Stress ulcers

　　I. Etiology

　　The main causes of stress ulcer occurrence are:

　　1. Severe trauma that causes the body to be in a state of stress includes severe外伤, extensive burns, intracranial diseases, brain trauma, and abdominal surgery.

　　2. Long-term hypotension such as shock, chronic renal insufficiency, and multiple organ failure.

　　3. Long-term use of drugs such as aspirin and indomethacin after the use of anticancer drugs and corticosteroid hormones.

　　4. Other factors such as gastric acid, ischemia, and the destruction of the gastric mucosal barrier.

　　5. Stress ulcers are caused by the digestion and destruction of gastric mucosal cells by gastric acid and pepsin. Gastric acid is a necessary condition for the formation of ulcers; without gastric acid, ulcers would not occur. Normal gastric mucosa contacts gastric acid and pepsin without being digested due to the protective action of the gastric mucosa. The protective action of the gastric mucosa includes the following three aspects:

　　(1) Gastric mucus barrier The gastric mucosa secretes mucus. The mucus is thick and gelatinous, adhering to the surface of the gastric mucosa, separating the gastric lumen from the mucosal surface (luminal surface) of the gastric mucosal epithelial cells. The mucus layer, due to its special molecular structure, has static water within it, which is not stirred. The diffusion rate of H+ and pepsin is extremely slow within it, so the mucus barrier can maintain a pH gradient between the epithelial cells and the gastric lumen.

　　(2) Gastric mucosal barrier The cell membrane on the luminal surface of gastric mucosal epithelial cells is composed of lipoproteins. H+ in the gastric lumen cannot pass through the cell membrane and reverse diffuse into the cell along the concentration gradient. The cell membrane forms a barrier of H+ between the gastric lumen and the epithelial cells. A small amount of H+ that passes through the mucus barrier is also blocked by the epithelial cell membrane. The connections between gastric mucosal epithelial cells are very tight, and H+ cannot enter the cell through this route.

　　(3) Neutralizing effect of HCO3- There are a large number of carbonic anhydrase in gastric mucosal cells that can combine the CO2 and H2O produced by intracellular oxidative metabolism, as well as CO2 and H2O from the blood, to form H2CO3. The latter dissociates into HCO3- and H+, and HCO3- enters the blood or interstitial fluid from the basolateral surface (serosal surface) of the cell, or can be transported to the gastric lumen from the mucosal surface. In the mucus layer adjacent to the mucosa, HCO3- neutralizes a small amount of H+ that penetrates through the mucus layer. Even if a small amount of H+ enters the mucosal epithelial cells, it can be neutralized by HCO3- within the epithelial cells, maintaining the acid-base balance of the cells.

　　There is a large amount of prostaglandins in the gastric mucosa, which stimulate the secretion of mucus and HCO3- and have a protective effect on gastric mucosal cells. However, substances such as aspirin, indomethacin, phenylbutazone, bile salts, corticosteroids, and urea can destroy the gastric mucosal barrier and cause acute gastric mucosal lesions.

　　The maintenance of the normal function of the gastric mucosal barrier relies on the normal metabolism and continuous renewal of gastric mucosal epithelial cells. Metabolism requires oxygen and substrates. In stress conditions such as shock, patients have varying degrees of hypotension and gastric microcirculatory disorders for unequal periods of time, leading to ischemia and hypoxia of the gastric mucosa, affecting the function of mitochondria, reducing ATP synthesis, insufficient energy supply, dysfunction of cells, and the loss of the ability to produce and secrete mucus and HCO3-. Both the mucus barrier and mucosal barrier lose their function, and H+ is reversed diffused into the cell, while the cell lacks HCO3- to neutralize the H+ entering the cell. As a result, the cell becomes acidotic, lysosomes within the cell break down, releasing lysosomes, and the cell undergoes autolysis, destruction, and death. At the same time, due to insufficient energy, DNA synthesis is affected, and cells cannot regenerate. Necrotic cells are not replaced by regenerating cells, leading to the formation of ulcers. The energy (glycogen) reserve of gastric mucosal cells is very little while the metabolic rate is high, making them more susceptible to metabolic disturbances due to ischemia than other organs (such as the liver, muscles, etc.). The metabolic rate of the epithelial cells in the gastric fundus is the highest among gastric mucosal epithelial cells, which can explain why stress ulcers often occur in the gastric fundus.

　　Second, pathogenesis

　　1. Pathogenesis of SU: SU is an acute gastric ulcer. The pathogenesis of peptic ulcer is related to that of SU, but they are not completely the same. SU has its own characteristics of onset. Szabo (1984) proposed the ulcer disease triangle, which clearly illustrates the relationship between several factors involved in the occurrence of gastric peptic ulcers.

　　(1) Increased excitability of the central nervous system: The stomach is the most sensitive organ under stress conditions. Emotions can inhibit the secretion of gastric acid and peristalsis, while tension and anxiety can cause erosion of the gastric mucosa, which has long been proven by cold restraint animal experiments. Rats are tied to a wooden board or placed in an iron wire cage of the same volume as their body size, constrained in their activity, and then placed in a refrigerator at 4℃. Or immerse the lower part of the rat's neck and chest in cold water, and after 2 hours, the gastric mucosa will appear erosion and bleeding. The experiment also found that after cold restraint, the level of serum gastrin increased, which may be related to the excitation of the vagus nerve. The central nervous system directly affects the secretion of gastric acid and gastric motility through three pathways, namely the anterior hypothalamus-vagus nervous system, the posterior hypothalamus-sympathetic nervous system, and the posterior hypothalamus-pituitary-adrenal system. Whether it is through one or more pathways during stress is not yet clear.

　　(2) Injury to the gastric mucosal barrier: For SU, it is a very important pathogenic cause, and can also be said to be a necessary condition for the onset of the disease. The gastric mucosa is a complex tissue structure with a highly functional nature, with numerous gastric pits distributed on the mucosal surface. Each pit contains openings of many bottle-shaped gastric glands with narrow necks, and the glandular epithelium is composed of several different functionally diverse cells. Parietal cells secrete gastric acid, chief cells secrete pepsinogen, and goblet cells near the neck of the glands secrete mucus. Between the pits are superficial epithelial cells, which are rich in carbonic anhydrase and can produce HCO3-, although their secretion rate is only 5% to 10% of that of H+. However, its basic secretion rate is 300 to 400 μmol/h, so the gastric mucosa simultaneously exists with both acid secretion and anti-acid mechanisms to serve as a self-protective function. The gastric acid and pepsin secreted by the gastric mucosa are highly effective digestive fluids. When the concentration of gastric acid reaches its highest, the H+ gradient inside and outside the mucosa can differ by up to 10 million times. According to the principle of the semi-permeable membrane in physics, H+ must diffuse in large quantities into the mucosa. In order to fully utilize the function of HCO3-, it is necessary to rely on the function of mucus. The mucus covering the gastric mucosal surface is a colloidal gel of glycoprotein with a concentration of 30 to 50 mg/ml and a thickness of 0.5 mm. It is not enough to prevent the penetration of H+, but it can allow the HCO3- secreted by the superficial epithelial cells to accumulate in the mucus, preventing loss, and slowly diffuse into the gastric cavity, becoming an effective buffering layer to prevent the retrograde invasion of H+. In addition, when the gastric acid increases, in addition to the continuous secretion of HCO3-, alkaline tide (alkalinetide) can also occur to maintain balance.

　　The mucus on the mucosal surface is gradually degraded by gastric acid and proteases, while new mucus is continuously secreted to supplement it. In addition, new epithelial cells at the base of gastric pits in the surface epithelial cells of the gastric surface migrate to the mucosal surface for renewal, and they are replaced every 3 days. The various functional activities of epithelial cells are an energy-consuming process, and the necessary condition to ensure their function is the blood flow of the gastric mucosa. The blood circulation in the gastric wall is rich, with serosal vessels passing through the muscular layer to reach the submucosal layer. In this layer, there are a few arteriovenous anastomoses, with arteries and veins branching into small arteries and veins. After passing through a very thin mucosal muscular layer, the small arteries branch into posterior arteries, and then enter the mucosal layer through precapillary vessels and precapillary sphincters to become capillaries, and return through veins at the same level.

　　Any factor that affects blood flow in the gastric wall will have an impact on the function of gastric mucosal epithelial cells, weakening the gastric mucosal barrier. Major surgery, severe trauma, systemic infection, and especially hypoperfusion caused by shock, can reduce blood flow in the gastric wall, leading to the occurrence of SU.

　　(3) The role of gastric acid and H+: Gastric acid and H+ have always been considered as important factors in the pathogenesis of peptic ulcer disease. An increase in gastric acid obviously increases the burden on the gastric mucosal defense system, but during SU, the level of gastric acid is generally not high, even reduced. Despite this, the role of H+ in the pathogenesis of SU cannot be denied.

　　Due to the damage of the gastric mucosal barrier, even though the concentration of H+ is not high, it can still reverse diffuse and cause acidification within the gastric wall. The normal pH within the gastric wall is higher than 7.2, and if it drops below 6.5, it can lead to acute gastric mucosal damage. H+ can promote histamine release, stimulate cholinergic nerves, cause an increase in the secretion of gastric acid and proteases, and can also increase capillary permeability, block the production of HCO3- on the mucosal surface epithelial cells. At the same time, due to the reduction in blood flow in the gastric wall, H+ that has diffused into the gastric wall cannot be cleared in time, and all these factors can lead to the occurrence of SU. Persistent acidosis that has not been corrected can also cause the pH of the gastric wall to drop, which has an impact on the occurrence of SU.

　　The influence of metabolites: The frequent renewal of various cells in the gastric mucosa, especially the surface epithelial cells, leads to an increase in the metabolites of membrane phospholipids—arachidonic acid. As a substrate, it is synthesized into prostaglandins under the catalysis of cyclooxygenase. Among them, PGl2 and PGE2, which have a high yield, have strong biological activity and a protective effect on the gastric mucosa. PGl2 can inhibit the secretion of gastric acid, increase blood flow to the gastric mucosa, increase the secretion of mucosal HCO3- and mucus, and prevent the retrograde diffusion of H+. PGE2 dilates blood vessels, and its effect on improving the blood circulation of the gastric mucosa is particularly obvious. In the gastric mucosa, the content of PGl2 is more than 10 times higher than that of PGE2. Due to the protective effect of prostaglandins, it is called the PG-mediated defense system. Aspirin and alcohol can induce acute gastric mucosal lesions because they can severely inhibit the synthesis of prostaglandins. Animal experiments have shown that feeding PGE2 to animals before giving aspirin can prevent the occurrence of SU. Under stress conditions, especially in cases of ischemia and hypoxia of the gastric mucosa, the production of prostaglandins decreases, and there will also be the uncontrolled production of other inflammatory mediators, such as when the production of prostaglandins decreases due to the reduction in the activity of cyclooxygenase, arachidonic acid is converted into leukotrienes and platelet-activating factor (PAF) due to the enhancement of the 5-lipoxygenase activity. Leukotrienes are vasoconstrictive substances, and PAF has the effect of aggregating platelets. The production of these mediators further aggravates the ischemia and ischemic damage of the gastric mucosa. In addition, mast cells (MC) under the gastric mucosa can also produce some mediators. MC is a common cell in loose connective tissue, which is mostly distributed along small blood vessels and is a highly sensitive tissue response cell to external stimuli. In the parts of the human body where the opportunity to contact external antigens is the most, such as the skin, respiratory tract, and digestive tract, the number of MC is particularly high. There are a large number of MC under the gastric mucosa, which can produce

　　(5) Helicobacter pylori (Hp) infection: Since Hp was cultured from the gastric mucosa of patients with chronic active gastritis in 1983, its relationship with peptic ulcer and gastritis has always been of interest to people. Hp can produce highly active urease, which rapidly decomposes urea on the surface of the gastric mucosal epithelium, producing NH3. Although NH3 is weakly alkaline, Hp can produce enzymes that decompose mucopolysaccharide polymers, destroying the mucus layer covering the mucosal surface. In addition, it can produce catalase, phospholipase, protease, and other enzymes that can damage epithelial cells. It is reported that the detection rate of Hp in duodenal ulcer patients is 85%, and in gastric ulcer patients is 53%, but it is difficult to determine whether Hp is the pathogen causing peptic ulcer or a concurrent bacterium after the occurrence of ulcers. It is now believed that Hp can cause acute gastritis, but rarely produces acute ulcers and will not cause overt bleeding.

　　(6) The role of bile salts: Many abdominal surgeries are often accompanied by loss of omental function, which can be either organic, such as the reconstruction of a bile-enteric shunt after subtotal gastrectomy, or functional, such as gastrointestinal dilatation. The more difficult the postoperative recovery, the more likely this phenomenon of digestive fluid reflux occurs, often involving both organic and functional causes. The effect of bile salts on the gastric mucosa should not be overlooked. Bile salts are considered the third most harmful substance to the gastric mucosa after aspirin and alcohol. Bile salts can reduce the potential difference of the gastric mucosa, increase its permeability, and make cations such as H+ and Na+ easily penetrate the mucosa and diffuse. Bile salts have a solubilizing effect on the lipid of the mucosal epithelial cell membrane, which can damage the gastric mucosa. Animal experiments have shown that taurine bile acid can inhibit the secretion of isolated gastric mucosa and can also inhibit the ATPase of mucosal epithelial cells.

　　From the perspective of etiology, the occurrence of surgical SU is often the result of a combination of factors. For some critically ill patients, it can even be considered that SU is actually the manifestation of multiple organ dysfunction syndrome (MODS) in the stomach (upper gastrointestinal tract).

　　2. Pathophysiology is divided into erosion and ulcer based on the depth of gastric mucosal damage. Erosion refers to superficial lesions that do not extend beyond the basement membrane of the epithelial layer, while the base of the ulcer extends beyond the basement membrane to the submucosa, entering the muscular layer, but acute ulcers rarely extend beyond the muscular layer, while chronic ulcers can invade the subperitoneal and peritoneal layers. Erosion rarely bleeds due to its superficial nature, acute ulcers extend to the submucosa and muscular layer, and if they invade the exposed blood vessels in the ulcer, massive bleeding can occur.

　　In addition to the depth of the mucosal lesions, the degree of inflammation in the adjacent tissues also varies. The normal gastric mucosa has almost no neutrophils, and the number of chronic inflammatory cells including lymphocytes, plasma cells, and phagocytes is very few, only 2 to 5 per high-power field, and lymphocytes can occasionally be seen between the surface epithelial cells. According to the Sydney classification, acute gastric mucosal erosion has epithelial desquamation, and the erosion surface is covered with inflammatory exudate. There is infiltration of neutrophils in the epithelium, and acute ulcers have a large number of inflammatory cells infiltrating, with neutrophils predominating, with pinpoint hemorrhage, and can also have pinpoint suppurative lesions (pit abscesses). The characteristics of chronic ulcers are the infiltration of a large number of chronic inflammatory cells, with an increase in neutrophils, and varying degrees of fibrosis.

　　The number and location of the lesions are extremely inconsistent. The erosion lesions are often widely distributed in the gastric mucosa, and ulcers can be multiple, or they can coexist with erosion. The lesions are generally the most severe in the gastric antrum, followed by the gastric body, and even the entire gastric mucosa may have lesions. Huang Quting and others observed large areas of mucosal defects with a diameter of nearly 10 cm in the gastric body and antrum during surgery for patients with extensive burns and acute massive hemorrhage, with submucosal exposure and severe bleeding. The lesions can extend to the lower esophagus and duodenum, but it will not occur that only the duodenum or esophagus has lesions while the gastric mucosa remains intact.

　　When acute ulcers invade exposed blood vessels, they can cause massive bleeding. Patients may experience hematemesis, even hypovolemic shock.

　　Stress ulcer may not present with clinical symptoms if it does not cause massive bleeding, or even if symptoms are present, they may be masked by the symptoms of stress and not diagnosed. Since stress ulcer is superficial, barium meal造影 often cannot be detected, so it is often only discovered after surgery exploration or post-mortem examination after death, with many missed diagnoses. The reported incidence rate was not high in the past, but since the advent of fiberoptic endoscopy, the clinical incidence rate has increased, but since not all patients with stress conditions undergo routine endoscopic examination, the reported incidence rate may still be much lower than the actual number.

　　Patients in the intensive care unit with shock, extensive burns, severe trauma or infection, or organ failure (such as acute renal failure, adult respiratory distress syndrome, liver failure) may experience upper gastrointestinal bleeding. The first consideration should be the possibility of stress ulceration, as the lesion is too superficial for barium meal X-ray examination to have diagnostic value. Fiberoptic gastroscopy can exclude other bleeding lesions, make an accurate diagnosis, and if the bleeding is severe and unclear, selective arteriography can be performed.

　　In the few hours after the occurrence of stress, almost all patients can be found to have pale gastric mucosa with scattered red ecchymotic spots localized in the gastric fundus upon fiberoptic gastroscopy. Microscopic examination shows mucosal edema, submucosal vascular congestion, and rarely inflammatory cell infiltration. Electron microscopy shows multiple epithelial cell membrane damage, and in some places, entire sheets of epithelial cells may be shed, exposing the underlying mucosal lamina propria. After 24-48 hours of stress, the entire gastric body mucosa has erosions of 1-2mm in diameter. Microscopic examination shows localized hemorrhage and coagulative necrosis. If the patient's condition improves, about 90% of the patients will show signs of healing in 3-4 days. Generally, it takes 10-14 days to heal completely. If the patient's condition continues to worsen, the erosion sites may fuse and expand, causing the mucosa to fall off completely, forming ulcers that can reach the submucosal layer and muscle layer of the mucosa, exposing the nutrient vessels. If the vessels rot and rupture, bleeding may occur.

　　The initial manifestation is bleeding, which does not occur at the beginning of the lesion. The lesion has been present for some time before bleeding occurs. Initially, the mucosal lesion is shallow and few, and does not cause bleeding. Later, the lesions increase and deepen, and bleeding may occur if preventive measures are not taken. Bleeding usually occurs 5-10 days after the onset of stress conditions, and bleeding is intermittent. Sometimes there may be several days between two episodes, possibly due to the batch appearance of lesions, with the healing of old lesions and the formation of new ones at the same time.

　　Stress ulcers are most common 5-10 days after stress, and the most common clinical manifestation is gastrointestinal bleeding during severe trauma, infection, and shock. After the action of gastric acid, the drained gastric juice appears dark brown or coffee-colored and forms a flocculent substance. When bleeding is severe, it can lead to hematemesis, black stools, and even hypovolemic shock. Endoscopy can show widespread erosion of the gastric mucosa and multiple superficial small ulcers, which are different from peptic ulcers and acute gastritis.

　　The prevention of stress ulcers is more important than treatment. Prevention should consider both general and local aspects.

　　1. General measures:This includes removing stress factors, correcting insufficient blood and oxygen supply, maintaining water, electrolyte, and acid-base balance, and providing nutritional support early on. Nutritional support mainly involves early enteral nutrition, with the application of formula diet increased from 25ml/h to 100ml/h within 24-48 hours. In addition, it includes the prophylactic use of acid-suppressing agents and the use of antibiotics, as well as measures to control infection.

　　2. Local measures:This includes gastrointestinal decompression, injection of sucralfate into the gastric tube to protect the gastric and duodenal mucosa, as well as the injection of H2 receptor antagonists and ion pump inhibitors.

　　The possibility of stress ulceration in patients with stress conditions is very high, so timely treatment is required for such patients, including blood volume supplementation, correction of circulatory disorders, improvement of tissue perfusion, ensuring ventilation, oxygen supply, and the use of antibiotics to prevent infection. Although the gastric acid of stress ulcer patients may not necessarily be over-secreted, gastric acid is a necessary condition for the development of stress ulcers. Therefore, it is best for patients with severe stress conditions to have a gastric tube placed to continuously aspirate gastric juice, both to maintain an acidic-free stomach and to prevent the exacerbation of ischemia in the gastric wall due to gastric dilation. However, the gastric mucosa is fragile and prone to bleeding, so the suction force should not be too strong. At the same time, intravenous injection of H2 receptor antagonists (cimetidine) to inhibit gastric acid secretion and the use of antacids (magnesium hydroxide or aluminum hydroxide) to lavage the stomach through the gastric tube at intervals to neutralize gastric acid. If conditions permit, 30ml of antacid can be infused into the stomach tube every hour, and the tube should be clamped for 45 minutes after infusion, then aspirate the gastric juice, and measure the pH of the gastric contents after 15 minutes of aspiration. If the pH is 5. Some people do not advocate the use of H2 receptor antagonists because when parietal cells produce gastric acid, every secretion of an H+ also produces an HCO3- (alkaline tide) that is secreted into the gastric cavity. H2 receptor antagonists inhibit gastric acid secretion while also affecting the production of HCO3-, which is not as effective as antacids in neutralizing gastric acid without affecting the secretion of HCO3-.

　　Because the lesions are too shallow, barium meal X-ray examination has no diagnostic value. Fiberoptic gastroscopy can exclude other bleeding lesions, make an accurate diagnosis, and if the bleeding is severe and unclear, selective arteriography can be performed.

　　In the few hours after the occurrence of stress, almost all patients can be found to have pale gastric mucosa with scattered red ecchymotic spots localized in the gastric fundus upon fiberoptic gastroscopy. Microscopic examination shows mucosal edema, submucosal vascular congestion, and rarely inflammatory cell infiltration. Electron microscopy shows multiple epithelial cell membrane damage, and in some places, entire sheets of epithelial cells may be shed, exposing the underlying mucosal lamina propria. After 24-48 hours of stress, the entire gastric body mucosa has erosions of 1-2mm in diameter. Microscopic examination shows localized hemorrhage and coagulative necrosis. If the patient's condition improves, about 90% of the patients will show signs of healing in 3-4 days. Generally, it takes 10-14 days to heal completely. If the patient's condition continues to worsen, the erosion sites may fuse and expand, causing the mucosa to fall off completely, forming ulcers that can reach the submucosal layer and muscle layer of the mucosa, exposing the nutrient vessels. If the vessels rot and rupture, bleeding may occur.

　　1. Decreased hemoglobin and hematocrit in blood routine.

　　2. Positive occult blood test in stool.

　　3. Fiberoptic gastroscopy is of special importance. Early in the proximal gastric mucosa, multiple scattered pale spots can be seen. After 24-36 hours, multiple superficial red erosive spots can be observed, and ulcers can appear later, even black in color. Some may present as active bleeding.

　　4. Selective arteriography can determine the location and extent of bleeding, and drugs can be infused for hemostasis through the catheter.

　　1. Stress ulcer patients should choose easily digestible foods rich in sufficient calories, proteins, and vitamins. Such as congee, thin noodles, milk, soft rice, soy milk, eggs, lean meat, tofu, and soy products; foods rich in vitamins A, B, C, such as fresh vegetables and fruits, because vegetables and fruits are rich in nutrients.

　　2. Stress ulcer patients should not eat spicy foods or drink alcohol to avoid recurrence of the disease.

　　1. Treatment

　　Firstly, treat the primary disease, and secondly, maintain the intragastric pH above 4.0. This includes the following measures:

　　1. Correct the general condition: rapid fluid replacement, blood transfusion, and restoration and maintenance of sufficient blood volume.

　　2. Control infection.

　　3. Avoid taking drugs that irritate the stomach, such as aspirin, hormones, and vitamin C.

　　4. Intravenous application of hemostatic agents such as Argon, PAMBA, VitK1, and posterior pituitary extract. In addition, intravenous administration of Losec (losec) and famotidine can be given to inhibit gastric acid secretion.

　　5. Local treatment: placement of a gastric tube for drainage and irrigation, or injection of enzyme inhibitors such as Losec and thrombin into the gastric tube. It is feasible to rinse the stomach with ice physiological saline or bicarbonate water until the gastric juice becomes clear.

　　6. Endoscopic application: hemostasis under gastroscopy can be achieved by electrocoagulation, laser coagulation, and local medication under gastroscopy.

　　7. Interventional treatment can use selective arterial angiography, embolization, and injection of vasoconstrictors, such as vasopressin.

　　8. For patients with severe bleeding due to stress ulcer, due to poor general condition of the patient, unable to tolerate surgery, and high incidence of postoperative rebleeding, general medical treatment is usually used first, and surgical treatment is considered only when medical treatment is ineffective. The methods of medical treatment include:

　　(1) Gastric tube aspiration Continuous aspiration of the gastric tube can prevent gastric dilation and can clear gastric acid and accumulated blood, and understand the bleeding situation.

　　(2) Ice saline or vasoconstrictor lavage Ice saline lavage (60ml each time) or vasoconstrictor (norepinephrine 8mg placed in 100ml glucose solution) is infused, which can cause mucosal blood vessels to contract to achieve hemostasis.

　　(3) Extragastric use of vasoconstrictors norepinephrine 8mg is placed in 250ml normal saline and infused into the peritoneal cavity or performed by selective arterial catheterization, at a rate of 0.2u per minute. Vasopressin is administered in the left gastric artery, for 24 hours, and gradually reduced in dose after bleeding stops.

　　(4) Antacid drug interval lavage H2 receptor antagonist cimetidine and prostaglandins can cause hyperemia and dilatation of gastric mucosal blood vessels, increasing bleeding, so some people advocate not using them in cases with bleeding.

　　(5) Surgical treatment is only required for 10% of patients with stress ulcer bleeding. The indications for surgery are: ① The bleeding is severe from the beginning, and rapid blood transfusion cannot maintain blood pressure; ② Continuous or intermittent bleeding, with a blood transfusion volume of 2 to 31 within 24 to 48 hours. There is a divergence of opinions on the choice of surgical methods. The earliest was to perform a subtotal gastrectomy. However, there is often rebleeding after surgery, indicating that the subtotal gastrectomy does not remove enough mucosa, and does not remove all bleeding foci, or prevent residual mucosa from producing new bleeding foci. Total gastrectomy has good hemostatic effects, but the general condition of patients with stress ulcer is extremely poor, with a high mortality rate and many postoperative sequelae. Now, generally, surgery to reduce gastric acid production and/or remove part of the mucosa, as well as gastric vessel ligation, is adopted. The former includes subtotal gastrectomy, vagotomy, and vagotomy combined with partial gastrectomy. Vagotomy not only reduces gastric acid secretion but also opens the arteriovenous shunts in the stomach, reducing blood flow to the gastric mucosa. Some data show that the hemostatic effect of vagotomy is similar to that of subtotal gastrectomy, but the rebleeding rate and mortality rate are both lower than those of subtotal gastrectomy. The hemostatic effect of partial gastrectomy combined with vagotomy is better than both of the former, and the rebleeding rate is lower than both of the former. Gastric vessel ligation involves ligating and tying off all gastric vessels except the short gastric artery (including the left and right gastric arteries and the left and right gastroepiploic arteries). Some reports indicate a low rebleeding rate after surgery, with no necrosis of the stomach and no complications after partial gastrectomy. Some advocate using the Roux-en-Y method to reconstruct the gastrointestinal tract after partial gastrectomy to prevent bile reflux and damage to the gastric mucosa. For patients with postoperative rebleeding, surgery should be performed as soon as possible, and it is best to use near-total gastrectomy or total gastrectomy, which is a reliable hemostatic surgery, because these patients cannot tolerate a second postoperative hemorrhage or a third hemostatic surgery.

　　II. Prognosis

　　Generally speaking, in young patients with low risk, vagotomy and gastrectomy (usually resection of 70% to 75% of the stomach) can be performed, along with the excision of hemorrhagic ulcers. The hemorrhagic ulcers remaining at the bottom of the stomach are sutured and ligated. In elderly patients with high risk, vagotomy and pyloroplasty can be performed, and the hemorrhagic ulcers are sutured. Regardless of which surgery is performed, the overall mortality rate is quite high, reaching 35% to 40%.