There has long been a debate about the advantages and disadvantages of enteral nutrition (EN) and parenteral nutrition (PN). In patients with intestinal function, EN is undoubtedly the best mode of nutritional support. However, intestinal obstruction, intestinal mucosal lesions, short bowel, and intestinal fistulae have limited the use of EN in patients with intestinal dysfunction to varying degrees. since the 20th century, the understanding and experience with PN has evolved considerably, and survival time in patients who have relied on PN support for a long time no longer depends on the implementation of PN, but mainly on the extent of the underlying lesion. Therefore, when considering the optimal mode of nutritional support for intestinal dysfunction, different patients may require different ratios of EN and PN support depending on the degree of intestinal dysfunction to ensure that the patient receives adequate amounts of nutritional substrate. The nutritional substrate provided to patients with type II bowel dysfunction not only meets the patient’s needs, but also helps the patient to recover rapidly from the process of abdominal infection’1I. Total parenteral nutrition (TPN) can replace the gastrointestinal tract to provide known nutrients needed by the body, leaving the gastrointestinal tract in a functional state of quiescence, thus having a therapeutic effect on certain gastrointestinal diseases. Since PN enters the circulation directly without passing through the gastrointestinal tract, it is the only way to supply nutrients to patients who cannot apply the gastrointestinal tract for anatomical or functional reasons. Therefore, when TPN first began to be used in the clinic, clinicians embraced this new therapy with great enthusiasm, applied it widely, and played a significant role. So many patients recovered from TPN that some physicians still believe that only central venous line infusion is the only way to support nutrition. Clinical and experimental evidence suggests that protein malnutrition can promote inflammation and lead to intestinal bacterial translocation. The cause of this may be related to the decline in immune function, intestinal mucosal damage and dysbiosis of intestinal flora day J. However, critically ill patients with long-term TPN application can develop medical intestinal starvation syndrome, manifested by slowed intestinal peristalsis, significantly reduced intestinal mucosal cell population, mucosal atrophy, reduced height of villi, protein and DNA content, as well as a significant reduction in secretory IgA in the intestinal lumen. Experimentally, rI’PN can lead to a significant increase in the number of intestinal bacteria and their metastasis to mesenteric lymph nodes ij. Possible reasons for the altered intestinal anatomy and immune dysfunction caused by this TPN standard formula are: (i) damage to intestinal mucosa and immune system function due to the patient’s pre-existing diseases, such as major surgery, severe infection, malnutrition, etc.; (ii) damage to intestinal mucosa and immune system function due to fasting and lack of effective stimulation of intestinal mucosa by intestinal food; (3) TPN reduces the production of pancreatic and biliary fluid and other GI secretions, which weakens their nutritional effect on intestinal mucosa; @ the lack of nutrients specific to intestinal mucosa cells, such as glutamine (Gin), in the standard formula of TPN. EN helps maintain the structural and functional integrity of intestinal mucosal cells, supports the intestinal mucosal barrier, and can significantly reduce the occurrence of enteric-derived infections. The mechanisms of action include: (1) maintaining the normal structure, intercellular junctions and villi height of intestinal mucosal cells, maintaining the mechanical barrier of the mucosa; (2) maintaining the normal growth of the intrinsic intestinal flora, maintaining the biological barrier of the mucosa; (3) contributing to the normal secretion of IrA by intestinal cells, maintaining the immune barrier of the mucosa; (4) stimulating the secretion of gastric acid and pepsin, maintaining the chemical barrier of the mucosa; (5) stimulating the secretion of digestive juices and gastrointestinal hormones secretion, promote gallbladder contraction and gastrointestinal peristalsis, increase visceral blood flow, and make the metabolism more in line with the physiological process, thus reducing the incidence of liver and biliary complications. Especially when the condition is critical, the immune function of the body decreases, and the low blood flow in the intestine leads to nutritional damage to the intestinal mucosa, while the metabolism is impaired in the critical condition, TPN tends to make the metabolism deviate from the physiological process, and the metabolic complications increase. EN is particularly important at this time. In recent years, there have been many discussions on the methods of nutritional support, and now the view is more consistent, that is, the two methods of enteral and parenteral nutritional support have their own advantages and disadvantages, and have their own indications, and TPN, TEN or PN + EN combined nutritional support can be selected according to different patients and different stages of the patient’s disease. The principles of choosing a reasonable nutrition support method are: ① between PN and EN, EN should be preferred; ② between trans-peripheral vein and trans-central vein PN, trans-peripheral vein PN should be preferred; ③ when EN is insufficient, PN can be used to strengthen; ④ when the nutritional needs are high or when short-term improvement of nutritional status is expected, PN can be used; ⑤ when longer-term nutritional supporters are needed, EN should be applied. Most intestinal Most patients with intestinal dysfunction do not require complete fasting for intestinal rest. In addition to supplying nutrition, EN also has the effect of promoting the growth and repair of intestinal mucosal cells and helps maintain the barrier function of the intestinal mucosa. Among the types of EN, intact protein formulations stimulate intestinal mucosal renewal and repair more than peptide or pure amino acid formulations, but intact protein formulations require an intact digestive capacity of the intestine, which is what is lacking in intestinal dysfunction, especially in critically ill patients. Therefore, peptide formulations are more frequently used. In recent years, the application and research of EN has been increasing, and EN formulations and infusion methods are being improved and developed, the most notable of which are Gin and dietary fiber, Gin is a tissue specific nu. trient for intestinal mucosal cells, and the intestinal uptake of Gin far exceeds that of any other amino acid. Many studies have shown that intestinal administration of Gin reduces intestinal wall permeability, prevents intestinal bacterial translocation, and improves patient survival. It maximizes intestinal function by improving the absorption of glucose, sodium, and other substances. These pharmacological effects have important clinical implications for patients with intestinal dysfunction in malabsorption, diarrhea and malnutrition. Combined application of Gin and growth hormone (GH) significantly improves protein synthesis in intestinal mucosal cells and promotes compensatory hyperplasia of the remaining small intestine after extensive resection of the small intestine, thus better improving the structure and function of the intestine. In the diet, both water-soluble and non-water-soluble fibers stimulate and promote mucosal growth and cell proliferation in the small intestine and colon, but different dietary fibers play different roles on the morphological structure of the intestine, gastrointestinal motility and nutrient absorption. Insoluble fiber (cellulose) increases stool volume and promotes intestinal peristalsis, while specific water-soluble fiber (if gum) delays gastric emptying and slows down intestinal food transport time, thus having anti-diarrheal effects. Fermentable water-soluble fiber (non-starch polysaccharides) can be catabolized by anaerobic bacteria to produce short-chain fatty acids (SCFA), which are readily absorbed by the colonic mucosa and utilized as energy, and have a nutritional stimulating effect on both small intestine and colonic mucosa, promoting intestinal mucosal cell proliferation, especially the absorption of water and sodium in the colon. Since the 1990s, a series of related studies have shown that. Certain nutrients can not only prevent and treat nutritional deficiencies, but also stimulate immune cells in a specific way, enhance immune response function, regulate cytokine production and release, reduce harmful or excessive inflammatory responses, maintain intestinal barrier function, etc. HJ. This therapeutic concept is called immunonutrition. Currently, nutrients with immunopharmacological effects that have begun to be applied in clinical practice include arginine, ∞-3 fatty acids and nucleotides, in addition to the aforementioned Gin and dietary fiber. On the basis of immune nutrition, ecological immune nutrition (ecoimmune nutirtion) has been proposed in recent years, i.e., in addition to the aforementioned nutrients, Lactobacillus and Bifidobacterium are added to the EN formula, such as Lacto.bacillus plantamn 299, Lactobacilhs ruteri o which has strong adhesion to the colonic mucosa It is believed that it is rich in Gin, glutamic acid and phospholipids. Some studies have shown that it can change the intestinal flora and reduce the growth of pathogenic bacteria and intestinal bacterial translocation DJ. Certain chronic lesions (such as Crohn’s disease or pseudo-intestinal obstruction) often progress over a long period of time before developing into intestinal dysfunction; while certain lesions (such as extensive intestinal necrosis due to superior mesenteric artery thrombosis) often develop overnight into intestinal failure. The surgical planning for these different types of bowel dysfunction, which may vary, often requires a multidisciplinary treatment model that includes controlling abdominal infection, improving nutritional status, determining intestinal anatomy, and developing definitive treatment measures to reduce the incidence of patient complications and morbidity and mortality. Bowel dysfunction is difficult and costly to treat, so clinicians must focus on prevention of bowel dysfunction. For example, early diagnosis and early treatment of potential intestinal ischemic lesions, avoiding fistulas and abdominal infections caused by surgical errors, careful surgical treatment to prevent abdominal adhesion formation, and not performing definitive surgery when abdominal infections are still present or when the patient is still malnourished to avoid complications and more intestinal tube loss. These are all noteworthy issues in preventing the occurrence of bowel dysfunction.