.

Long-term increase temperature, significant tachycardia, high leukocytosis, and symptoms of severe intoxication may indicate suppuration of such an ulcerative infiltrate.

Radiologically, these patients have ulcerative niches large sizes with the flow of contrast mass into neighboring areas (organs).

Treatment.

Treatment of penetrating ulcers in the absence of effect from conservative therapy - surgical. The method of operation depends on the location of the ulcer and the topographic, anatomical and pathomorphological characteristics of the tissues involved in the penetration. The selection method may be following operations: gastric resection according to Billroth -I and Billroth -II, vagotomy with anthrumectomy (economical gastrectomy), vagotomy with drainage operation and removal of the ulcer from the lumen of the gastrointestinal tract (exterritorialization of the ulcer). In some cases, surgery for penetrating ulcers can be extended and combined with resection of the liver and spleen, atypical resection of the pancreas and some other surgical procedures.

Ulcerative gastrointestinal bleeding

Ulcerative gastrointestinal bleeding is the most common and serious complication of gastroduodenal ulcers. It develops in 15-20% of patients with peptic ulcer disease. There is a high mortality rate for this complication - up to 10% or more. The ratio of bleeding gastric and duodenal ulcers is 1:4. It occurs equally often in men and women.

Etiology, pathogenesis

There are bleedings arterial, venous And capillary The source of bleeding is small and large arrozed vessels located in the area of ​​the bottom or edges of an acute or chronic ulcer. Bleeding can also be diffuse against the background of inflammatory and destructive changes in the wall of the organ and erosive or hemorrhagic gastroduodenitis accompanying the ulcer. Most often, bleeding develops from ulcers of the lesser curvature of the stomach and the posteromedial surface of the duodenum, which is associated with the characteristics of the blood supply in these areas.

The patient's response to blood loss is determined by its volume and speed, the resulting deficiency of fluid and electrolytes, the patient's age, and the presence of concomitant diseases.

With blood loss up to 50-100 ml, there is no clinical bleeding and its signs can only be detected by laboratory methods (examination of stool for occult blood - Gregersen reaction). Such bleeding is more common chronic nature but over a certain period of time they can lead to massive blood loss and anemia in patients. In this regard, they are an indication for surgical treatment.

Acute bleeding, which occurs with rapid blood loss of 500 ml or more, is accompanied by characteristic clinical manifestations: hemothemesis - vomiting with contents the color of “coffee grounds” and melena - the release of liquid tarry feces. It is especially necessary to highlight profuse bleeding, when up to 1 liter of blood simultaneously enters the lumen of the gastrointestinal tract and a characteristic symptom complex develops: vomiting blood, melena and hemorrhagic shock.

The compensatory mechanism for blood loss of 500 ml is the rapid redistribution of blood and interstitial fluid.

Systemic vasoconstriction leads to the mobilization of blood from blood depots - the spleen, liver, and the release of antidiuretic hormone and aldosterone restores intravascular volume due to the entry of interstitial fluid into the vascular bed. These changes are accompanied by a decrease in hemoglobin and hematocrit levels, hypoproteinemia, decreased cardiac output, tachycardia, and systolic pressure remains normal or even increased.

With blood loss of more than 1 liter of blood, compensatory mechanisms may fail due to a significant discrepancy between the blood volume and volume vascular bed. This leads to the development of hemorrhagic shock immediately after blood loss or several hours after it.

Clinic and diagnosis, classification of severity of blood loss

When examining a patient with ulcerative gastrointestinal bleeding to select treatment tactics, it is important to obtain answers to the following questions:

1) whether a patient with a peptic ulcer really has blood in the stomach and intestines.

2) exact localization of the ulcer and its characteristics (acute, chronic).

3) what is the severity of blood loss.

4) bleeding has stopped or continues, its nature (arterial, venous, capillary) and intensity, the presence of thrombosed vessels.

The examination plan for a patient with ulcerative bleeding includes studying the medical history, complaints, conducting an objective examination, laboratory tests, and emergency fibrogastroduodenoscopy.

A significant number of patients have a history of symptoms typical of a peptic ulcer: pain after eating or hunger pain, heartburn, nausea and vomiting, seasonality - exacerbations in the spring-autumn period. Bleeding often occurs against the background of an exacerbation of peptic ulcer disease, but it can develop without it, with a generally satisfactory condition.

Even before the classic signs of bleeding from an ulcer appear - vomiting coffee grounds and melena, patients begin to complain of weakness, dizziness, increased sweating, flashing spots before the eyes, tinnitus, nausea, thirst, palpitations, drowsiness. In case of severe blood loss, its first manifestation is loss of consciousness, which often develops while the patient is moving or during physical activity, for example, after defecation. The appearance of vomiting coffee grounds indicates the presence of a source of bleeding in the stomach, and melena indicates the localization of an ulcer in the duodenum.

The results of an objective examination of a patient with ulcerative bleeding depend on the intensity and degree of blood loss. The general condition of the patient ranges from satisfactory to mild degree blood loss to coma in severe cases. Common signs of bleeding are pronounced pallor of the skin and visible mucous membranes, a dry tongue, and a rapid thread-like pulse. Blood pressure initially increases and then tends to progressively decrease. Central venous pressure also decreases.

When examined, the abdomen participates in the act of breathing, is not tense, and is almost always painless on palpation. The disappearance of pain when bleeding from an ulcer occurs due to alkalization of acidic gastric contents by blood is one of characteristic features this complication. Rectal examination reveals tar-colored stool.

An increase in hemoglobin levels is observed in the peripheral blood in the first 2-4 hours after the onset of bleeding. However, subsequently its level decreases, as does the hematocrit level. This decrease is the result of hemodilution, which progresses as bleeding continues. BCC also decreases progressively.

Decisive importance in determining the program of diagnostic and therapeutic measures for ulcerative bleeding is given to emergency fibrogastroduodenoscopy. In terms of information content, it surpasses all other diagnostic methods.

Before the examination, the patient's stomach is washed with cold water through a thick probe. Atropine and promedol are administered over 20-30 minutes, local anesthesia mucous membrane oral cavity and pharynx at the entrance to the esophagus with 1% dicaine solution.

Fibrogastroduodenoscopy allows you to diagnose a bleeding gastroduodenal ulcer, differentiate a benign ulcer from a malignant one, identify other causes of bleeding - stomach tumors, varicose veins of the esophagus, hemorrhagic gastritis, etc. Based on determining the size of the ulcer, the presence or absence of thrombosed vessels at the bottom of the ulcer, assessing the reliability of hemostasis with Taking into account the severity of blood loss during fibrogastroduodenoscopy, the possibility of recurrent bleeding is predicted. If hemostasis is reliable, conservative therapy is carried out, and if there are signs of ongoing bleeding, emergency surgery is performed.

Great importance to determine treatment tactics has an accurate assessment of the severity of blood loss. In surgical practice, it is convenient to assess the severity of bleeding based on clinical data and the results of studies of the blood volume.

There are three degrees of blood loss (according to A.A. Shalimov):

I degree -light- observed with a loss of up to 20% of circulating blood volume (up to 1000 ml in a patient weighing 70 kg). The general condition is satisfactory or moderate, the skin is pale (vascular spasm), sweating appears; pulse 90-100 per minute, blood pressure 100-90/60 mm. rt. Art., anxiety gives way to slight retardation, consciousness is clear, breathing is somewhat rapid, reflexes are decreased, muscles are relaxed, leukocytosis with a shift of the leukocyte formula to the left, oliguria. Without compensation for blood loss, no significant circulatory disorders are observed.

II degree -moderate severity- observed with a loss of 20 to 30% of circulating blood volume (from 1000 to 1500 ml in a patient weighing 70 kg). The general condition is of moderate severity, the patient is inhibited, speaks in a low voice, slowly, marked pallor of the skin, sticky sweat, pulse 120-130 per minute, weak filling, blood pressure 90-80/50 mm. rt. Art., rapid shallow breathing, severe oliguria. Due to vasospasm, blood pressure may be normal or even elevated. However, it can decrease at any time due to the depletion of compensatory mechanisms and vasodilation. Without compensation for blood loss, the patient can survive, but significant disturbances in blood circulation, metabolism and function of the kidneys, liver, and intestines remain.

III degree -heavy- observed with a loss of more than 30% of the circulating blood volume (from 1500 to 2500 ml in a patient weighing 70 kg). The general condition is severe or very severe, the motor reaction is depressed, the skin and mucous membranes are pale cyanotic or spotted (vasospasm is replaced by dilatation). The patient answers questions slowly, in a whisper, often loses consciousness, the pulse is threadlike, 130-140 per minute, periodically cannot be counted or palpated, the maximum blood pressure is from 0-60 to 50 mm. rt. Art., central venous pressure is low, breathing is shallow, rare, limbs and body are cold to the touch, body temperature is reduced. Oliguria gives way to anuria. Replenishment of blood loss can lead to rapid recovery of hemodynamics (labile form). If rapid improvement does not occur, this indicates damage to vital parenchymal organs (torpid form). In this case, as in the labile form, there is dilation of the arteriometarteriolovenular complex with open arteriovenous anastomoses.

Hemorrhagic phenomena are often observed, indicating widespread intravascular thrombus formation; blood oxygen saturation and arteriovenous difference decrease, the general condition worsens, and intoxication symptoms increase.

Without timely compensation for blood loss, patients die due to the death of cells in a number of organs, primarily the liver, kidneys, severe metabolic disorders, and a decrease in cardiac activity. Blood loss of 50-60% of the circulating blood volume causes rapid death from cardiac arrest due to insufficient blood supply to the heart muscle.

Differential diagnosis of ulcer bleeding is carried out with bleeding of non-ulcer etiology and pulmonary hemorrhage. The source of bleeding from the lumen of the gastrointestinal tract can be the following diseases:

1. Varicose veins of the esophagus and stomach with portal hypertension.

2. Mallory-Weiss syndrome (crack in the mucous cardia of the stomach).

3. Erosive hemorrhagic gastroduodenitis.

4. Benign and malignant tumors of the stomach, diverticula.

5. Strangulated hiatal hernia.

6. Bleeding from chemical burns of the stomach.

7. Solinger-Ellison syndrome (endocrine ulcer).

The following lead to the development of acute bleeding ulcers: systemic diseases How hypertonic disease, atherosclerosis, capillary toxicosis, liver cirrhosis, uremia, shock of various etiologies, as well as toxic and medicinal effects on the mucous membrane of the stomach and duodenum (taking salicylates, steroid hormones). Bleeding can also develop from peptic ulcers of previously performed gastrointestinal anastomoses.

All these diseases have clinical symptoms that differ from those of gastric and duodenal ulcers, which should be taken into account first of all when the general signs of gastrointestinal bleeding appear, which are outlined above.

Pulmonary genesis bleeding is established based on the presence of discharge from the oral cavity during coughing of scarlet foamy blood, percussion data, auscultation, and x-ray examination of the lungs.

Treatment

If gastrointestinal bleeding is suspected, the patient is hospitalized in a surgical hospital. Transportation must be carried out lying on a stretcher. After performing emergency fibrogastroduodenoscopy, laboratory tests, and physical examination of the patient, the optimal volume of conservative therapy, indications and urgency of surgical intervention are determined.

Complex hemostatic therapy is carried out. Strict bed rest is prescribed, cold is applied to the epigastric region, the stomach is washed with chilled water. 0.1% is injected into the stomach through a tube solution of adrenaline- 4 ml along with 100-150 ml of 5% aminocaproic acid or give this solution one tablespoon after 15 minutes. Hemostatic therapy is carried out in the following volume (infusion): aminocaproic acid 5%-200 ml, decinone 250 mg, calcium chloride 10%-10 ml, fibrinogen 1-2 g per 250 ml of isotonic sodium chloride solution, vikasol 1%-3 ml in /m. Elimination of volemic disorders and replenishment of bcc is carried out using blood transfusions and its components (in a volume of 60-80% of bcc deficiency), native, dry and frozen plasma up to 200-800 ml, as well as dextrans, albumin, proteins and crystalloids. The objectives of conservative therapy for ulcerative bleeding also include stabilization of hemodynamics using cardiac, vascular and respiratory agents, elimination of metabolic acidosis - sodium bicarbonate 4% -200 ml is administered and restoration of microcirculation with the introduction of rheopolyglucin - 400 ml and trental - up to 10-15 ml per 250 ml of isotonic sodium chloride solution.

In the arsenal of methods for stopping ulcer bleeding, therapeutic fibrogastroduodenoscopy plays an important role. For the purpose of hemostasis, the ulcer is injected with 0.1% solution of adrenaline or noradrenaline, electrocoagulation of the bleeding vessel is performed, the vessel is sutured with a metal clip, laser coagulation, filling the ulcer with medical glue MK No. 6, 7, 8. In specialized institutions, it is possible to embolize a bleeding vessel in the ulcer using superselective injection of an artificial embolus through the femoral artery.

There are emergency, urgent and planned operations for ulcerative bleeding. Emergency surgery is performed within up to 2 hours if bleeding continues II-III degrees severity of blood loss and recurrence of profuse bleeding. Urgent surgery is performed on the first or second day of the disease when bleeding has stopped and there is a blood clot in the ulcer (unstable hemostasis), as well as when bleeding recurs in the hospital.

Planned operations are performed with stable hemostasis, small ulcers, the presence of blood clots and mild blood loss.

When blood pressure drops below 60 mm Hg. and a pulse rate of more than 120-130 beats/min against the background of clinical manifestations of ongoing bleeding, it is necessary to carry out a complex of conservative therapeutic measures in full directly in the operating room. When hemodynamics are restored to level II-III of blood loss severity (BP>60/80 mm Hg, pulse no more than 120-130 beats/min, emergency surgery is performed immediately.

The main goal of the operation is to stop bleeding. At in serious condition The patient's bleeding ulcers of the stomach or duodenum are excised and sutured on the back wall with interrupted sutures. If the patient’s condition allows (BP> 100 mm Hg), then not only stopping bleeding is performed, but also one of the pathogenetically substantiated methods of radical surgical treatment of peptic ulcer. For gastric ulcers - resection of 2/3 with anastomosis according to Billroth-I or Billroth-II in the Hofmeister-Finsterer modification. For bleeding duodenal ulcers, stem or selective vagotomy is performed with excision of the ulcer and pyloroplasty according to one of the methods.

In the postoperative period, patient management is carried out taking into account the severity of blood loss and the volume of surgery. Treatment is carried out in the intensive care unit or intensive care unit. Taking into account the degree of anemia and the severity of the operation, bed rest is prescribed for 4-5 days. After the operation, from the third day, table zero is prescribed, on the fourth or fifth - table 1a, and at the end of the second week - table 1. The gastric tube, which during the operation is left in the stomach or in its stump after washing and the absence of stagnant masses, is usually removed on the third day. On the third day they give a cleansing enema. Sutures from the postoperative wound are removed on days 7-10.

The volume of infusion therapy depends on the deficit of bcc and in the first or second days is 3000 ml - 4000 ml. It contains plasma, protein, albumin, rheopolyglucin, glucose solution, Ringer-Locke solution, other crystalloids, as well as trental, vitamin C, Vicasol. The criterion for the volume and composition of infusion therapy, in addition to the BCC indicator, is the level of central venous pressure, biochemical parameters of blood and urine, and other indicators of homeostasis. Considering that anemic patients are predisposed to infection, antibiotics are prescribed. For patients who have undergone palliative surgery (suturing or excision) for gastrointestinal ulcer bleeding, an examination is recommended after a year and, if an ulcer is detected, a planned radical operation is performed.

Ulcerative pyloroduodenal stenosis

In 5-10% of patients with ulcers, gastric outlet stenosis develops. Its cause in 80% of cases is multiple relapses of duodenal ulcer. Less commonly, narrowing in this zone develops with ulcers of the prepyloric and pyloric parts of the stomach.

Etiology and pathogenesis.

The narrowing of the pyloroduodenal region due to peptic ulcer is cicatricial or inflammatory-spastic in nature. This degeneration of the pylorus leads to its rigidity and non-closure, which creates conditions for constant duodeno-gastric reflux. Penetrating into the stomach, bile components change the pH of the environment to alkaline and this stimulates the secretion of gastrin with an increase in the production of hydrochloric acid and pepsin. The resulting antrum gastritis and hypersecretion of hydrochloric acid create favorable conditions not only for the recurrence of duodenal ulcers, but also for the formation of ulcers in the antrum of the stomach. Constantly alternating periods of exacerbation of peptic ulcer disease and scarring processes are the direct cause of progressive stenosis of the pyloroduodenal region.

In the initial stage of the disease, the size of the stomach is not changed, the wall is somewhat thickened, there is cicatricial deformation of the pyloroduodenal canal, as well as a cicatricial process around the ulcer. The tone of the stomach is normal, and the tone of the pylorus is increased, with symptoms of spasm, and the motility of the antrum of the stomach is increased. Then the stomach stretches, the hypertrophy of its wall increases. In addition to cicatricial narrowing of the pyloroduodenal canal, a pronounced adhesive process in the form of perigastritis and periduodenitis is determined in this area. The tone and motility of the stomach decrease at this stage. Subsequently, as the disease progresses, the stomach becomes sharply distended, its wall becomes thinner, and the patency of the pyloroduodenal canal is reduced to its complete obstruction. In the circumference of the pyloric region, a rough adhesive peri-process in the form of a scar-adhesive “mantle” is determined. The tone and motility of the stomach are sharply reduced, practically absent.

Ulcerative pyloric stenosis is accompanied by severe violations homeostasis associated with the inability to digest food and the loss of large amounts of fluid and electrolytes through vomiting. There may be a significant deficiency of potassium, sodium, chlorine ions, and water deficiency can reach 4-5 liters. As a result of fasting, profound metabolic disorders, intoxication, and severe acidosis develop. The phenomena of catabolism with the breakdown of proteins, fats and carbohydrates are pronounced.

Clinic, diagnosis, classification of stenoses.

Patients with stenosis usually have a long history of ulcers. Many of them had undergone surgery for a perforated ulcer in the past. General symptoms are: weight loss, feeling of early satiety, feeling of fullness in the epigastrium, nausea and vomiting undigested food, eaten several hours or days before.

The severity of clinical, biochemical, radiological and endoscopic changes in a patient with peptic ulcer disease depends on the stage of stenosis

Classification. The following stages of stenosis are distinguished:

1.Compensated stenosis ;

2.Subcompensated stenosis ;

IN stages of compensated stenosis patients complain of nausea, vomiting, a feeling of heaviness in the epigastrium, and belching. The general condition in this stage of stenosis suffers little. With a contrast X-ray examination, the stomach is slightly enlarged or of normal size, peristalsis can be enhanced, there is a moderate narrowing of the pylorus, the contrast agent is retained in the stomach for no more than 12 hours. Fibrogastroduodenoscopy reveals cicatricial deformation of the pyloroduodenal canal with a narrowing of its lumen to 1 cm. Clinical and biochemical parameters are without significant changes.

In phase subcompensated stenosis patients note weakness, thirst, a constant painful feeling of heaviness in the epigastrium, nausea, sour belching, vomiting of stagnant food, rumbling in the stomach. At clinical examination a decrease in body weight, dehydration, decreased skin turgor, and pronounced pallor of the skin are detected. A physical examination reveals splashing of gastric contents, and sometimes gastric peristalsis is visible to the eye through the skin of the anterior abdominal wall. Blood tests show a decrease in hemoglobin levels, moderate leukocytosis, protein and casts appear in the urine. Biochemical studies reveal hypoproteinemia, increased levels of urea and creatinine, increased levels of ALT, AST, changes in the ionogram with a decrease in the content of sodium, chlorine, potassium, magnesium.

On X-ray examination, the stomach is already significantly dilated, has the shape of a bowl, and peristalsis is weakened. There is a pronounced narrowing of the pylorus, a delay in evacuation from the stomach into the duodenum for up to 12-24 hours.

During fibrogastroduodenoscopy, the stomach is distended, contains liquid and poorly digested food. The pyloroduodenal canal is narrowed to 0.3 - 0.8 cm.

Decompensated stenosis characterized by severe weakness, constant thirst, rotten belching, repeated and profuse vomiting of food eaten the day before, which brings temporary relief. In severe cases, seizures may occur. Sharp weight loss, up to cachexia. The skin is earthy in color. The stomach is significantly enlarged in size, its contours are determined when examining the abdomen through the anterior abdominal wall, and the sound of splashing is clearly audible.

Due to severe hypokalemia, the development of gastric or chloriprival tetany is possible, manifested by the occurrence of paresthesias and convulsions, the identification of Trousseau's symptom (“obstetrician’s hand”)

Clinical and biochemical tests determine gross pathological changes.

At x-ray examination there is a sharp expansion of the stomach, sometimes it can occupy the entire abdominal cavity, and the greater curvature in the form of a bowl is visualized in the pelvis. The pyloric region is sharply narrowed or does not fill contrast agent at all. Delay in gastric evacuation - more than 24 hours. On fibrogastroscopy, the stomach is sharply dilated and contains a lot of fluid - up to 8-10 liters. The pyloric canal is cicatricially narrowed to 0.1 cm.

Differential diagnosis ulcerative pyloroduodenal stenosis is carried out with stenosis due to cancer. Cancer stenosis is characterized by a shorter history and absence of clinical manifestations of peptic ulcer disease. The final diagnosis is established based on fluoroscopy and endoscopy. Pyloric stenosis can also be caused by extragastric formations, for example, a tumor of the head of the pancreas. The clinical picture of stenosis is combined with symptoms of obstructive jaundice. The diagnosis is confirmed by ultrasound examination of the pancreas.

Treatment.

Ulcerative pyloroduodenal stenosis - absolute reading to the operation. The objectives of the operation include: removing obstacles to the movement of food from the stomach into the intestines, restoring the passage of food into the duodenum or small intestine, reducing the secretion of hydrochloric acid.

In case of ulcerative pyloroduodenal stenosis, preoperative preparation is required, the volume and nature of which depend on the degree of stenosis and the resulting pathological disturbances and changes in homeostasis.

Without fail, within 4-5 days before surgery, in order to mechanically cleanse and restore the tone of the stomach, it is washed through a probe with solutions of sodium chloride, Ringer-Locke. Infusion therapy for significant fluid losses (during vomiting) can reach a volume of 6-8 liters. It includes correction of the aqueous electrolyte composition of the blood by infusion of Krokhalev solution, physiological sodium chloride solution, Ringer-Locke solution; correction of carbohydrate metabolism with the introduction of 5-10-20% glucose solution; correction of hypoproteinemia with the introduction of plasma, albumin, protein; the introduction of hemodez, rheopolyglucin, dextrans eliminates hypovolemic disorders; in case of anemia, blood is transfused; Vitamin therapy and restorative therapy are carried out. Preparation for surgery includes the elimination of other disorders that are revealed during the examination.

The nature of surgical treatment depends on the stage of stenosis. With compensated and subcompensated stenosis, it is preferable to perform organ-preserving operations: trunk or selective vagotomy with a drainage operation - pyloroplasty, or economical gastrectomy - anthrumectomy. In some cases, gastric resection may be performed using the Billroth-I or Billroth-II method.

At decompensated stenosis, due to significant depression of the motor function of the stomach, its resection is indicated, and vagotomy in in this case inappropriate.

In severe cases, it is possible to perform a stomach drainage operation - gastrojejunostomy.

In the postoperative period, special attention is paid to the early restoration of the motor-evacuation function of the stomach and intestines, as well as syndromic correction of homeostasis disorders.

Malignancy of stomach ulcers

Malignancy– degeneration of a stomach ulcer into cancer. Duodenal ulcers become malignant extremely rarely. This complication is observed in 5-10% of patients with peptic ulcer disease with a long course of the disease. Callous ulcers of the lesser and especially greater curvature (80-90% of ulcers) and the antrum and cardia of the stomach are most often malignized. The size and location themselves cannot be decisive in the differential diagnosis of ulcers and cancer; however, if the size of the ulcerative defect in the stomach is more than 2 cm, one should always think about the possibility of malignancy and, in this regard, it is necessary to conduct a thorough examination of the patient.

Pathomorphological signs of malignant ulcers are the following:

a) in the area of ​​the bottom of the ulcer there is complete destruction of the muscle layer and a wide area of ​​scarring;

b) there is no submucosal layer at the edge of the ulcer, there is infiltration cancer cells from the very initial stages diseases;

c) in the area of ​​the ulcer, signs of cancerous neuritis, endarteritis, and thrombophlebitis are revealed.

Histologically, a malignant ulcer is an adenocarcinoma.

Clinic .

Clinical manifestations of the early stages of degeneration of an ulcer into cancer do not have any features characteristic only of them. The possibility of malignancy of an ulcer may be indicated by Savitsky’s “small signs” syndrome: deterioration in general condition, loss of appetite, aversion to certain types of food, for example, meat, fast fatiguability, mental depression. In the early stages of malignancy, clinical manifestations are insignificant, but as the process progresses, they become more pronounced and are characterized by increasing general weakness, emaciation, changes in the nature of pain, and a decrease in the acidity of gastric juice. In this case, signs of anemia, accelerated ESR are observed, and a positive reaction to occult blood in the stool is often noted.

To recognize the nature of the ulcer, use clinical method, based on the principle of studying the degree of effectiveness of conservative treatment.

Under the influence of active therapeutic treatment within 4-6 weeks, a benign ulcer decreases in size and subsequently scars, while a malignant ulcer does not change significantly. B early diagnosis cancer and in assessing the effectiveness of conservative treatment, the most effective use of radiological and endoscopic methods. An additional X-ray examination will be carried out small defect filling, the periulcer inflammatory shaft becomes wider and asymmetrical. A malignant ulcer niche often has an irregular trapezoidal shape, high, undermined, uneven edges. Fibrogastroscopy currently plays the main diagnostic role. It allows not only to examine the gastric mucosa, but also to perform a targeted biopsy of an ulcer suspicious for malignancy. Be sure to take at least 4-5 pieces from the edge of the ulcer for subsequent histological examination.

Treatment.

If it is established that the ulcer has degenerated into cancer or malignancy is suspected, even in the absence of histological confirmation, surgical intervention is indicated. In his classic monograph “Studies of Gastric Surgery” S.S. Yudin formulated the principles of surgical tactics for a stomach ulcer suspected of malignancy: “The larger the ulcer, the deeper the niche, the older the patient, the lower the acidity - the greater the danger of cancer arising from the ulcer, and therefore, the sooner gastric resection is indicated.”

If during an operation undertaken for an ulcer there is doubt about its nature, then for the differential diagnosis of a callous ulcer and an ulcerated stomach tumor, data on the nature of the lymph nodes of the greater and lesser omentum can be used. With a peptic ulcer, although the lymph nodes may be enlarged in size, they are soft and mobile. When a gastric ulcer becomes malignant, the lymph nodes are usually firm to the touch and have limited mobility. A cytobiopsy of such a lymph node can finally confirm the diagnosis.

The extent of surgical intervention depends on the location of the malignant ulcer. When it is located in the lower and middle third of the stomach, it is performed subtotal resection stomach with removal of the greater and lesser omentum and regional lymph nodes. In cases where the ulcer is located in the upper parts of the stomach, total-subtotal gastrectomy or gastrectomy also with resection of the greater and lesser omentum. The prognosis for malignant gastric ulcers in the case of timely surgery is usually better than for primary gastric cancer, as evidenced by a higher (7 times) five-year survival rate after operations for ulcer degeneration.

CONCLUSION

Prognosis of peptic ulcer depends largely on the age and gender of the patient, the location of the ulcer, the characteristics of the course of complications, concomitant diseases, working and living conditions. With timely recognition and comprehensive comprehensive treatment in the absence of complications, it is usually favorable, and complete recovery is possible.

Prevention is aimed at eliminating possible etiological factors ulcer formation: quitting smoking and alcohol, organizing a work and rest schedule, proper nutrition. Patients with peptic ulcer disease should be under medical supervision. Anti-relapse treatment should be comprehensive, long-term (courses lasting 1.5 - 2 months for at least 5 years from the moment of the last exacerbation). In the normal course of the disease, anti-relapse courses are carried out 2 times a year during the most probable occurrence relapse, i.e. in spring and autumn, with frequent and prolonged exacerbations - 3-4 times a year.

BIBLIOGRAPHY:

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3. Lychev V.G., Nabiulin M.S., Arkhipov A.G. et al. Gastroenterology. Textbook method. allowance. / Barnaul. - 1998. - 159 p.

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Ulcerative bleeding- one of the most common and dangerous complications of peptic ulcer disease, and duodenal ulcers bleed more often than gastric ulcers. Ulcer bleeding usually occurs against the background of symptoms of exacerbation of a peptic ulcer (hunger pain, heartburn, etc.), but in some patients it may be the first sign of a relapse of the ulcer. Hidden (occult) bleeding almost always accompanies an exacerbation of peptic ulcer disease, although, as a rule, it goes unnoticed and is not considered a complication. Usually only massive (profuse) bleeding with hematemesis and melena is diagnosed.

Ulcerative bleeding usually occurs during exacerbation of gastric ulcer, but more often during exacerbation of duodenal ulcer against the background of chronic active gastritis and duodenitis associated with helicobacter pylori infection in patients who have either not undergone eradication therapy or it has not resulted in the elimination of this bacterium in the gastroduodenal mucous membrane. Often, provoking factors in the development of ulcer bleeding, according to our data, are non-steroidal anti-inflammatory drugs (NSAIDs), alcohol and other aggressive factors (coagulants, etc.). Most patients at the time of blood loss experience a fainting state, often short-term, dry mouth, weakness, cold sticky sweat, palpitations, shortness of breath, the urge to defecate with the release of unformed black feces ( tarry stool), bloody vomiting (hematemesis), often with contents like “coffee grounds”. As noted earlier, these symptoms, with varying degrees of severity, are observed in almost all patients with ulcerative bleeding from the upper sections digestive tract.

Depending on the severity of the patients’ condition, they are admitted either to the surgical (stable condition) or to the intensive care (unstable condition) department of the emergency hospital, but all of them need to undergo urgent diagnostic and therapeutic measures, including:

1. Urgent endoscopy of the upper digestive tract and, if indicated, endoscopic hemostasis (irrigation of the inflamed and bleeding gastroduodenal mucosa with liquid thrombin, electro- or laser photocoagulation, clipping and ligation of a bleeding vessel, organoplasma coagulation and other procedures in order to ensure effective hemostasis, which with the help of these measures, according to our data, is ensured in 99.8% of cases).

2. Laboratory and instrumental studies: electrocardiography, general blood test with counting of reticulocytes and platelets, determine hematocrit, creatinine, urea, iron, K, Na+, Ca2+ in the blood, urine and feces analysis, coprogram).

3. Along with endoscopic hemostasis, it is necessary to simultaneously administer an inhibitor intravenously proton pump, for example, the drug Losek 40 mg every 8 hours (in the absence of contraindications, a proton pump inhibitor can be given orally in a triple daily dose) for 3 days. or at least a histamine H2 receptor blocker (quamatel 20 mg or ranitidine 50 mg every 6 hours for 3 days) and at the same time take the drug sucralfate 2 g orally every 6 hours for 3 days.

4. From the 4th day, carry out a 7-day course of eradication therapy, including a proton pump inhibitor (standard dose 2 times a day in the morning and evening hours + clarithromycin 500 mg 2 times a day at the same hours for 7 days), amoxicillin according to 1000 mg 2 times a day or metronidazole (tinidazole) 500 mg 2 times a day at the same hours for 7 days + colloidal bismuth substrate (de-nol, etc.) 240 mg 2 times a day at the same hours for 7 days.

5. After completing the eradication course, it is immediately advisable to prescribe a proton pump inhibitor in a standard dose of 15 g for 6 months. or other antisecretory drug.

If it is possible to implement such tactics for managing patients with ulcerative bleeding associated with helicobacter pylori infection, then relapses of bleeding and exacerbation of peptic ulcer disease stop provided that this bacterium is successfully eradicated from the gastroduodenal mucosa.

Main goals drug treatment peptic ulcer associated with helicobacter pylori and complicated by ulcerative bleeding are:

1) destruction of helicobacter pylori infection in the mucous membrane of the stomach and duodenum;

2) a sharp weakening of the aggressiveness of the gastric and duodenal contents (at a pH level above +, thrombolysis is prevented);

3) increased resistance of the mucous membrane of the stomach and duodenum to aggressive factors(when colonization of the mucous membrane is eliminated, its resistance increases significantly).

Along with this, in the acute period it is necessary to ensure hemostasis, compensate for hemodynamic and other vital resources of the body. If modern scientific and technological achievements are fully used, then success can be guaranteed even without surgical interventions.

Perforation of an ulcer into the abdominal cavity- a serious complication of peptic ulcer disease and symptomatic ulcers. Ulcers often perforate during exacerbations of peptic ulcer disease. Perforation of ulcers is often preceded by physical exertion, filling the stomach with food, drinking alcohol, and neuropsychic stress.

The clinical picture of perforation usually develops acutely, but a careful study of the anamnesis often reveals symptoms associated with exacerbation of peptic ulcer disease. Before perforation, increased pain and the appearance of low-grade fever are possible. often chills, nausea, “unreasonable” vomiting. But the most characteristic symptoms of perforation are undoubtedly a sharp “dagger” pain in the epigastric region, a plank-like tension in the muscles of the anterior abdominal wall, especially the epigastrium, a positive Shchetkin-Blumberg sign, disappearance of hepatic dullness, and bradycardia. pallor of the skin.

6-8 hours after perforation, peritonitis usually develops, characterized by sharp deterioration general condition of the patient (frequent thready pulse, arterial hypotension, fever, phenomena of dynamic intestinal obstruction, leukocytosis with neutrophilic shift). In the first hours, stool and gases are possible, but then flatulence increases, and stool, gas, and even urine are retained. Vomiting is rare.

The diagnosis of ulcer perforation becomes certain if the following signs are present:

1. Sudden onset of acute continuous pain. It should be borne in mind that temporary improvement sometimes occurs 3 hours after its appearance, but it is false and can lead to loss of vigilance of the patient, and sometimes the doctor. In the elderly and patients taking it for a long time steroid hormones, pain and symptoms of peritonitis may be absent.

2. The stomach does not participate in the act of breathing.

3. There are no bowel sounds.

4. When X-ray examination in most patients, gas is detected under the diaphragm, which has diagnostic value, but its presence is not mandatory. Sometimes gas is found in other parts of the abdominal cavity. but this symptom is difficult to interpret, and therefore it is not typical for perforation.

In case of an atypical clinical picture of a perforated ulcer of the stomach and duodenum (covered perforation, perforation into the lesser omentum or into a hollow organ), when a perforated ulcer is combined with other atypically occurring diseases of the abdominal organs, urgent laparoscopy is indicated. If the laparoscopic picture of a perforated ulcer is questionable, a test is recommended that involves pumping air into the stomach through a thin probe.

It is important to note that duodenal ulcers most often perforate, followed in frequency by perforation of the sigmoid colon diverticulum, Crohn's disease and gastric ulcers.

Surgery

1. In all cases, emergency surgical intervention is indicated.

2. Surgical treatment includes suturing the ulcer and covering it with an omentum, as well as excision of the ulcer area with plastic surgery. Conservative treatment is indicated only for some patients who refuse surgery or have a high surgical risk. They need to be provided with intravenous fluids and antibiotics, and continuously pump out gastric contents through a nasogastric tube.

Some surgeons believe it is possible to perform surgical intervention only on those patients who have no effect from conservative treatment, however, this approach to the treatment of perforated ulcers is not justified, moreover, at present, the possibilities of surgical treatment have increased significantly due to the introduction of abdominal laparoscopy into practice.

Most frequent complications perforated ulcers are peritonitis and the formation of a subphrenic abscess.

Peritonitis

Clinical manifestations: fever, forced position, abdominal wall rigidity, symptoms of peritoneal irritation (not always clearly expressed in patients receiving corticosteroid therapy). Bowel sounds are always absent.

Causes: in addition to perforated ulcers, one should keep in mind appendicitis, cholecystitis, pancreatitis, diverticulitis, salpingitis; There are also primary infectious, tuberculous, sclerosing, granulomatous peritonitis, peritonitis in periodic illness (familial Mediterranean fever).

Treatment consists of resuscitation measures and also includes intravenous antibiotics (cefuroxime 750 mg and metronidazole 500 mg 3 times a day). Laparotomy is indicated.

Primary infectious peritonitis is most often associated with infection of the peritoneum by Escherichia coli and Str. pneumoniae and develops predominantly in patients with liver cirrhosis with ascites. To identify the pathogen and determine the sensitivity of the bacterial flora to antibiotics, it is necessary to urgently collect ascitic fluid for microbiological examination. It is necessary to immediately begin intravenous administration of cefotaxime (claforan and other synonyms) - 1 g 2 times a day and then continue antibiotic therapy depending on the results of culture of ascitic fluid.

Tuberculous peritonitis is most often diagnosed by laparoscopy, but it can also be suspected by examining ascitic fluid. Standard anti-tuberculosis therapy should be carried out for 9 months.

Subphrenic abscess- accumulation of pus below the diaphragm and above the liver, spleen or stomach. It is a late complication of a perforated ulcer.

An abscess may also be associated with diverticulitis, destruction of the appendix, or injury to the abdominal cavity with infection of the peritoneum. In some cases, an abscess occurs after abdominal surgery.

Clinic and diagnosis - pain in the abdomen and shoulder, fever, leukocytosis. The diagnosis is suggested by identifying unilateral elevation of the dome of the diaphragm on an x-ray. Typically, a CT scan or ultrasound is required to identify the abscess cavity.

Surgical drainage and prescription of broad-spectrum antibiotics that suppress gram-negative and anaerobic microorganisms.

Penetration of gastric and duodenal ulcers

Penetration refers to the spread of an ulcer beyond the wall of the stomach or duodenum into surrounding tissues and organs. A distinction is made between the stage of ulcer penetration (necrosis) through all layers of the wall of the stomach or duodenum, the stage of fibrous fusion with the adjacent organ, and the stage of completed perforation and penetration into the tissue of the adjacent organ. Ulcers of the posterior and lateral walls of the bulb and postbulbar ulcers of the duodenum often penetrate into the head of the pancreas, biliary tract, liver, hepatogastric or duodenal ligament, into the large intestine and its mesentery; stomach ulcers - in the lesser omentum and body and pancreas.

Penetration is accompanied by the development of the inflammatory process and the formation of fibrous adhesions, sometimes quite extensive. In this case, the pain becomes almost constant, very intense, loses its natural connection with food intake, and does not decrease from taking antacids; Nausea and vomiting intensify, signs of inflammation appear - low-grade fever, leukocytosis, ESR increases. In the area of ​​the pathological focus, pronounced palpation pain is often determined and it is possible to palpate the inflammatory infiltrate.

If an ulcer is diagnosed, its penetration into the pancreas can be suspected if the patient complains of constant persistent back pain, worsening after meals and at night, not relieved by antacids and antispasmodics. The pain is visceral-somatic: from the epigastrium it radiates to the back to the spinous processes of the vertebrae, which often become sensitive upon palpation, sometimes it also spreads to the left, less often to the right, and even becomes encircling.

When an ulcer penetrates into the lesser omentum (more often with an ulcer of the lesser curvature of the stomach), pain from the epigastrium usually spreads under the right costal arch; when penetrating in the direction of the diaphragm (ulcers of the upper parts of the stomach), pain radiates from the epigastrium to the retrosternal space, neck, humeroscapular region, often simulating “coronary” disease; when the ulcer spreads into the mesentery of the colon or small intestine (more often with postbulbar ulcers and anastomotic ulcers), pain extends down to the navel and even to the hypogastrium.

The diagnosis is confirmed by x-ray (deep “niche”, low mobility of the ulcer zone) and endoscopic (deep ulcer, steep crater, edges are usually high, in the form of a shaft) examinations. A penetrating ulcer is often resistant to therapy or continuously recurs, and changes in the wall of the organ and surrounding tissues progress. Treatment is usually surgical.

Perivisceritis (perigastritis, periduodenitis)

During exacerbation of gastric and duodenal ulcers, periulcerous inflammation often reaches the serous membrane. Clinical manifestations of perivisceritis in peptic ulcer disease are determined by both the prevalence of the inflammatory process and its localization. In the acute phase, as a rule, there is some reaction of the serous membrane, detected by palpation (symptom of local muscle tension) and “effleurage” (Mendelian symptom), disappearing in the remission phase. From a practical point of view, not only the severity and localization of inflammation are important, but also adhesive periulcerous processes that change the picture of peptic ulcer disease, disrupting the activity of the stomach, duodenum and other digestive organs. Most often, adhesions form between the pylorobulbar region and the pancreas, between the stomach and liver, adhesions with gallbladder and the colon, even less often scar changes develop in the area of ​​the lesser omentum. With the addition of perivisceritis, the pain of a peptic ulcer becomes more intense, intensifying soon after eating, especially after a heavy meal, with physical activity, change in body position. In the phase of exacerbation of perivisceritis, along with local muscle tension, percussion and palpation pain, radiating pain is often determined by palpation of the abdomen (visceral syndrome with radiating pain).

The localization and irradiation of palpation and percussion pain depend on the location of the ulcer and perivisceritis: “posterior” - perigastritis and “medial” - periduodenitis occur with sharp pain, reminiscent of pain with damage to the pancreas.

Perivisceritis of the gastric outlet and duodenal bulb in the acute phase is often accompanied by impaired patency of the pyloric canal caused by an inflammatory infiltrate around the ulcer, and possibly adhesive process. Typically, adhesive deformity develops during a long-term recurrent course of peptic ulcer disease.

With perigastritis in the area of ​​the lesser curvature of the stomach, according to the localization of the ulcer and periulcerous inflammation, palpation pain is determined in the epigastrium and often radiates to the right hypochondrium. Far advanced recurrent perigastritis of this localization can lead to shortening and wrinkling of the lesser curvature of the stomach and the pyloric region being pulled towards it. When the ulcer is localized in the duodenum, periduodenitis is often accompanied by deformation of its bulb.

Fibrous and inflammatory changes in the serous membrane of the duodenum, its adhesions with neighboring organs and scars can cause deformation of the intestine with a narrowing of its lumen.

Perivisceritis may be accompanied by low-grade fever, increased ESR, hyperfibrinogenemia, the appearance of C-reactive protein in the blood and other indicators of inflammation. During laparoscopy, signs of the inflammatory process and adhesions are detected serosa stomach and/or duodenum, during gastroduodenoscopy - along with an ulcer, often deep and large, pronounced and widespread inflammation of the mucous membrane, deformation of the wall and impaired mobility of the affected organ are revealed.

Treatment of peptic ulcer disease in the acute phase, complicated by perivisceritis, does not differ significantly from generally accepted guidelines. In some cases, the use of physiotherapeutic procedures (sinusoidal modulated currents, microwave therapy, peat and mud applications) is justified.

Pyloric stenosis- a complication of peptic ulcer disease, more often occurs when a recurrent ulcer is localized in the pyloric canal and the initial part of the duodenal bulb.

Violation of the pyloric patency during exacerbation of peptic ulcer disease is aggravated by periulcerous inflammatory edema and its spasm. An exacerbation of a peptic ulcer with developing pyloric stenosis is accompanied by a feeling of pressure and fullness in the epigastric region that occurs immediately after eating. nausea and vomiting, which brings relief. Appetite disappears, and body weight may drop. Antiulcer treatment provides subjective improvement, but with a recurrent ulcerative process, pyloric stenosis quickly progresses and enters an organic, decompensated stage. Vomiting becomes constant, and splashing sounds appear. On an empty stomach, a large amount of contents is detected in the stomach. Progressive weight loss is observed and hypochloremia and hypokalemia occur. azotemia, alkalosis. During X-ray examination, at this stage the stomach takes the form of a “stretched bag” with weak peristalsis, its emptying is slowed down to 24 hours or more.

The endoscopic picture of decompensated stenosis with a sharp depression of the motor function of the stomach, active pangastritis, and rough relief of the mucous membrane, although typical, still often complicates the visual differential diagnosis of cicatricial ulcerative and cancerous stenoses. In this situation, the diagnosis should be based on the result of histological examination of the biopsy material.

Before surgical treatment, it is necessary to pump out gastric contents through a nasogastric tube and intravenously administer an isotonic sodium chloride solution (2-Zl/day), glucose solution (1-2 l/day). vitamins (ascorbic acid, nicotinamide, cocarboxylase, vitamins B6, B12, etc.). Transfusion of polyglucin and rheopolyglucin is often required. albumin, red blood cells, potassium chloride. Under the control of a coagulogram, vikasol and dicinone are used. In connection with the introduction of parenteral nutrition into clinical practice, it has become possible to correct disorders of nitrogen metabolism both before surgery and in the early postoperative period (see parenteral nutrition).

Currently, endoscopic balloon dilatation is used in some cases for pyloric stenosis, but it is less effective than surgery.

Regardless of the method of surgical treatment, it is advisable for patients to undergo a full course of antiulcer therapy in the preoperative period.