Stress ulcer

Introduction to stress ulcer Stress ulcers generally refer to acute gastritis that occurs during shock, trauma, postoperative surgery, and severe systemic infections, often accompanied by bleeding symptoms, and is an acute gastric mucosal lesion. The incidence of stress ulcers has increased in recent years, mainly due to the strengthening of intensive care, the effective support of vital organs, and the renewal of anti-infectives, increasing the chance of developing stress ulcers. basic knowledge The proportion of the disease: the probability of the population is 0.9% Susceptible people: no special people Mode of infection: non-infectious Complications: hypovolemic shock

Causes of stress ulcer

Trauma factor (25%)

Severe trauma causes the body to be in a state of stress: severe trauma, extensive burns, intracranial diseases, brain trauma, acute gastritis that occurs after abdominal surgery and severe systemic infections, often accompanied by bleeding symptoms.

Body factor (15%)

Long-term hypotension in the body can easily lead to stress ulcers such as shock, chronic renal failure, and multiple organ failure. After gastric acid action, the gastric juice drained is dark brown or brown and forms flocculent. When the amount of bleeding is large, there is hematemesis, melena, and even hypovolemic shock.

Drug factor (10%)

Long-term use of aspirin, indomethacin, etc. after treatment with anticancer drugs and steroids.

Other factors (5%)

Such as stomach acid, ischemia and destruction of the gastric mucosal barrier.

Stress ulcer is caused by gastric mucosal cells being destroyed by gastric acid and pepsin. Gastric acid is a necessary condition for ulceration. If there is no stomach acid, it will not produce ulcers. Normal human gastric mucosa is exposed to gastric acid and pepsin without being digested. Because the gastric mucosa has its own protective effect, the protective effect of the gastric mucosa includes the following three aspects:

(1) gastric mucus barrier

The mucous membrane of the stomach secretes mucus, the mucus is thick and jelly-like, and it is closely attached to the surface of the gastric mucosa. The gastric cavity is separated from the mucosal surface (cavity surface) of the epithelial cells of the gastric mucosa. The mucus layer has a special molecular structure and its internal moisture. Static, undisturbed, H+ and pepsin diffuse very slowly, so the mucus barrier maintains a pH gradient between epithelial cells and the gastric cavity.

(two) gastric mucosal barrier

The cell membrane of the luminal surface of gastric mucosal epithelial cells is composed of lipoprotein. The H+ in the gastric cavity cannot be reversely diffused into the cells through the gradient of the cell membrane. The cell membrane forms an H+ barrier between the gastric cavity and the epithelial cells, and a small amount of H+ through the mucus barrier. It is also blocked by the epithelial cell membrane, and the connections between the gastric mucosal epithelial cells are very tight, and H+ cannot enter the cells thereby.

(III) Neutralization of HCO3-

A large amount of carbonic anhydrase in gastric mucosal cells can produce intracellular oxidative metabolism, and CO2 and H2O from blood combine to form H2CO3, which dissociates into HCO3- and H+, and HCO3- from the basal surface of the cell (serosal surface) Entering the blood or interstitial fluid, can also be transported from the mucosal surface into the gastric cavity, neutralizing a small amount of H+ through the mucus layer in the mucus layer close to the mucosa, even if a small amount of H+ enters the mucosal epithelial cells can be infected by epithelial cells The internal HCO3- is neutralized to maintain the acid-base balance of the cells.

There are a large number of prostaglandins in the gastric mucosa. Prostaglandins stimulate the secretion of mucus and HCO3-, which has protective effects on gastric mucosal cells, while aspirin, indomethacin, phenylbutazone, cholate, corticosteroids, urea and other substances can destroy the stomach. Mucosal barrier, causing acute gastric mucosal lesions.

The maintenance of normal function of gastric mucosal barrier depends on the normal metabolism and constant renewal of gastric mucosal epithelial cells. Metabolism requires oxygen and substrate. Under stress conditions such as shock, patients have unequal hypotension and gastric microcirculation disorders, gastric mucosa. Ischemia, hypoxia, affecting mitochondrial function, resulting in decreased ATP synthesis, insufficient energy supply, dysfunction of cells, loss of ability to produce and secrete mucus and HCO3-, mucus barrier and mucosal barrier function, H+ reverse diffusion into cells The cells lack HCO3-neutralizing H+ into the cells, resulting in acidosis of the cells, lysis of intracellular lysosomes, release of lysozymes, autolysis of cells, destruction, and death. At the same time, DNA synthesis is affected due to insufficient energy, and cells cannot be Regeneration, necrotic cells do not regenerate cells to replace the renewal, forming ulcers, gastric mucosal cells have little energy (glycogen) reserves and high metabolic rate, which is more susceptible to ischemia than other organs (such as liver, muscle, etc.) Metabolism, the highest rate of epithelial cell metabolism in the gastric mucosal epithelial cells, which explains why stress ulcers occur in the fundus.

Stress ulcer prevention

The prevention of stress ulcers is more important than treatment, and prevention must be considered from both the systemic and local parts.

1. Systemic measures

Including removing stress factors, correcting blood supply, insufficient oxygen supply, maintaining water, electrolytes, acid-base balance, early nutrition support, etc. Nutritional support is mainly for early enteral nutrition, within 24 to 48 hours, using formula diet, from 25ml / h increased to 100ml / h, in addition to the use of preventive application of antacids and antibiotics, as well as measures to control infection.

2. Local measures

Including gastrointestinal decompression, gastric mucosal injection of sucralfate to protect the gastric duodenal mucosa, as well as injection of H2 receptor antagonists and ion pump inhibitors.

Patients with stress may have stress ulcers, so they should be treated promptly, supplement blood volume, correct circulation disorder, improve tissue perfusion, ensure ventilation, give oxygen, use antibiotics to prevent infection, and stress. Although gastric acid in patients with ulcers does not necessarily have excessive secretion, gastric acid is a necessary condition for the production of stress ulcers. Therefore, it is better for patients with severe stress to retain the gastric tube to continuously attract gastric juice, and one to maintain acid deficiency in the stomach. Second, to prevent gastric wall ischemia due to gastric dilatation, but the gastric mucosa is vulnerable to bleeding, suction should not be too large, while intravenous H2 receptor antagonist (cimetidine) inhibits gastric acid secretion and antacids (magnesium milk or Aluminum hydroxide) is inserted into the stomach through the stomach tube to neutralize gastric acid. Conditionally, 30 ml of antacid can be infused from the stomach tube every hour, and the tube is filled for 45 minutes, then the gastric juice is aspirated, and the blood is taken for 15 minutes. The pH of the stomach content, if the pH is <5, the 60 ml is irrigated for the second hour, and the pH of the stomach contents is maintained at >5, and some people do not advocate the use of the H2 receptor antagonist, because every one of the H+ is secreted when the parietal cells produce gastric acid. Generate one at the same time HCO3- (alkaline tide) secreted into the lumen of the stomach, H2 receptor antagonists inhibit gastric acid secretion at the same time also affects the generation of HCO3-, as antacid to neutralize gastric acid and without affecting the secretion of HCO3-.

Stress ulcer complications Complications hypovolemic shock

When an acute ulcer invades a bare blood vessel, it can cause major bleeding, and the patient may have hematemesis or even hypovolemic shock.

Stress ulcers can have no clinical symptoms if they do not cause major bleeding, or they can be covered by symptoms of stress without being diagnosed. Stress ulcers are superficial, and barium meal imaging is often not found, so often After major bleeding, after surgical exploration or death, it can be found through autopsy. Many cases of missed diagnosis have not been reported in the past. The clinical incidence rate has increased since the end of fiberoptic endoscopy, because not all patients with stress All routine endoscopy, the statistical incidence may be much lower than the actual number.

Stress ulcer symptoms Common symptoms Hemorrhoids peptic ulcer edema Upper gastrointestinal bleeding Mucosal congestion Peritonitis Renal failure Low blood volume shock Hepatic failure

Patients in intensive care unit or shock, extensive burns, severe trauma or infection, organ failure (such as acute renal failure, adult respiratory distress syndrome, liver failure) in patients with upper gastrointestinal bleeding, first consider stress The possibility of ulceration, because the lesion is too shallow, X-ray examination has no diagnostic value, fiber gastroscopy can rule out other bleeding lesions, clear diagnosis, if the amount of bleeding is large, can not see clearly, can be used for selective angiography.

In a few hours after a stressful condition, almost all patients can be found to have pale gastric mucosa within a few hours of stress. There are scattered red spots that are confined to the fundus. Microscopic examination reveals mucosal edema, submucosal vascular congestion, and few inflammatory cells. Infiltration, electron microscopy, multiple epithelial cell membrane destruction, in some places, the whole epithelial cells are detached, and the lamina propria of the mucous membrane is exposed. After 24 to 48 hours of stress, the entire gastric mucosa has a diameter of 1 to 2 mm, under the microscope. Visible mucosa has localized bleeding and coagulative necrosis. If the condition of the patient in the Soviet Union is improved, 90% of the patients will start to heal after 3 to 4 days. Generally, it will heal completely in 10 to 14 days. If the patient's condition continues to deteriorate, it will smash. The foci expand and expand, the whole layer of mucosa falls off, forms an ulcer, reaches the mucosal muscle layer and the submucosa, exposes the nutrient blood vessels, and if the blood vessel rots and ruptures, it causes bleeding.

The first manifestation is hemorrhage. When the bleeding is not the beginning of the lesion, there has been a period of time before the lesion. At first, the mucosal lesion is shallow and less, and no bleeding is caused. After the lesion is deepened, the bleeding can be caused if no preventive measures are taken. 5 to 10 days after the onset of stress, there is no pain during bleeding, and the bleeding is intermittent. Sometimes it is intermittent for several days, which may occur due to the presence of lesions, and the old lesions heal and new lesions form.

Stress ulcers are more common in 5 to 10 days after stress. The most common clinical manifestation is gastrointestinal bleeding in severe trauma, infection and shock. After gastric acid, the gastric juice drained is dark brown or brown and forms floccules. Shape, when the amount of bleeding is large, there is hematemesis, melena, and even hypovolemic shock, gastroscopy shows that the gastric mucosa is extensively erosive, and there are multiple superficial small ulcers, these changes and peptic ulcer, acute gastritis The difference.

Stress ulcer examination

X-ray examination of the shallow sputum meal has no diagnostic value. Fiberoptic gastroscopy can exclude other hemorrhagic lesions and confirm the diagnosis. If the amount of bleeding is large, it can not be seen clearly, and can be used for selective angiography.

In a few hours after a stressful condition, almost all patients can be found to have pale gastric mucosa within a few hours of stress. There are scattered red spots that are confined to the fundus. Microscopic examination reveals mucosal edema, submucosal vascular congestion, and few inflammatory cells. Infiltration, electron microscopy, multiple epithelial cell membrane destruction, in some places, the whole epithelial cells are detached, and the lamina propria of the mucous membrane is exposed. After 24 to 48 hours of stress, the entire gastric mucosa has a diameter of 1 to 2 mm, under the microscope. Visible mucosa has localized bleeding and coagulative necrosis. If the condition of the patient in the Soviet Union is improved, 90% of the patients will start to heal after 3 to 4 days. Generally, it will heal completely in 10 to 14 days. If the patient's condition continues to deteriorate, it will smash. The foci expand and expand, the whole layer of mucosa falls off, forms an ulcer, reaches the mucosal muscle layer and the submucosa, exposes the nutrient blood vessels, and if the blood vessel rots and ruptures, it causes bleeding.

1. Blood routine hemoglobin decreases and hematocrit decreases.

2. Fecal occult blood test was positive.

3. Fiber gastroscopy has special importance. In the early stage, most scattered pale spots can be seen on the proximal mucosa of the stomach. After 24 to 36 hours, multiple superficial red spots can be seen, and ulcers can appear later, even in black. Some manifested as active bleeding.

42. Selective angiography can determine the location and extent of bleeding, and can be injected via a catheter to stop bleeding.

Diagnosis and diagnosis of stress ulcer

Differential diagnosis

Stress ulcers differ from other mucosal lesions or ulcers in the stomach:

(1) Acute mucosal lesions caused by alcohol, hormones and non-hormonal anti-inflammatory preparations (such as aspirin, indomethacin, etc.) are not accompanied by severe infection, trauma and other stress conditions. The lesion is multiple superficial erosions, the site of occurrence Similar to stress ulcers, but limited to mucous membranes, does not invade the muscle layer, does not leave scars after healing, generally does not cause a lot of bleeding, bleeding can stop by itself, no need for surgical treatment.

(2) Curing ulcers caused by burns are also acute ulcers, which occur during the recovery period of burns, while stress ulcers caused by burns occur 3 to 5 days after burns. Curling ulcers are single and located in the duodenum. , often penetrate the intestinal wall leading to perforation.

(3) Cushing ulcer caused by brain trauma, brain tumor or intracranial neurosurgery occurs in the esophagus, stomach or duodenum, can penetrate the gastrointestinal wall, and has hypersecretion of gastric acid and pepsin (due to excessive stimulation of the vagus nerve). Serum gastrin levels are elevated, while stress ulcers are not hypersecremic to gastric acid or pepsin.

Stress ulcers can have no clinical symptoms if they do not cause major bleeding, or they can be covered by symptoms of stress without being diagnosed. Stress ulcers are superficial, and barium meal imaging is often not found, so often After major bleeding, after surgical exploration or death, it can be found through autopsy. Many cases of missed diagnosis have not been reported in the past. The clinical incidence rate has increased since the end of fiberoptic endoscopy, because not all patients with stress All routine endoscopy, the statistical incidence may be much lower than the actual number.

Burns caused by stress ulcers generally have a burn area of more than 35%, and the area is less than 50%. If no sepsis occurs, only 2% of the sepsis develops stress ulcers. If the sepsis is complicated, the incidence increases to 19%. , trauma, severe infection after surgery is prone to stress ulcers, chest and abdomen combined injury is more likely than chest, soft tissue or limb injury to cause stress ulcers, chronic gastroduodenal ulcer or cirrhosis esophageal vein Stress ulcers often occur after variceal bleeding.

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