Acute gastric mucosal bleeding is an acute lesion characterized by superficial gastric mucosal damage with changes such as congestion, edema, erosion, bleeding, or even the formation of a transient superficial ulcer, and is a common complication of severe psychological disorders and critical clinical conditions. Its main manifestation is upper gastrointestinal bleeding, which can endanger the patient’s life in severe cases. It has been clinically named many different names, such as acute erosive gastritis, acute hemorrhagic gastritis, acute stress hemorrhage, and stress ulcer. Widely distributed multiple erosions or ulcers are common pathological changes of various acute gastric mucosal lesions complicated by bleeding, and their exact pathogenesis has not been fully elucidated, but is generally believed to be related to ischemic necrosis of the gastric mucosa, weakened gastric mucosal barrier function and persistence of a hyperacidic environment in the gastric lumen. On the basis of damage to the gastric mucosa due to ischemia and hypoxia, capillary permeability increases, mucosal congestion and edema, histamine release further increases gastric acid secretion, and this vicious cycle eventually leads to severe hypoxic necrosis of the mucosa and loss of large portions of the mucosa, forming mucosal erosions and superficial ulcers, which in turn cause upper gastrointestinal bleeding. When the disease progresses further and erodes larger blood vessels, it can cause hemorrhage. From the pathological point of view, it is now considered more reasonable to refer to acute gastric mucosal damage and stress superficial ulcers caused by various stress factors as acute gastric mucosal hemorrhage. The etiology and pathogenesis of acute gastric mucosal hemorrhage have not been fully elucidated, and there are many triggers that can cause this disease. It is mainly believed that various stress factors act on the central nervous system and the gastrointestinal tract, and through the interaction of the neuroendocrine and digestive systems, the balance between protective and damaging factors that maintain the integrity of the gastroduodenal mucosa is disrupted. From the available data stress, drugs and alcohol consumption are the most important causative factors. Drugs, alcohol, microbial infection and other factors as exogenous damage factors, damage the gastric mucosal barrier and lead to gastric mucosal erosion; various stress factors stimulate the body to produce stress response, produce endogenous damage factors and stimulate the body to secrete a lot of glucocorticoids, so that gastric acid increases, mucus decreases, and the gastric mucosa is vulnerable to damage. Commonly used antipyretic and analgesic drugs such as aspirin have a strong apoptogenic effect on gastric mucosa and can inhibit the proliferation of mucosal cells. The diagnosis of this disease is mainly based on medical history and clinical manifestations, and the confirmation of diagnosis depends on emergency gastroscopy. The key to treatment is to reduce the causative factors as much as possible and to actively treat the underlying disease. Reducing the acidity in the stomach is the key to treatment, and treatment of the underlying disease is the key to treatment. The commonly used potent acid-control agents are H2 receptor antagonists and H+-K+ ATP pump inhibitors, including famotidine, omeprazole, lansoprazole, etc., which have the characteristics of fast-acting, strong and long-lasting effect of inhibiting gastric acid. Most of the acute gastric mucosal bleeding can be treated conservatively with non-surgical treatment, and some of the bleeding lesions with more limited lesions can be stopped locally by endoscopy. Acute gastric mucosal hemorrhage occurs mostly in the gastric body and gastric fundus. It is rare that the lesion involves only the gastric sinus and duodenum, but not the gastric body and fundus. Since the lesions are mostly confined to the mucosal layer and are relatively superficial, perforation does not usually occur. In most cases, the effect of conservative treatment is positive, but there is a certain mortality rate, and the cause of death is usually due to rebleeding and multi-organ failure, so it must be given sufficient attention in clinical practice. Acute gastric mucosal hemorrhage presents mainly as upper gastrointestinal bleeding with no obvious specificity. The main symptoms are vomiting blood and/or black stool, and most patients only have the resolution of tarry black stool without vomiting blood. Before the resolution of black stool, there is often a sudden feeling of bowel movement, and there may be dizziness, palpitations, weakness, or even fainting before and after defecation. If the bleeding volume is large, compensatory manifestations such as increased heart rate, mild increase in diastolic blood pressure due to peripheral vasoconstriction and decreased pulse pressure difference may occur. The bleeding in this disease is usually characterized by intermittent episodes, and there are few prodromal symptoms. Sometimes, vague epigastric pain, nausea, and burning sensation can be felt. The medical history often includes a history of severe systemic illness or trauma, as well as the use of non-steroidal antipyretic analgesics (NSAIDs) or heavy alcohol consumption. From the physical examination, there are usually no obvious signs in the abdomen, but there may be mild pressure pain in the upper abdomen and hyperactive bowel sounds; if the bleeding volume is large, there may be compensatory manifestations of the circulatory system such as accelerated heart rate and reduced pulse pressure difference; if the bleeding volume reaches 800 ml or more, there may be obvious manifestations of shock, including irritability or apathy, cold sweat, wet and cold hands and feet, shortness of breath, fine and rapid pulse rate and decreased blood pressure. Because the clinical manifestations of this disease lack specificity, it is not very different from upper gastrointestinal bleeding caused by other causes, and sometimes it can be masked by the symptoms of the primary disease or concomitant diseases. In clinical observation, changes in gastrointestinal symptoms and abdominal signs should be noted. There are two more specific types of acute gastric mucosal bleeding. Gastroduodenal ulcers that form after severe burns, often referred to as Curling ulcers. Gastroduodenal ulcers caused by traumatic brain injury, brain surgery, or central nervous system disease are usually referred to as Cushing ulcers. These two specific types of ulcers have higher than normal levels of gastric acid secretion and serum ghrelin. The latter usually invades deeper into the gastroduodenal wall and is prone to complications such as bleeding or perforation, which is not identical to the usual type of acute gastric mucosal bleeding. The etiology of non-steroidal antipyretic and analgesic drugs such as aspirin, anti-inflammatory pain and alcohol is not related to severe trauma or disease, which also mainly manifests clinically as upper gastrointestinal bleeding, but is characterized by healing once the drug is discontinued, and the treatment is easier and more effective. Acute gastric mucosal bleeding is one of the common causes of acute upper gastrointestinal bleeding and should be diagnosed and treated rapidly. In the process of treatment of this disease, firstly, internal medicine is the main treatment, which can generally achieve better results. For a few patients with serious bleeding and ineffective conservative treatment, emergency surgery should be considered when necessary. I. Non-surgical treatment 1. general treatment; 2. removal of etiology and volume supplementation; 3. antacid and inhibition of digestive secretion; 4. gastrointestinal decompression and infusion of hemostatic drugs; 5. gastroscopic hemostasis. When various non-surgical treatments fail to stop bleeding, some scholars have selectively cannulated the left gastric artery via the femoral artery and drip injected vasoconstrictive drugs, which has achieved certain efficacy in some patients. For example, vasopressin dripping through the left gastric artery can make the small gastric mucosal arteries contract and reduce mucosal congestion to stop bleeding. Non-surgical treatment can achieve the purpose of hemostasis in most of the patients, but sometimes surgery must be considered when the hemorrhage cannot be stopped by non-surgical treatment or is repeated after it has stopped, or even when it is life-threatening. However, there are many controversial and divergent views on surgical methods. There are various surgical methods, including suture of bleeding point in the stomach, ligation of blood vessels outside the stomach, vagus nerve trunk cut plus pyloroplasty, vagus nerve trunk cut plus major gastric resection and total gastrectomy. In addition to the hemostatic effect, the patient’s tolerance of the procedure must be fully considered when choosing the surgical approach. From the current literature, most scholars prefer vagotomy with major gastrectomy or vagotomy with bleeding point suturing and pyloroplasty.