Acute and stress ulcers

Acute or stress ulceration of the mucous membrane of the organs of the gastrointestinal tract is a frequent complication in the victims with burns, severe injuries and in the wounded with gunshot wounds.

Especially often, these complications occur in patients and patients with severe cardiovascular, respiratory, hepatic and renal insufficiency, as well as in the development of purulent-septic complications. Acute erosion and ulcers of the gastrointestinal tract are often complicated by bleeding or perforation. The frequency of stress ulcers in the stomach and duodenum in patients after wounds is 27%, in patients with mechanical trauma - 67%. The total frequency of occurrence of stress ulcers is 58%. Stress ulcers were complicated by bleeding in wounded in 33%, in victims with mechanical trauma - in 36% of cases. The overall lethality with complicated acute erosions and ulcers of the digestive canal remains very high and, according to different authors, varies from 35 to 95%.

A characteristic feature of these lesions is that they quickly arise and in most cases heal with a favorable course of the main pathological process and normalization of the patient's general state for a short time.

[1], [2], [3], [4], [5], [6], [7], [8], [9]

How do stress ulcers develop?

Until recently, it was believed that stress ulcers affect mainly the stomach and less often the duodenum. However, in reality they are found in all parts of the intestinal tube. And for each site of the gastrointestinal tract, certain damaging agents are characteristic.

The proximal parts of the gastrointestinal tract (stomach and duodenum) are affected most often. Firstly, almost all aggressive factors act here on the mucous membrane: hydrochloric acid, proteolytic enzymes, intestinal contents in antiperistalsis and reflux, microorganisms with achlorhydria, lysosomal enzymes with aggravation of autolytic processes, ischemia of the mucosa and filtration of slags through it. Thus, the number of aggressive agents damaging the mucosa in these departments is maximal. Secondly, the essential point is that qualitatively these factors of aggression far exceed those that act in other parts of the digestive canal. In thin and especially in large intestines, food has largely been decomposed into constituent parts, having previously undergone mechanical and chemical treatment. Therefore, in the distal direction along the intestinal tube the intensity of the "destructive" forces decreases, the chyme adapts ever more to the environment of the organism.

In the victims with multiple and combined trauma, complicated by shock, we can feel the energy deficit, in connection with which the "emergency reserve" of energy in the body is consumed - glucose. Its mobilization from the liver depot occurs very quickly and hyperglycemia is observed within a few hours after trauma or injury.

Later, against the background of energy hunger, there are sharp changes in blood glucose level (intravenous infusions play a role in this), which is a stimulating factor for the vagus nerve nuclei, which leads to an increase in acidic gastric secretion and an increase in the digestive capacity of gastric juice. In conditions of stress, this mechanism can cause the predominance of factors of aggression over the factors of protection, that is, be jazvagenennym.

Severe trauma, as well as endogenous intoxication lead to dysfunction of the adrenal cortex, which, in turn, leads to increased secretion of glucocorticoid hormones. The expediency of "ejecting" glucocorticoid hormones into the bloodstream is to stabilize the hemodynamic parameters. But there is another side to the action of these hormones, which consists in stimulating the vagus nerves, loosening the mucous membrane of the stomach and reducing the production of mucopolysaccharides. The situation described above is traced - there is a stimulation of the digestive capacity of the stomach with reduced resistance of the mucous membrane.

In the first 8-10 days after a severe trauma, an increase in acidic gastric secretion is observed with maximum figures on the third day, which can be regarded as a reaction of the body to stress.

In the immediate time after the injury, a significant decrease in pH occurs, and the "peak" of acidity corresponds to the most probable time of ulceration. In the following, starting from the second week after the injury, the level of acidic gastric secretion decreases.

In the next 24 hours after injury, the rate of intragastric proteolysis is significantly increased. In patients with uncomplicated stress ulcers and in patients with ulcers complicated by hemorrhage, the indices of acid-peptic aggression of the stomach are significantly higher than the corresponding average indicators. These data indicate that in patients with shock in the next few hours and days after injury, increased acidic gastric secretion and intragastric proteolysis plays an important role in the formation of stress ulcers of the stomach and duodenum.

In the case of stress ulceration of the mucous membrane of the stomach and duodenum, a number of proteolytic enzymes are activated, the pH-optimum of which varies from 1.0 to 5.0. A high enzymatic activity was also established at pH 6.5-7.0. The source of such activity can be lysosomal enzymes, released as a result of the destruction of lysosomal membranes.

One of the reasons for the destruction of lysosomal membranes and the release of intracellular cathepsins under stress can be the activation of lipid peroxidation (LPO) and excessive accumulation of its products, which leads to the development of lipid peroxidation syndrome. This syndrome includes such pathogenetically related components as damage to membrane lipids, lipoproteins and proteins, swelling followed by destruction of mitochondria and lysosomes, and as a result - cell death and local destruction of the mucous membrane. In addition, oxygen radicals interact with the products of arachidonic acid metabolism and stimulate the formation of thromboxanes, which reduce blood supply to the gastric mucosa due to vascular spasm.

Many authors have shown that under stress, the stability of lysosomal membranes is reduced, accompanied by the release of lysosomal enzymes beyond the lysosomes into the cytosol of the cell, and then into the stomach cavity. This process provides the initial formation of a defect in the gastric mucosa, and the subsequent connection of the secretory protease system is the final formation of the ulcer.

In the first few days after a severe trauma, the activation of LPO processes in the tissues of the body, including in the mucous membrane of the stomach, results in the destruction of cell and lysosomal membranes, the release of activated lysosomal enzymes, and excessive blood circulation and the tissues of aggressive peroxidation intermediates and free radicals (Figures 9.5 and 9.6).

The activity of lipid peroxidation in the blood serum and gastric juice in patients with shock is not the same in the absence of complications and with the development of multi-organ failure and acute ulcers of the gastrointestinal tract.

The formation of stressful or acute ulcers of the gastrointestinal tract is characterized by significant differences in the level of LPO processes. The first peak of LPO activity is observed in the first 2-4 days after trauma, when, as a rule, stress ulcers occur. The second peak of lipid peroxidation activity and the formation of true acute ulcers are observed in the victims with severe complications resulting in the development of multiple organ dysfunction on the 9-17th day after the trauma.

A similar picture is observed in gastric juice. Most violations of systemic hemodynamics, acid-base state, protein and electrolyte metabolism in patients with various complications begin to develop from 7-8 days after injury, that is, at the time when acute gastrointestinal ulcers are formed, complicated by bleeding or perforation.

Already in the first hours after the injury, there are signs of acute local or total inflammation of the mucous membrane of the stomach and duodenum. By the end of the first day there is swelling and loosening of the mucosa. After 2-3 days, the folds become coarser, thicken and poorly straightened with air insufflation. The mucous membrane gradually acquires increased vulnerability and bleeding. Often reveals submucous hemorrhages, sometimes becoming a drainage character.

After 3-4 days against the background of an inflammatory reaction of the mucous membrane, there are stress erosions of a linear or oval form, which, when combined, form defects of irregular shape.

What do stress ulcers look like?

Stress ulcers that occur against the background of an inflammatory reaction of the mucous membrane have distinct edges, a round or oval shape. The bottom of them is usually flat, with necrosis of superficial epithelium of black color, sometimes on the periphery of the ulcer there is a bright rim of hyperemia. Subsequently, after rejection of necrotic tissues, the bottom of the ulcer becomes bright red and sometimes bleeds. The size of the ulcerative defect, as a rule, does not exceed 2 cm, although ulcers and large diameter are sometimes found.

Such stressful erosive and ulcerative lesions of the mucous membrane of the stomach and duodenum occur in the majority of the affected. The degree of severity of the inflammatory reaction depends on the severity of the injury.

Another morphological picture of the mucous membrane of the gastrointestinal tract is observed in the development of severe purulent complications. The mucous membrane of the stomach is ischemic and atrophied. There are true acute ulcers. Ulcerative defects are usually large in size and are localized, as a rule, in the outlet stomach. Inflammation of the mucosa is absent. The leading role in the genesis of acute ulcers is played by vascular disorders leading to ischemia and suppression of the protective factors of the mucous membrane.

These disorders consist in an increase in the tone of small arteries and arterioles, plasma saturation, proliferation, and sloughing of the endothelium. In the capillaries adjacent to the hemorrhagic infarction zone, thrombi are often detected. Often, the pathological process involves the muscle layer of the wall of the stomach or intestine, hemorrhages occur in the submucosa. There are desquamation and degeneration of the epithelium and often - focal necrosis in the mucosa and submucosal layer. A characteristic feature of all changes is the predominance of dystrophic processes over inflammatory and, as a consequence, a greater probability of perforation of acute ulcers.

Excretion of the mucous membrane of stomach slag (urea, bilirubin, etc.) is an additional factor that damages the mucous membrane.

With progressive peritonitis and wound infection, the affected patients develop an enteral insufficiency syndrome, one of the clinical manifestations of which are acute ulcers of the gastrointestinal tract. The occurrence of such ulcers is associated with impaired function of the intestinal tube and other organs and systems (violation of microcirculation in the wall of the stomach and intestine, increased thrombus formation in small vessels of the gastrointestinal tract wall, aggressive influence on the mucous membrane of the stomach and urea and other aggressive metabolic factors and t etc.). Thus, damage to the mucous membrane of the gastrointestinal tract is one of the first manifestations of multiple organ failure.

Localization of stress ulcers

Ulcerations at various sites of the digestive tract can be represented as follows.

In the proximal part of the stomach, hypersecretion of hydrochloric acid and increased intragastric proteolysis occur. It is at this stage that the main mechanism for the occurrence of acute ulcers is the intensification of the factors of aggression.

In the output department of the stomach, the factors of acid-peptic aggression act on the mucous membrane (as well as in its proximal parts). In addition, a sufficiently aggressive factor is bile, which enters the stomach as a result of duodenal gastral reflux. Ischemia of the mucous membrane plays an important role in the acute gastric ulcer in the outlet stomach. Therefore, in the genesis of acute ulcer formation, against the background of the intensification of the factors of aggression, the weakening of defense factors begins to play a significant role. The destruction of the mucous membrane, as a rule, large, single, often complicated by bleeding, sometimes perforation. There are, as a rule, stress ulcers, but marked by the formation and acute ulcers.

In the duodenum, bile acids, lysolecithin and enzymes of the pancreas are added to the aggression factors acting on the mucous membrane in the output stomach. Acute ulcers in the duodenum especially occur when the function of pyloric pulp and the preservation of the secretory function of the stomach. In this case, the acid-peptic factor, strengthened by proteolytic enzymes of the pancreas, with all its might crashes onto the mucous membrane of the duodenum, the protective forces of which are largely weakened due to a violation of the blood supply to its wall and a violation of the synthesis of mucopolysaccharides. In addition, the microbial factor can act in the duodenum. Stress ulcers prevail over the acute ones.

In the small intestine, the effect on its mucous membrane of the acid-peptic factor is minimal. Of acid-peptic aggression, only pancreatic enzymes play an important role. In the emergence of destruction of the mucous membrane, the role of the microbial factor increases. Disturbances of microcirculation in the intestinal wall are quite significant, and as a result, trophic disorders of the mucosa in their importance come out on top. These are true acute ulcers, which were sometimes called trophic ulcers. This title reflects the essence of the formation of these ulcers. Acute ulcers in the small intestine, as a rule, are solitary and occur against the background of purulent-septic complications in the development of enteric insufficiency. Strictly speaking, acute ulcers are one of the morphological manifestations of enteral insufficiency. Moreover, the true acute ulcers of the gastrointestinal tract are often also a manifestation of multi-organ failure, as a rule, its "markers". Acute ulcers are most often complicated by perforation of the intestine due to thrombosis of the vessels in its wall at the level of the microcirculatory bed. Bleeding acute ulcers of the small intestine is complicated extremely rarely, since they occur in the ischemic wall. Stress ulcers in the small intestine are rare.

In the large intestine, with the development of multiple organ failure, pronounced ischemia of the intestinal wall takes place, which leads to a significant weakening of the protective properties of the mucosa. Disturbances in the protective properties of the mucosa are aggravated by metabolic disorders in the intestinal wall. Against this background, exposure to the mucosa of active lysosomal enzymes leads to the formation of local, most often single, destruction of the mucosa. Additional factors of aggression are slags (creatinine, urea, bilirubin), the excretion of which is carried out by the mucosa of the colon, as well as highly pathogenic microbial associations that grow on the ischemic and weakened mucosa. Acute ulcers in the large intestine are also a manifestation of multiple organ failure, but are rare. Multiple organ failure is either amenable to intensive therapy, or progresses, and such patients usually do not live up to the formation of acute ulcers in the large intestine.

Differential diagnosis of stressful and acute ulcers

Between the stressful and acute ulcers of the gastrointestinal tract, there are fundamental differences. Stress ulcers occur against the background of stress - mental, surgical, traumatic, wounded. Usually it occurs in the time from several hours to several days after the impact of stress factors. Acute ulcers occur much later - from 11-13 days after the onset of the disease, performing surgery, getting injured or injured. As a rule, acute ulcers occur due to depletion of the body's defenses against the backdrop of development of severe (most often purulent) complications and multiple organ failure. They are sometimes the first manifestation of enteric insufficiency.

In recent years, more attention has been paid to the syndrome of enteric insufficiency, which develops in victims who are in serious condition, the intestinal tube of which may be a kind of reservoir of pathogenic bacteria and a source of various infections. The number and pathogenicity of bacteria contained in the lumen of the gastrointestinal tract, significantly increase in patients in critical condition. To describe such states, a special term is proposed - "intestinal sepsis". Under certain circumstances, bacteria can penetrate the mucosal barrier of the intestinal wall and cause a clinical picture of sepsis. This process is called microbial translocation.

Initially, there is an excessive colonization of bacteria, and then "sticking" them to the surface of epithelial cells. Further live bacteria penetrate the mucous barrier and reach the lamina propria, after which they actually turn out to be outside the gastrointestinal tract.

Mechanical gut protective factors normally limit the ability of bacteria to reach the mucosal epithelium. In the small intestine, normal peristalsis prevents a prolonged bacterial stasis in the immediate vicinity of the mucous membrane, which reduces the likelihood of bacteria entering through the mucus layer and "sticking" to the epithelium. When peristalsis of the intestine is broken, most often due to paresis and mechanical intestinal obstruction, there is an increased risk of bacteria penetrating through the mucus layer and "sticking" to the mucosal epithelium.

Complete replacement of epithelial cells of the small intestine occurs within 4-6 days. Thus, the process of renewal of epithelial cells leads to a significant limitation of the number of bacteria that "stick" to the surface of the epithelium.

Many protective mechanisms that prevent the occurrence of bacterial translocation are violated in patients in serious condition, with the risk of multiple organ dysfunction. In such patients, there are often significant disorders of the immune system and the administration of antibiotics can significantly disrupt the ecology of the intestinal microflora, leading to an excessive growth of pathogenic bacteria. The use of antacids through the mouth and H2-histamine receptor blockers can lead to excessive colonization of bacteria in the stomach due to their increased survival. Hyperosmolar nutrient mixtures administered enterally and parenterally not only disrupt the normal ecology of the intestinal microflora, but can lead to mucosal atrophy and damage to the mechanical barrier of the intestine. Hypoalbuminemia, as a rule, leads to edema of the intestinal wall, a decrease in peristalsis of the intestine, stasis of intestinal contents, excessive growth of bacteria and disruption of the permeability of the intestinal wall.

Of all the organs of the gastrointestinal tract, the stomach is most sensitive to hypoxia. Hypoxia, often observed in the wounded and injured, helps reduce the tone of the pyloric sphincter, which leads to reflux of the contents of the duodenum into the stomach. In combination with hypercapnia, hypoxia increases gastric secretion.

The small intestine is also sensitive to ischemia, and in a critical situation the organism "sacrifices" it to save vital organs.

One of the main causes of gastrointestinal ischemia in blood loss, along with a significant decrease in the volume of circulating blood, is the release of a large number of vasopressor substances - adrenaline, angiotensin, vasopressin, as well as endotoxins of E. Coli, having sympathetic properties. In this case, the most affected part of the intestine, the blood supply of the upper mesenteric artery. It is in this area of the intestinal tube (in the duodenum and jejunum) that the a-receptors predominate, that already at the very onset of the development of hemodynamic disorders leads to ischemia and deep hypoxia of the intestinal wall. As a rule, much less lesions are noted in the colon, in the wall of which beta receptors predominate.

With the progression of pathological changes, primary vasospasm is replaced by congestive fullness due to the expansion of precapillary sphincters and the preservation of increased tone of postcapillary venules.

Rapidly increasing disturbances of microcirculation lead to damage to the mucous membrane that spreads from the submucosal layer to the lumen of the intestine. The development of hypoxia leads to an increase in the permeability of cell and lysosomal membranes for enzymes. Activated proteolytic enzymes (pepsin, trypsin) and lysosomal hydrolases (acidic phosphatase, beta-glucuronidase) destroy the mucosa, the resistance of which is reduced due to impaired blood supply, inhibition of synthesis and destruction of mucin. The proteolytic enzymes of bacteria play a great role in the pathogenesis of the intestinal mucosa lesion.

A large number of microbes and toxins, aggravating endogenous intoxication, enters the systemic bloodstream due to violation of the barrier function of the gut. Significant restriction of the blood supply to the small intestine leads to disruption of parietal digestion. In the lumen of the small intestine microorganisms multiply rapidly, the processes of fermentation and decay are activated with the formation of toxic under-oxidized products and fragments of protein molecules. The enzymes released by enterocytes enter the systemic circulation and activate proteases. The development of the syndrome of enteral insufficiency leads to the emergence of a vicious circle of pathological processes.

[10], [11]

Treatment of stressful and acute ulcers

Preventive treatment of stress ulcers must necessarily be divided into two groups - general measures, the so-called nonspecific prevention, and activities that directly affect the mucosa of the gastrointestinal tract.

Treatment of general order is aimed at eliminating violations of hemodynamics, hypoxia, metabolic disorders, and also requires adequate anesthetic management.

Activities that directly affect the mucous membrane of the gastrointestinal tract include the use of drugs that reduce the damaging effect of aggressive factors on the mucosa.

A good measure to prevent the formation of stress ulcers of the stomach and duodenum is the intragastric administration of concentrated (40%) solutions of glucose. Glucose helps to restore the energy balance of mucosal cells, increases blood sugar, which is accompanied by a decrease in the excitation of the nucleus of the vagus nerve, the weakening of the neuro-reflex phase of gastric secretion and stimulation of secretion of bicarbonates and mucus. And, finally, it can be assumed that concentrated glucose solutions entering the duodenum inhibit the third, intestinal, phase of gastric secretion. Usually, the patient is injected into the stomach 50-70 ml of a 40% glucose solution twice a day.

To prevent self-digestion of the gastric mucosa in conditions of increased activity of the factors of acid-peptic aggression, it is necessary to introduce protein preparations into the stomach, which to a large extent "distract" the active proteolytic enzymes. To this end, during a day through the probe patients are injected into the stomach solution of egg protein (a protein of three eggs, mixed in 500 ml of water).

With the purpose of reducing the activity of lysosomal enzymes and suppressing intracellular proteolysis, it is advisable to inject patients with contraceptives of 40-60 thousand units daily.

Reduction of the ulcerative action of serotonin is achieved by the introduction of a peritol through the gastric tube 30 ml 3 times a day as a syrup. Peritol (cyproheptadine hydrochloride) has a pronounced antihistaminic and antiserotonin effect, has anticholinesterase activity, antiallergic effect. In addition, this drug has a sedative effect.

Given that the main factor in the formation of stress ulcers of the gastrointestinal tract is acid-peptic aggression, preventive measures against the formation of stress ulcers in the wounded and those with severe trauma, should be carried out under the control of the pH of the intragastric environment. Ideally, especially in patients with an increased risk of stress ulcers, it is necessary to organize pH-metric monitoring. If the pH of the intragastric content is lower than 4.0, antacid and antisecretory drugs should be prescribed. It is optimal to maintain the pH at 4-5, since it is in this range that practically all hydrogen ions are bound, and this is quite enough to significantly suppress the activity of intragastric proteolysis. Raising the pH above 6.0 is not advisable, since it leads to the activation of pepsin secretion.

All antacid substances are divided into preparations of systemic and local action. Antacid preparations of systemic action include sodium bicarbonate (soda) and sodium citrate. Of antacid preparations of local action, mention should be made of calcium carbonate precipitated (chalk), magnesia and magnesium hydroxide, magnesium carbonate basic, magnesium trisilicate and aluminum hydroxide. Alkaline mineral water and food antacids are also used as antacid agents of local action.

In addition to these antacid preparations, combined preparations are currently used - vikalin, vicar (roter), almagel, phosphalugel, gaviscon, gastalus, galusillac, aludrox, kompensan, azidrin, etc.

The greatest curative effect among antacids has aluminum preparations, combining such properties as duration of action, pronounced adsorbing, neutralizing, enveloping and cytoprotective effects.

Abroad, antacids such as maalox, maalox-1K, maalox TC, alyudrox, milant, milant II, delicid, gastrogel, gelucil, ulcasan, talcide are most often used abroad. In our country, Maalox is the most common of these drugs. Using it to prevent stress ulcers reduces the risk of their development to 5%. The most optimal for this purpose is the use of maalox-70. Maalox-70 is injected 20 ml every hour into the gastric tube.

Prevention of stress ulcers

Adequate prevention of stress ulcers is ensured by the maximum reduction of acid production by parietal cells. There is no doubt that one of the most powerful drugs that suppress acidic gastric secretion are blockers of histamine H2-receptors. The first effective drug from this group, widely used, was cimetidine (cinamed, cimetine, tagamet, histodil, belomet).

When carrying out complex prophylaxis of stress ulcers, it is preferable to appoint blockers of histamine H2 and H2 receptors of the second and third generations once in maximum doses per night (ranitidine 300 mg or famotidine 40 mg), since it is important to prevent nighttime hypersecretion in the prevention of stress ulcers, and in the daytime the use of antacids, special nutrient mixtures, as well as early enteral nutrition provides a sufficient reduction in the acidity of the intragastric contents and an adequate counter Gov. Effect.

As antisecretory drugs, compounds selectively acting on M-cholinergic receptors are used. Of the entire large number of anticholinergic drugs for the prevention of stress ulcers of the gastrointestinal tract, only a few are used. It is gastrobamate (a combination drug with ganglion blocking, cholinolytic and sedative effect), atropine, metacin (besides antisecretory it also has an antacid effect and normalizes gastric motility), probantine (more pronounced anticholinergic action than atropine), chlorosyl (has a more pronounced and longer , than atropine, anticholinergic action).

The most effective drug from this group to prevent the occurrence of stressful gastroduodenal ulcers is gastrotsepin (pyrenesin). The combination of gastrocepin with H2-receptor blockers of histamine and antacid preparations is a highly effective means of preventing the occurrence of stressful gastroduodenal ulcers.

Decompression of the stomach and prevention of the dilatation of its antrum in the early period after surgery, injury or trauma to a certain extent reduces the gastrin stimulation mechanism of secretion.

Of the medicinal preparations that are important for the prevention of stressful gastroduodenal ulcers, it should be noted proglumida, somatostatin and secretin. Secretin is administered intravenously drip in a dose of 25 units / h. At the same time, it stimulates not only the formation of bicarbonates, but also the production of somatostatin, produced by antrum D-cells of the stomach. On the one hand, somatostatin brakes on the paracrine mechanism the production of gastrin, on the other - it inhibits insulin, thus suppressing vagal secretion. Enter somatostatin intravenously in a dose of 250 mcg / h. In addition, secretin and somatostatin reduce blood flow in the mucous membrane of the stomach and duodenum, and therefore are prescribed to patients with stress gastroduodenal ulcers complicated by bleeding.

From preparations that promote mechanical protection of the mucous membrane of the gastrointestinal tract, bismuth preparations, vikalin, vicair, vinylin (balm Shostakovskogo, de-nol) have become widely spread in clinical practice. De-nol has a pronounced bactericidal action against Helicobacter pylori due to the de-nol release of a free active bismuth ion that penetrates into the bacterial wall. And, unlike other antibacterial agents, de-nol due to close contact with the mucous membrane has a bactericidal effect not only on the surface of the integument epithelium, but also in the depth of folds. It is most convenient to prescribe to patients a liquid form of the drug, while diluting 5 ml of the drug in 20 ml codes.

Another effective preparation that protects the mucous membrane of the gastrointestinal tract from the influence of aggressive factors is the complex aluminum-containing sulfated disaccharide sucralfate (venter).

Of domestic drugs of a similar effect, two are worth mentioning - zinc sulfate and ampol. Zinc sulfate is administered orally 220 mg three times a day and has an antiseptic and astringent effect, and also stimulates the production of mucus. Amipol, produced as a dietary cookie "Amipol", when it gets into the stomach dissolves (it can be introduced through a probe, previously dissolved in water) and as a result of the reaction with hydrochloric acid, a protonated amipol is formed. Upon contact with the damaged surface of the mucous membrane, the protonated amyl is a gel-like layer that covers this surface and protects it from the influence of aggressive factors.

It is well known that any hypovitaminosis adversely affects the vital activity of the organism and during reparative processes after injuries, injuries and surgeries. Forced starvation of victims in the first few days after injuries and injuries, especially if they underwent surgery, creates additional prerequisites for the development of hypovitaminosis, so the appointment of balanced multivitamin mixtures is all the more justified.

The biostimulants - aloe extract, bilsed, FIBS, pelloidodistillate, peolidin, polybiolin, colanchoe juice, etc., were quite widespread for the restoration and stimulation of the body's defenses.

To a large extent, the regenerative function of the patient's body increases the parenteral administration of protein preparations (plasma, albumin solution), as well as protein hydrolysates (aminopeptide, aminocrine, etc.). The regenerative capacity of the organism increases the combination of the introduction of protein preparations with anabolic hormones - methandrostenolone, nerobol, turinabol, retabolil, and methylandrostenediol.

To prevent the formation of acute ulcers of the gastrointestinal tract, retabolil is best suited for the victims, since it improves the repair processes in the mucous membrane of the gastrointestinal tract to the greatest extent and, in addition, causes a significant increase in protective mucus formation. To prevent the formation of acute ulcers, the drug should be administered in a dose of 1-2 ml per day of admission of patients to the hospital.

Pyrimidine derivatives (methyluracil (methacil), pentoxyl, potassium orotate) also have a beneficial effect in preventing the occurrence of acute gastrointestinal ulcers.

The overwhelming majority of victims, especially with the development of multi-organ failure, there are violations of immune homeostasis, leading to a violation of the regulation of regenerative processes and the development of dystrophic changes in the patients' body. In this regard, for the prevention of acute ulcers of the gastrointestinal tract, it is absolutely necessary to use the means regulating the state of immunity. These are drugs such as feracryl, decaris (levamisole), thymopentin and sodium nucleate. They combine the effects of immunostimulants and reparants.

Decaris (levamisole) restores the functions of T-lymphocytes and phagocytes, increases the production of antibodies, complement components, enhances the phagocytic activity of neutrophilic leukocytes and macrophages.

Timalin stimulates the immunological reactivity of the body (regulates the number of T and B lymphocytes), the reaction of cellular immunity, enhances phagocytosis. To a large extent, thymaline also stimulates regeneration processes. In order to prevent the formation of acute ulcers, thymalin is administered daily 10-20 mg intramuscularly.

Drugs capable of increasing the stability of the gastrointestinal mucosa include prostaglandins, antihypoxants and antioxidants, nonspecific stabilizers of cell membranes, agents that correct energy metabolism disorders, blockers of the functional activity of mast cells and neutrophilic granulocytes, stimulants of mucosal metabolic activity, neuroleptics, derivatives phenothiazine, epidermal growth factor, retinol, pentagastrin, and others.

The increase in the resistance of the organism and the stability of the cells of the gastric epithelium to various aggressive influences is to a great extent due to the elimination of hypoxia and its consequences, in particular, to a decrease in the activity of lipid peroxidation processes.

Hypoxia is a condition that results from either limiting the flow of oxygen into the cell, or in connection with the loss of the ability to utilize it in biological oxidation reactions. A new approach to eliminating hypoxia is the use of antihypoxic drugs. Antihypoxants are a class of pharmacological substances that facilitate the reaction of tissues to hypoxia or even prevent its development, as well as accelerating the processes of normalizing functions in the posthypoxic period and increasing the resistance of tissues and the body as a whole to oxygen deficiency.

A number of substances with antihypoxic effect have been synthesized in our country and abroad. These include sodium oxybutyrate (GHB), piracetam (nootropil), amtisole. Sodium oxybutyrate serves as a redox buffer, eliminating the deficit of the oxidized form of nicotinamide adenine dinucleotide (NAD) developing during hypoxia, normalizes the processes of oxidative phosphorylation, binds toxic products of nitrogen metabolism, and also stabilizes cell membranes. To prevent the formation of acute ulcers of the gastrointestinal tract, GHB should be administered intravenously at a dose of 50-75 mg / kg per day in 200 ml of physiological saline in combination with potassium preparations.

Amtizol is an antihypoxant of the second generation, which has proven itself in severe shockogenic trauma, accompanied by massive blood loss and hypoxia of various genesis. The inclusion of amtisol in the complex therapy leads to an improvement in hemodynamics and functions of the central nervous system, an increase in the oxygen content in tissues and an improvement in microcirculation, normalization of blood COS parameters and energy supply of cells. Amtizol is used in a dose of 2-6 mg / (kg * day).

Along with these so-called reference antigipoksantami for the prevention of the formation of acute ulcers of the gastrointestinal tract, other drugs with an antihypoxic effect are used: triamine, gliosis, etomerisol, perfluorocarbon emulsions, mafusol, allopurinol, and others.

An extremely important role in increasing the resistance of the mucous membrane of the gastrointestinal tract to the action of various factors is played by the intensity of the blood flow. In most cases, the basis for the development of acute ulcers of the gastrointestinal tract is ischemia of the mucous membrane. Increased blood flow in the mucous membrane with the use of drugs that improve the peripheral circulation - isoproterol, trental, parmidin (prodectin, anginin), theonikola, troxovazine, curantilum - significantly reduces the development of acute ulcers of the gastrointestinal tract. In addition, the traditional means used in surgery-countercrital, trasanol, pantripine, M-cholinolytics, ganglion blockers, spasmolytic drugs, anabolic steroids, dimedrol, histaglobulin and alpha-aminocaproic acid, also have a positive effect on blood circulation in the mucous membrane of the gastrointestinal tract. It has been established that alpha-aminocaproic acid reduces perivascular, vascular and extravascular disorders; ganglioblokator temohin and myotropic antispasmodics (no-spa, papaverine) - vascular and extravascular; Dimedrol and histaglobulin - perivascular and vascular; anabolic steroid hormones (retabolil, methandrostenolone) - perivascular and intravascular; peripheral M-holinolipitiki (atropine, metacin, platifillin) - vascular disorders.

In the clinic at the present time, various drugs stimulating metabolic activity and accelerating repair processes in the mucosa of the gastrointestinal tract are widely used. This mucostabil, gastropharm, trichopol (metronidazole), reparone, methyluracil (metacil).

Metiluracil (metacil) stimulates the synthesis of nucleic acids and proteins, has an anti-inflammatory effect, promoting the rapid healing of acute ulcers of the gastrointestinal tract. At present, the interest of clinicians to trichopolum has increased considerably, since trichopol is an effective drug that suppresses the activity of Helicobacter pylori, bacteria that can cause the development of acute erosions and ulcers of the gastrointestinal tract.

Effective drug, with pronounced protective properties, is dalargin. It enhances reparative and regenerative processes, improves microcirculation in the mucosa, has an immunomodulating effect, and moderately inhibits gastric and pancreatic secretion.