I. Definition
Stress ulcers (SU) are acute gastrointestinal erosions and ulcers that occur in the body under severe stress conditions such as various types of severe trauma and critical illnesses, which can eventually lead to gastrointestinal bleeding, perforation, and deterioration of the original lesions. Thus, prevention of SU is a non-negligible aspect of rescuing critically ill patients. su is also known as acute gastric mucosal lesion (AGML), acute erosive gastritis, acute hemorrhagic gastritis, etc.
Second, the etiology of the occurrence of stress ulcers (stressors)
A variety of diseases can lead to the occurrence of SU, the most common stressors are:
1, heavy cranial trauma (also known as Cushing’s ulcer)
2, severe burns (also known as Curling ulcers)
3, severe trauma and a variety of difficult and complex postoperative major surgery
4.Serious systemic infection
5.Multi-organ dysfunction syndrome (MODS) and / or multi-organ failure (MOF)
6, shock, heart, lung, brain resuscitation after surgery
7, cardiovascular and cerebrovascular accidents
8, severe psychological stress, such as trauma, excessive stress, etc.
III. Stress ulcer pathogenesis
The weakening of gastric mucosal defense function and the relative enhancement of gastric mucosal damage factor are the main mechanisms of SU pathogenesis.
1, gastric mucosal defense function is reduced: microcirculatory disorders occurring locally in the mucosa under stress, and the mucosal barrier (bicarbonate) and epithelial barrier function are reduced.
2, increased gastric acid secretion: among the various injury factors, gastric acid plays an important role in the early onset of the disease, other injury factors include increased secretion of pepsinogen, as well as various types of inflammatory mediators produced in the case of ischemia.
3, neuroendocrine dysregulation: hypothalamus, paraventricular nucleus and limbic system are the integration centers for stress, and central mediators such as thyrotropin-releasing hormone (TRH), 5-hydroxytryptamine (5-HT) and catecholamines may be involved in and mediated the occurrence of SU.
IV. Clinical manifestations of stress ulcers
1. Clinical features:
(1) The more severe the primary disease, the higher the incidence of (SU), the more aggressive the disease, and the higher the mortality rate.
(2) No obvious prodromal symptoms (such as stomach pain, acid reflux, etc.), the main clinical manifestations are upper gastrointestinal bleeding (vomiting blood or black feces) and symptoms of hemorrhagic shock. In patients without overt bleeding, a positive gastric fluid or fecal occult blood test and an unexplained decrease in hemoglobin concentration ≥20 g/L should be considered as a possible stress ulcer with bleeding.
(3) When perforation occurs in SU, signs and symptoms of acute abdomen may be present.
(4) The occurrence of SU is mostly concentrated within 3 to 5 days of the primary disease production, and a few can be delayed up to 2 weeks.
2. Endoscopic features of radical ulcers.
(1) The lesions are most frequent in the body of the stomach, but are also seen in the esophagus, duodenum and jejunum.
(2) The morphology of lesions is mainly multiple erosions and ulcers, the former showing multiple bleeding spots or bleeding patches, and the depth of ulcers may reach the submucosa, intrinsic muscular layer and plasma membrane layer.
V. Diagnostic methods of stress ulcers
With a history of stress, upper gastrointestinal bleeding, perforation and other symptoms occurring within 2 weeks after the original disease, endoscopic examination should be done immediately when the condition allows, and if lesions such as erosions and ulcers exist, the SU diagnosis can be established.
VI. Prevention of stress ulcers
Stress ulcers are important for prevention and should be the focus of prevention in high-risk patients with gastrointestinal monitoring.
1. The following conditions are listed as high-risk groups for SU.
(1) Advanced age (age ≥ 65 years);
(2) severe trauma (craniocerebral trauma, burns, thoracic and abdominal complications, difficult major surgery, etc.);
(3) Combined shock or persistent hypotension;
(4) Severe systemic infection;
(5) Complicated MODS, mechanical ventilation >3d;
(6) Severe jaundice;
(7) Combined coagulation disorders;
(8) Post-transplantation of organs;
(9) Long-term application of immunosuppression and extra-gastrointestinal nutrition;
(10) History of ulcer within 1 year;
2, actively deal with the original disease, eliminate the source of stress; anti-infection, anti-shock, prevention and control of intracranial hypertension, protection of heart, brain, kidney and other important organ functions.
3.Gastrointestinal monitoring, insertion of gastric tube, regular testing of gastric pH or 24h gastric pH test, and regular testing of fecal occult blood.
4.For those who have a history of ulcers, gastroscopy can be performed before the perioperative period of major surgery to clarify whether there are combined ulcers.
5.Drug prevention
(1) Acid-suppressing drugs.
① Pre-operative prevention: for patients who are to undergo major surgery, it is estimated that there is a possibility of post-operative complications SU, oral acid suppressants or antacids can be applied within a week before the perioperative period to raise the gastric pH. Commonly used drugs are: proton pump blocker (PPI) omeprazole 20mg, 1 time/d; histamine receptor blocker: famotidine 20mg, 2 times/d; ranitidine 150mg, 2 times/d, cimetidine 400mg, 2 times/d.
(2) Prevention for severe trauma and high-risk people: PPI should be given intravenously after the onset of the disease to make the pH in the stomach rise rapidly to above 4, such as omeprazole (40mg,2 times/d).
(2) Antacids include: aluminum hydroxide, magnesium aluminum carbonate, 5% sodium bicarbonate solution, etc., which can be injected from the gastric tube to make the intragastric pH ≥ 4.
(3) mucosal protective agents are: aluminum thioglycollate, prostaglandin E, etc., the duration of medication is not less than 2 weeks.
6.Supportive therapy
(1) If the condition permits, encourage early feeding to neutralize gastric acid and enhance gastrointestinal mucosal barrier function.
(2) If there is hypoproteinemia, electrolyte and acid-alkaline balance disorder, timely supplementation and adjustment should be made.
VII. Treatment of stress ulcer complicated by gastrointestinal bleeding
Once the symptoms of gastrointestinal bleeding such as vomiting blood or black stool are found, it indicates that SU has occurred. At this time, in addition to continuing to treat the original disease, various hemostatic measures and treatment of stress ulcer must be taken immediately.
1.Immediately transfuse blood and rehydrate to maintain normal blood circulation.
2.Rapidly raise the intragastric pH to ≥6 to promote platelet aggregation and prevent thrombus lysis to create the necessary conditions for intragastric hemostasis.
(1) The recommended medication is PPI injection (omeprazole, first dose 80mg, later 40mg,q8h maintenance)
(2) H2 blocker injection, famotidine (40mg), cimetidine (800mg) intravenous twice daily.
(3) Intragastric infusion of alkaline drugs (e.g. aluminum hydroxide, etc.) to keep gastric juice pH above 6.
(4) Conditions permitting, growth inhibitors can also be considered.
3.For those who have bacterial infection in combination with burns, etc., the application of mucosal protective agents and antibiotics should be strengthened to prevent the displacement of flora.
4.For patients with coagulation mechanism disorders, platelet suspension, prothrombin complex, etc., and other drugs to promote coagulation can be transfused.
5.After drug treatment, if the condition cannot be controlled, emergency gastroscopy should be done immediately to clarify the diagnosis if the condition permits, and endoscopic hemostasis treatment can be done.
6.If the bleeding cannot be effectively stopped by medication and endoscopic intervention, surgical treatment can be considered if the situation permits in order to save the patient’s life.
7.After the bleeding stops, anti-ulcer drugs should continue to be applied until the ulcer heals. The recommended drugs are PPI, H2 blocker, etc. The course of treatment is 4-6 weeks.