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. Due to premature birth or low weight and admitted to the ward, during artificial feeding or for immature children due to incomplete establishment of swallowing reflex and placement of gastric tube during nasal feeding found retention in the stomach, followed by abdominal distension, vomiting, blood in the stool fever or temperature does not rise, tachycardia or slow heart rate, abdominal muscle tension, abdominal distension, abdominal wall erythema and other signs. (A) Pathogenesis 1, the presence of certain bacteria in the intestine and the toxins produced: Clostridium perfringens B toxin is more likely, because it was found that patients with this disease fecal anaerobic culture, the detection rate of this bacterium and its B toxin serum antibody positivity rate are significantly higher than the normal population, the bacteriological solution injected into the guinea pig small intestine, can make its intestinal hemorrhagic lesions and death. 2, sick children with reduced trypsin activity: the above B toxin can be intestinal trypsin hydrolysis and loss of pathogenic effect, long-term protein malnutrition and (or) frequent consumption of sweet potatoes, corn and other foods rich in trypsin inhibitors, can make the intestinal trypsin activity significantly reduced, so that the sick children easy to develop, which can explain why the disease is higher in poor rural areas. (The typical pathological changes of necrotizing small bowel infection are necrotizing inflammatory changes, starting from the submucosal layer, with the expansion of the lesion, can develop to the muscular layer and mucosal layer, so that the whole layer of the intestinal wall is congested and edematous focal necrosis, the necrotic mucosa is shed to form ulcers, continue to develop to the muscular layer, plasma layer, and perforation caused by peritonitis, the lesion is mostly seen in the lower jejunum and upper ileum, but also in the duodenum In severe cases, the entire small intestine can be involved, generally scattered, segmental arrangement, some for 1 to 2 segments or more than 2 segments, the length of each segment varies, the shortest more than 10 cm, the longest up to 100 cm, clearly delineated, the damaged intestinal wall thickened, brittle, loss of elasticity, dilated, heavy plasma membrane surface rough with fibrin adhesion, the intestinal lumen is filled with jam-like blood stool, microscopically visible lesions intestinal wall layers have Inflammatory cell infiltration, mainly lymphocytes, eosinophils, monocytes, plasma cells, mucosa can be necrotic or detached, the submucosa has a large area of hemorrhagic necrosis and edema, capillary dilatation and congestion, the abdominal cavity can be cloudy, purulent or hemorrhagic exudate, the lesion recovery does not leave chronic granulomatous changes, causing intra-abdominal adhesions is rare.