Infants and children with acute necrotizing enterocolitis have atypical symptoms, with the onset of the disease in the first 3 to 10 days of life. They are admitted to the intensive care unit due to prematurity or low birth weight, and during artificial feeding or during nasal feeding with a gastric tube placed in immature children due to incomplete establishment of the swallowing reflex, they are found to have retention in the stomach, followed by signs such as abdominal distention, vomiting, fever with blood in the stool or temperature not rising, tachycardia or slow heart rate, abdominal muscle tension, abdominal distension, and erythema of the abdominal wall. There is no single satisfactory explanation for the etiopathogenesis, but there is more agreement on certain susceptibility factors and reasoning. These susceptibility factors include: intestinal ischemia, intestinal infection, impaired intestinal barrier function, respiratory distress syndrome, hemorrhage, asphyxia, congenital heart disease combined with heart failure, sepsis, shock, hypothermia, erythrocytosis and/or high blood viscosity, artificial feeding, etc. 1, intestinal ischemia A variety of causes of visceral vasoconstriction, mesenteric vascular blood supply is insufficient can lead to intestinal ischemic damage, intestinal mucosa susceptibility to ischemia is most prominent. Experimentally, autolysis of the small intestinal mucosa was observed in rats 1 h after the onset of hemorrhagic shock. The clinical principle of dealing with ischemic damage should be to restore blood reperfusion as soon as possible to increase tissue oxygenation, but prolonged ischemia can lead to reperfusion damage after restoration of perfusion, which is caused by calcium overload, oxygen radical generation, release of various enzymes including elastase and collagenase triggered by activation of neutrophils, and imbalance of endothelial cell homeostasis. The intestinal tract is the largest bacterial reservoir in the human body, and bacteria and toxins cannot be invaded due to the protective effect of the intestinal mucosa itself, which is called a defense barrier. Shock, intestinal ischemia, asphyxia, poor artificial feeding, etc. can lead to the destruction of the intestinal barrier, which in turn causes the imbalance of bacterial microecology in the intestine and the invasion of bacteria and toxins to induce AHNE. These can lead to infection, necrosis, and perforation of the intestinal wall. C-type P. aeruginosa in the feces (Welchii bacterium that produces β toxin) can easily cause pathogenic effects, causing intestinal microcirculation disorders, and manifest patchy gangrenous intestinal lesions. 3, intestinal barrier insufficiency Intestinal barrier function includes mechanical, immune, biological, chemical and motor functional barriers. Under normal conditions, intestinal mucosal epithelial cells, intercellular connections and bacterial membranes form a mechanical barrier, and intestinal mucus and mucin form an elastin layer covering the surface of intestinal mucosa, which prevents bacteria from invading and protects against chemical and mechanical stimuli. Under normal conditions, secretory immunoglobulins (sIgA) secreted by the intestinal mucosa are extremely important for the local immune function of the mucosa and serve as an immune barrier, whose role is to form a protective layer on the mucosal surface, prevent bacterial adhesion, cause bacterial agglutination, inhibit bacterial activity and neutralize bacterial toxins and defend against viruses, as well as against various protein hydrolases. sIgA deficiency results in bacterial adhesion to the mucosal epithelium and formation of colonies, which in turn The lack of sIgA causes bacteria and endotoxin to invade the body circulation through the portal vein and lymphatic system, forming enterogenic endotoxemia and bacterial translocation. The role of inflammatory mediators in the pathogenesis of AHNE has recently focused more on the study of relevant inflammatory mediators. Platelet-activating factor (PAF), tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6) and endothelin 1 (ET-1) have been found to be important inflammatory mediators in the pathogenesis of AHNE in animal models.