Acute and stress ulcers

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

These complications occur especially frequently in patients and victims with severe cardiovascular, respiratory, hepatic and renal failure, as well as with the development of purulent-septic complications. Acute erosions and ulcers of the gastrointestinal tract are often complicated by bleeding or perforation. The incidence of stress ulcers of the stomach and duodenum in patients after injuries is 27%, in patients with mechanical trauma - 67%. The overall incidence of stress ulcers is 58%. Stress ulcers were complicated by bleeding in 33% of wounded patients, in 36% of victims with mechanical trauma. The overall mortality rate for complicated acute erosions and ulcers of the digestive tract remains very high and, according to various authors, ranges from 35 to 95%.

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

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How do stress ulcers develop?

Until recently, it was believed that stress ulcers mainly affect the stomach and, less frequently, the duodenum. However, in reality, they occur in all parts of the intestinal tube. Moreover, each section of the gastrointestinal tract is characterized by certain damaging agents.

The proximal sections of the gastrointestinal tract (stomach and duodenum) are affected most often. Firstly, almost all aggressive factors act on the mucous membrane here - hydrochloric acid, proteolytic enzymes, intestinal contents during antiperistalsis and reflux, microorganisms during achlorhydria, lysosomal enzymes during aggravation of autolytic processes, ischemia of the mucous membrane and filtration of waste through it. Thus, the number of aggressive agents damaging the mucous membrane in these sections is maximum. Secondly, an important point is that in qualitative terms these factors of aggression significantly exceed those acting in other parts of the digestive tract. In the small and especially in the large intestine, food is already largely broken down into its constituent parts, having previously undergone mechanical and chemical processing. Therefore, in the distal direction along the intestinal tube, the intensity of the “destructive” forces decreases, and the chyme becomes increasingly adapted to the body’s environment.

In victims with multiple and combined trauma complicated by shock, there is a noticeable energy deficit, due to which the body's "emergency reserve" of energy - glucose - is used up. Its mobilization from the liver depot occurs very quickly and hyperglycemia is observed within a few hours after the trauma or injury.

Subsequently, against the background of energy hunger, sharp fluctuations in blood glucose levels are observed (intravenous infusions play a certain role in this), which is a stimulating factor for the nuclei of the vagus nerve, leading to an increase in acidic gastric secretion and an increase in the digestive capacity of gastric juice. Under stress conditions, this mechanism can cause the prevalence of aggressive factors over protective factors, i.e. be ulcerogenic.

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 "release" of glucocorticoid hormones into the bloodstream is to stabilize hemodynamic parameters. But there is another side to the action of these hormones, which consists in stimulation of the vagus nerves, loosening of the gastric mucosa and reduction of mucopolysaccharide production. The situation described above is observed - stimulation of the digestive capacity of the stomach occurs with reduced resistance of the mucosa.

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

In the immediate period after the injury, there is a significant decrease in pH, and the "peak" of acidity corresponds to the most probable time of ulcer formation. Subsequently, starting from the second week after the injury, the level of acidic gastric secretion indicators decreases.

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

During stress ulceration of the gastric and duodenal mucosa, a number of proteolytic enzymes are activated, the pH optimum of which ranges from 1.0 to 5.0. High enzymatic activity has also been established at a pH of 6.5-7.0. The source of such activity may be lysosomal enzymes released as a result of the destruction of lysosome membranes.

One of the causes of lysosomal membrane destruction and release of intracellular cathepsins during stress may be 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 with subsequent destruction of mitochondria and lysosomes and, as a consequence, 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 the blood supply to the gastric mucosa due to vascular spasm.

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

In the first few days after a severe injury, against the background of stress, lipid peroxidation processes are activated in the body's tissues, including the gastric mucosa, which leads to the destruction of cellular and lysosomal membranes, the release of activated lysosomal enzymes, as well as to excess circulation in the blood and the presence in the tissues of aggressive intermediate peroxidation products and free radicals (Fig. 9.5 and 9.6).

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

The formation of stress 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 injury, when, as a rule, stress ulcers occur. The second peak of LPO activity and the formation of true acute ulcers is observed in victims with severe complications, ultimately leading to the development of multiple organ failure on the 9th-17th day after injury.

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

Already in the first hours after the injury, signs of acute local or total inflammation of the mucous membrane of the stomach and duodenum are detected. By the end of the first day, edema and loosening of the mucous membrane appear. After 2-3 days, the folds become rougher, thicker and do not straighten out well when insufflated with air. The mucous membrane gradually becomes more vulnerable and bleeding. Submucous hemorrhages are often detected, sometimes acquiring a confluent character.

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

What do stress ulcers look like?

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

Such stress erosive and ulcerative lesions of the mucous membrane of the stomach and duodenum occur in most victims. The degree of expression of the inflammatory reaction depends on the severity of the injury.

A different morphological picture of the mucous membrane of the gastrointestinal tract is observed with the development of severe purulent complications. The mucous membrane of the stomach is ischemic and atrophic. True acute ulcers occur. Ulcer defects are usually large in size and are localized, as a rule, in the outlet of the stomach. Inflammation of the mucous membrane is absent. The leading role in the genesis of acute ulcers is played by vascular disorders, leading to ischemia and suppression of protective factors of the mucous membrane.

These disorders consist of increased tone of small arteries and arterioles, plasmatic impregnation, proliferation and desquamation of the endothelium. Thrombi are often detected in the capillaries adjacent to the hemorrhagic infarction zone. The muscular layer of the stomach or intestinal wall is often involved in the pathological process, and hemorrhages occur in the submucosal layer. Desquamation and degeneration of the epithelium and often focal necrosis in the mucous membrane and submucosal layer occur. A characteristic feature of all changes is the predominance of dystrophic processes over inflammatory ones and, as a consequence, a high probability of perforation of acute ulcers.

Excretion of waste products (urea, bilirubin, etc.) by the gastric mucosa is an additional factor damaging the mucous membrane.

With progressive peritonitis and wound infection, the victims develop enteral insufficiency syndrome, one of the clinical manifestations of which is acute ulcers of the gastrointestinal tract. The occurrence of such ulcers is associated with dysfunction of the intestinal tube and other organs and systems (impaired microcirculation in the wall of the stomach and intestine, increased thrombus formation in small vessels of the gastrointestinal tract wall, aggressive impact on the mucous membrane of the stomach and intestine of urea and other aggressive metabolic factors, 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

Ulcer formation in various parts of the digestive tract can be represented as follows.

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

In the outlet of the stomach, the mucous membrane is exposed to factors of acid-peptic aggression (as in its proximal sections). In addition, bile entering the stomach as a result of duodenogastric reflux is a sufficiently aggressive factor. In the outlet of the stomach, ischemia of the mucous membrane plays a significant role in acute ulcer formation. Therefore, in the genesis of acute ulcer formation, against the background of increased aggression factors, a weakening of the protective factors begins to play a significant role. Destructions of the mucous membrane are usually large, single, often complicated by bleeding, sometimes perforation. As a rule, stress ulcers occur, but the formation of acute ulcers is also noted.

In the duodenum, bile acids, lysolecithin and pancreatic enzymes are added to the aggressive factors acting on the mucous membrane in the outlet of the stomach. Acute ulcers in the duodenum occur especially often when the function of the pyloric sphincter is impaired and the secretory function of the stomach is preserved. In this case, the acid-peptic factor, enhanced by the proteolytic enzymes of the pancreas, with all its power falls on the mucous membrane of the duodenum, the protective forces of which are significantly weakened due to the disruption of the blood supply to its wall and the disruption of the synthesis of mucopolysaccharides. In addition, a microbial factor can act in the duodenum. Stress ulcers prevail over acute ones here.

In the small intestine, the effect of the acid-peptic factor on its mucous membrane is minimal. Of the acid-peptic aggression, only pancreatic enzymes play a significant role. The role of the microbial factor increases in the occurrence of destruction of the mucous membrane. Microcirculation disorders in the intestinal wall are quite significant, and therefore trophic disorders of the mucous membrane come out on top in their significance. These are true acute ulcers, which were previously sometimes called trophic. This name reflects the essence of the formation of these ulcers. Acute ulcers in the small intestine are usually solitary and occur against the background of purulent-septic complications during the development of enteral insufficiency. In fact, acute ulcers are one of the morphological manifestations of enteral insufficiency. Moreover, true acute ulcers of the gastrointestinal tract are often also a manifestation of multiple organ failure, usually being its "markers". Acute ulcers are most often complicated by intestinal perforation due to thrombosis of vessels in its wall at the level of the microcirculatory bed. Acute ulcers of the small intestine are extremely rarely complicated by bleeding, since they occur in an ischemic wall. Stress ulcers in the small intestine occur quite rarely.

In the colon, with the development of multiple organ failure, there is pronounced ischemia of the intestinal wall, which leads to a significant weakening of the protective properties of the mucous membrane. Violations of the protective properties of the mucous membrane are aggravated by metabolic disorders in the intestinal wall. Against this background, the effect of active lysosomal enzymes on the mucous membrane leads to the formation of local, most often single, destruction of the mucous membrane. Additional factors of aggression are slags (creatinine, urea, bilirubin), the excretion of which is carried out by the mucous membrane of the colon, as well as extremely pathogenic microbial associations vegetating on the ischemic and weakened mucous membrane. Acute ulcers in the colon are also a manifestation of multiple organ failure, but are quite rare. Multiple organ failure either responds to intensive therapy or progresses, and such patients most often do not survive until the formation of acute ulcers in the colon.

Differential diagnosis of stress and acute ulcers

There are fundamental differences between stress and acute ulcers of the gastrointestinal tract. Stress ulcers occur due to stress - mental, surgical, traumatic, wound. This usually occurs within a few hours to several days after exposure to stress factors. Acute ulcers occur much later - starting from 11-13 days after the onset of the disease, surgery, injury or wound. As a rule, acute ulcers occur due to the depletion of the body's defenses against the background of the development of severe (usually purulent) complications and multiple organ failure. They are sometimes the first manifestation of enteral failure.

In recent years, more and more attention has been paid to enteral insufficiency syndrome, which develops in victims in serious condition, whose intestinal tube can 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 increase significantly in patients in critical condition. A special term has been proposed to characterize such conditions - "intestinal sepsis". Under certain circumstances, bacteria can penetrate the mucous 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 their "sticking" to the surface of epithelial cells. Then, live bacteria penetrate the mucous barrier and reach the lamina propria, after which they actually end up outside the gastrointestinal tract.

Mechanical intestinal protective factors normally limit the ability of bacteria to reach the epithelium of the mucous membrane. In the small intestine, normal peristalsis prevents prolonged stasis of bacteria in the immediate vicinity of the mucous membrane, which reduces the likelihood of bacteria penetrating through the mucus layer and "sticking" to the epithelium. When intestinal peristalsis is impaired, 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 epithelium of the mucous membrane.

Complete replacement of the 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 "sticking" to the surface of the epithelium.

Many protective mechanisms preventing bacterial translocation are impaired in critically ill patients at risk of multiple organ failure. These patients often have significant immune system dysfunction, and antibiotic administration can significantly disrupt the intestinal microflora ecology, leading to overgrowth of pathogenic bacteria. Oral antacids and H2-histamine receptor blockers can lead to excessive bacterial colonization in the stomach due to their increased survival. Hyperosmolar nutrient mixtures administered enterally and parenterally not only disrupt the normal intestinal microflora ecology, but can also lead to mucosal atrophy and damage to the intestinal mechanical barriers. Hypoalbuminemia typically leads to intestinal wall edema, decreased intestinal motility, intestinal content stasis, bacterial overgrowth, and impaired intestinal wall permeability.

Of all the organs of the gastrointestinal tract, the stomach is the most sensitive to hypoxia. Hypoxia, often observed in the wounded and injured, contributes to a decrease in 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 body “sacrifices” it to save vital organs.

One of the main causes of gastrointestinal ischemia during blood loss, along with a significant decrease in the volume of circulating blood, is the release of a large amount of vasopressor substances - adrenaline, angiotensin, vasopressin, as well as endotoxins of E. coli, which have sympathotropic properties. In this case, the section of the intestine supplied with blood by the superior mesenteric artery suffers the most. It is in this section of the intestinal tube (in the duodenum and jejunum) that a-receptors predominate, which already at the very beginning of the development of hemodynamic disorders leads to ischemia and deep hypoxia of the intestinal wall. As a rule, significantly less damage is noted in the colon, in the wall of which beta-receptors predominate.

As pathological changes progress, the primary vascular spasm is replaced by congestive plethora due to the expansion of precapillary sphincters and the maintenance of increased tone of postcapillary venules.

Rapidly increasing microcirculation disorders lead to damage of the mucous membrane, spreading from the submucous layer to the intestinal lumen. The development of hypoxia leads to an increase in the permeability of cellular and lysosomal membranes for enzymes. Activated proteolytic enzymes (pepsin, trypsin) and lysosomal hydrolases (acid phosphatase, beta-glucuronidase) destroy the mucous membrane, the resistance of which is reduced due to impaired blood supply, inhibition of synthesis and destruction of mucin. Proteolytic enzymes of bacteria also play a major role in the pathogenesis of damage to the intestinal mucous membrane.

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

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Treatment of stress and acute ulcers

Preventive treatment of stress ulcers must be divided into two groups: general measures, so-called non-specific prevention, and measures that have a direct impact on the mucous membrane of the gastrointestinal tract.

General treatment is aimed at eliminating hemodynamic disturbances, hypoxia, metabolic disorders, and also involves adequate anesthetic care.

Measures that have a direct impact on the mucous membrane of the gastrointestinal tract include the use of drugs that reduce the damaging effects of aggressive factors on the mucous membrane.

A good measure for preventing the formation of stress ulcers of the stomach and duodenum is the intragastric administration of concentrated (40%) glucose solutions. Glucose helps restore the energy balance of the mucous membrane cells, increases the blood sugar level, which is accompanied by a decrease in the excitation of the vagus nerve nuclei, a weakening of the neuroreflex phase of gastric secretion and stimulation of the 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 given 50-70 ml of a 40% glucose solution into the stomach twice a day.

To prevent self-digestion of the gastric mucosa under conditions of increased activity of acid-peptic aggression factors, it is necessary to introduce protein preparations into the stomach, which would significantly "distract" active proteolytic enzymes. For this purpose, a solution of egg white (the white of three eggs, mixed in 500 ml of water) is introduced into the stomach of patients through a tube during the day.

In order to reduce the activity of lysosomal enzymes and suppress intracellular proteolysis, it is advisable to administer Contrikal to patients at 40-60 thousand units daily.

The ulcerogenic effect of serotonin is reduced by administering 30 ml of peritol as a syrup through a gastric tube 3 times a day. Peritol (cyproheptadine hydrochloride) has a pronounced antihistamine and antiserotonin effect, has anticholinesterase activity, and has an antiallergic effect. In addition, this drug has a pronounced sedative effect.

Considering that the main factor in the formation of stress ulcers of the gastrointestinal tract is acid-peptic aggression, preventive measures aimed at preventing 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 contents decreases below 4.0, antacid and antisecretory drugs should be prescribed. Maintaining pH at 4-5 is optimal, since it is in this range that almost all hydrogen ions are bound, and this is quite sufficient to significantly suppress the activity of intragastric proteolysis. Increasing pH above 6.0 is inappropriate, since it leads to activation of pepsin secretion.

All antacid substances are divided into systemic and local action drugs. Systemic antacid drugs include sodium bicarbonate (soda) and sodium citrate. Local action antacid drugs include precipitated calcium carbonate (chalk), magnesium oxide and hydroxide, basic magnesium carbonate, magnesium trisilicate and aluminum hydroxide. Alkaline mineral waters and food antacids are also used as local action antacids.

In addition to the antacid drugs listed above, combination drugs are currently used: vikalin, vikar (roter), almagel, phosphalugel, gaviscon, gastal, galusillak, aludrox, kompensan, acidrin, etc.

Among antacids, the greatest therapeutic effect is possessed by aluminum preparations, which combine such properties as duration of action, pronounced adsorbing, neutralizing, enveloping and cytoprotective effects.

Abroad, the most commonly used antacid drugs are Maalox, Maalox-1K, Maalox TS, Aludrox, Milanta, Milanta II, Delcid, Gastrogel, Gelusil, Ulkasan, Talcid. In our country, Maalox is the most common of these drugs. Its use for the prevention of 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 administered 20 ml every hour into a gastric tube.

Prevention of stress ulcers

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

When carrying out complex prevention of stress ulcers, it is preferable to prescribe second- and third-generation histamine H2-receptor blockers once in maximum doses at night (ranitidine 300 mg or famotidine 40 mg), since suppression of nocturnal hypersecretion is of great importance in preventing the occurrence of stress ulcers, and during the daytime, the use of antacids, special nutritional mixtures, as well as early enteral nutrition ensures a sufficient reduction in the acidity of the intragastric contents and an adequate antiulcer effect.

Compounds that selectively act on M-cholinergic receptors are used as antisecretory drugs. Of the large number of anticholinergic drugs, only a few are used to prevent stress ulcers of the gastrointestinal tract. These are gastrobamate (a combination drug with ganglionic blocking, anticholinergic and sedative effects), atropine, metacin (in addition to antisecretory action, it also has an antacid effect and normalizes gastric motility), probantin (a more pronounced anticholinergic effect than atropine), chlorosil (has a more pronounced and longer-lasting anticholinergic effect than atropine).

The most effective drug from this group for preventing the occurrence of stress gastroduodenal ulcers is gastrocepin (pirenzepine). The combination of gastrocepin with histamine H2 receptor blockers and antacid drugs is a highly effective means of preventing the occurrence of stress gastroduodenal ulcers.

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

Of the medications that are important for the prevention of stress gastroduodenal ulcers, proglumide, somatostatin, and secretin should be noted. Secretin is used intravenously by drip at a dose of 25 units/hour. It stimulates not only the formation of bicarbonates, but also the production of somatostatin, which is produced by D-cells of the antrum of the stomach. On the one hand, somatostatin inhibits the production of gastrin by a paracrine mechanism, on the other hand, it inhibits insulin, thereby suppressing vagal secretion. Somatostatin is administered intravenously at a dose of 250 mcg/hour. 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.

Among the drugs that promote mechanical protection of the gastrointestinal mucosa, bismuth preparations are widely used in clinical practice - vikalin, vikair, vinylin (Shostakovsky's balm, de-nol). De-nol has a pronounced bactericidal effect on Helicobacter pylori due to the release of free active bismuth ion by de-nol, which penetrates into the bacterial wall. Moreover, 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 integumentary epithelium, but also in the depth of the folds. It is most convenient to prescribe the liquid form of the drug to patients, diluting 5 ml of the drug in 20 ml of coda.

Another effective drug that protects the gastrointestinal mucosa from the effects of aggressive factors is the complex aluminum-containing sulfated disaccharide sucralfate (Venter).

Of the domestic drugs with similar action, two should be noted - zinc sulfate and amipol. Zinc sulfate is prescribed orally at 220 mg three times a day and has an antiseptic and astringent effect, and also stimulates the production of mucus. The drug amipol, produced in the form of dietary cookies "Amipol", dissolves when it enters the stomach (it can be administered through a tube, having previously dissolved in water) and as a result of the reaction with hydrochloric acid, protonated amipol is formed. When in contact with the damaged surface of the mucous membrane, protonated amipol forms a gel-like layer that covers this surface and protects it from the effects of aggressive factors.

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

Biostimulants such as aloe extract, bilsed, FiBS, pelloid distillate, peolidin, polybiolin, Kalanchoe juice, etc. have become quite widespread for the restoration and stimulation of the body's defenses.

To a significant extent, the regenerative function of the patient's body is increased by parenteral administration of protein preparations (plasma, albumin solution), as well as protein hydrolysates (aminopeptide, aminokrovin, etc.). The regenerative capacity of the body is increased to an even greater extent by the combination of administration of protein preparations with anabolic hormones - methandrostenolone, nerobol, turinabol, retabolil, methylandrostenediol.

Retabolil is best suited for the prevention of acute gastrointestinal ulcers in victims, since it improves reparative processes in the gastrointestinal mucosa to the greatest extent and, in addition, causes a significant increase in protective mucus formation. To prevent acute ulcers, the drug should be administered at a dose of 1-2 ml on the day of admission to the hospital.

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

The vast majority of victims, especially with the development of multiple organ failure, have disorders of immune homeostasis, leading to a disruption in the regulation of regenerative processes and the development of dystrophic changes in the patient's body. In this regard, to prevent acute gastrointestinal ulcers, it is absolutely necessary to use agents that regulate the state of immunity. These are drugs such as feracryl, decaris (levamisole), thymopentin and sodium nucleinate. 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, and enhances the phagocytic activity of neutrophilic leukocytes and macrophages.

Thymalin stimulates the body's immunological reactivity (regulates the number of T- and B-lymphocytes), cellular immunity reactions, and enhances phagocytosis. Thymalin also significantly stimulates regeneration processes. To prevent the formation of acute ulcers, thymalin is administered daily at 10-20 mg intramuscularly.

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

The increase in the body's resistance and the resistance of gastric epithelial cells to various aggressive influences is largely associated with the elimination of hypoxia and its consequences, in particular, with a decrease in the activity of lipid peroxidation processes.

Hypoxia is a condition that occurs as a result of either limited oxygen supply to the cell or loss of the ability to utilize it in biological oxidation reactions. A new approach to eliminating hypoxia is the use of antihypoxants. Antihypoxants are a class of pharmacological substances that facilitate the reaction of tissues to hypoxia or even prevent its development, as well as accelerate the processes of normalization of functions in the post-hypoxic period and increase the resistance of tissues and the body as a whole to oxygen deficiency.

A number of substances with antihypoxic action have been synthesized in our country and abroad. These include sodium oxybutyrate (GHB), piracetam (nootropil), and amtizole. Sodium oxybutyrate acts as a redox buffer that eliminates the deficiency of the oxidized form of nicotinamide adenine dinucleotide (NAD) that develops during hypoxia, normalizes oxidative phosphorylation processes, binds toxic products of nitrogen metabolism, and 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 solution in combination with potassium preparations.

Amtizol is a second-generation antihypoxant that has proven itself in severe shock-producing trauma accompanied by massive blood loss and hypoxia of various origins. Inclusion of amtizol in complex therapy leads to improved hemodynamics and CNS functions, increased oxygen content in tissues and improved microcirculation, normalization of blood acid-base balance and cellular energy supply. Amtizol is used in a dose of 2-6 mg/(kg * day).

Along with these so-called reference antihypoxants, other drugs with an antihypoxic effect are used to prevent the formation of acute ulcers of the gastrointestinal tract - trimin, gliosiz, etomerzol, perfluorocarbon emulsions, mafusol, allopurinol, etc.

Blood flow intensity plays an extremely important role in increasing the resistance of the gastrointestinal mucosa to the action of various factors. In most cases, the development of acute gastrointestinal ulcers is based on mucosal ischemia. Increasing blood flow in the mucosa when using drugs that improve peripheral circulation - isoproteriol, trental, parmidine (prodectin, angina), theonikol, troxovazin, curantil - significantly reduces the development of acute gastrointestinal ulcers. In addition, traditionally used in surgery drugs - contrical, trasylol, pantrypine, M-anticholinergics, ganglionic blockers, antispasmodics, anabolic steroids, diphenhydramine, histaglobulin and alpha-aminocaproic acid - also have a positive effect on blood circulation in the gastrointestinal mucosa. It has been established that alpha-aminocaproic acid reduces perivascular, vascular and extravascular disorders; ganglion blocker temekhin and myotropic antispasmodics (no-shpa, papaverine) - vascular and extravascular; diphenhydramine and histaglobulin - perivascular and vascular; anabolic steroid hormones (retabolil, methandrostenolone) - perivascular and intravascular; peripheral M-cholinolytics (atropine, metacin, platifillin) - vascular disorders.

Various drugs that stimulate metabolic activity and accelerate reparation processes in the gastrointestinal tract mucosa are currently widely used in the clinic. These are mucostabil, gastropharm, trichopolum (metronidazole), reparon, methyluracil (metacil).

Methyluracil (metacil) stimulates the synthesis of nucleic acids and proteins, has an anti-inflammatory effect, promoting rapid healing of acute ulcers of the gastrointestinal tract. Currently, the interest of clinicians in trichopolum has increased significantly, since trichopolum 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.

An effective drug with pronounced protective properties is dalargin. It enhances reparative and regenerative processes, improves microcirculation in the mucous membrane, has an immunomodulatory effect, and moderately inhibits gastric and pancreatic secretion.