What Is Bolus Tube Feeding?

Intestinal infections are intestinal mucosal atrophy, barrier damage, and translocation of bacteria and endotoxin in the intestine 1 to 2 hours after a large area burn. If it is not handled promptly or improperly, bacteria enter the portal vein system and blood lines spread, causing intestinal infections. Gut-infected infection can occur very early after injury, and there are no obvious signs of infection in the wounds, lungs, veins, and urinary tract when symptoms of infection have just appeared. The preventive method is to perform effective liquid resuscitation as soon as possible after burns, and eat small amounts or stay in the small intestine catheter and nasal feeding early to reduce the destruction of the intestinal barrier and reduce the intestinal bacterial displacement. Immediately after intestinal infection, broad-spectrum antibiotics should be applied, supportive therapies should be strengthened, attention should be paid to energy and various nutrient supplements, and drugs to promote gastrointestinal mucosal repair should be provided. Ceftazidime has a good effect in preventing and treating enteric infections. ^[1]

Enteric infection

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Intestinal infections are intestinal mucosal atrophy, barrier damage, and translocation of bacteria and endotoxin in the intestine 1 to 2 hours after a large area burn. If it is not handled promptly or improperly, bacteria enter the portal vein system and blood lines spread, causing intestinal infections. Gut-infected infection can occur very early after injury, and there are no obvious signs of infection in the wounds, lungs, veins, and urinary tract when symptoms of infection have just appeared. The preventive method is to perform effective liquid resuscitation as soon as possible after burns, and eat small amounts or stay in the small intestine catheter and nasal feeding early to reduce the destruction of the intestinal barrier and reduce the intestinal bacteria displacement. Immediately after intestinal infection, broad-spectrum antibiotics should be applied, supportive therapies should be strengthened, attention should be paid to energy and various nutrient supplements, and drugs to promote gastrointestinal mucosal repair should be provided. Ceftazidime has a good effect in preventing and treating enteric infections. ^[1]

Gut derived infection

The intestine is the body's largest "bacteria store" and "endotoxin bank." In healthy conditions, the intestinal mucosa has a tight shielding function. In critically ill patients, such as intestinal mucosa shielding function is impaired or exhausted, intestinal pathogens and endotoxins can be translocated through the intestine and cause systemic infection.

Under normal circumstances, the intestinal mucosa is the main local defense barrier, preventing bacteria and endotoxins contained in the intestinal cavity from entering the systemic circulation, but in some cases, intestinal bacteria and endotoxins can escape from the intestine and enter the intestine Lymphatic and mesenteric lymph nodes, which in turn enter the portal vein system and systemic circulation, cause systemic infections and endotoxemia. This process of intestinal bacteria invading extra-intestinal tissue is called bacterial translocation. Many patients who died of sepsis and MOF can develop intestinal bacteria in their blood, but clinical and necropsy have not found infections. It is conceivable that these infections originate from the intestine and are called intestinal infection. There is a large amount of clinical data showing that severe trauma, burns, shock, and major surgery patients often cause systemic infection or endotoxemia due to intestinal barrier failure, leading to the occurrence of MODS. Therefore, it was proposed in the late 1980s that in the occurrence of MOF, the intestine is the "central organ" or "moving organ". In the occurrence of intestinal infection, liver Kupffer cell activity plays a key role. Bacteria and endotoxins brought by portal vein blood are eliminated by Kupffer cells after entering the liver. Impaired Kupffer cell activity will not prevent intestinal bacteria and endotoxins from entering the systemic circulation. Bacteria and endotoxins stay in the blood of the portal vein system and promote Kupffer cells to secrete various cytokines and inflammatory mediators, aggravating the systemic inflammatory response. Bacterial translocation therefore marks impaired gut barrier function.