What Is Enterocolitis?

Enterocolitis is an acquired disease that occurs mainly in premature babies or sick newborns. It is characterized by mucosal and even deep intestinal necrosis, most often in the terminal ileum, and the colon and proximal small intestine are rarely affected. "Bioremediation therapy" for the treatment of liver cirrhosis and colitis has been applied for the first time in the Gastroenterology Center of Beijing 304 Hospital. The use of "bioremediation therapy" for the treatment of liver cirrhosis has achieved significant results.

Enterocolitis

Enterocolitis is an acquired disease that occurs mainly in premature babies or sick newborns. It is characterized by mucosal and even deep intestinal necrosis, most often in the terminal ileum, and the colon and proximal small intestine are rarely affected. "Bioremediation therapy" for the treatment of liver cirrhosis and colitis has been first applied in the Gastroenterology Center of Beijing 304 Hospital. The use of "bioremediation therapy" for the treatment of liver cirrhosis has achieved significant results.

Western Medicine Name

Enterocolitis

Chinese Medicine Name

Enterocolitis

English name

Yersinia enterocolitica

Disease site

Small intestine

The main symptoms

Bloating, diarrhea, high fever

Main cause

Persistent intestinal ischemic damage, bacterial colonization, intestinal substrates (e.g. enteral feeding

Multiple groups

Premature or sick newborns, 75% of cases occur in preterm infants

Contagious

Non-contagious

way for spreading

Acquired disease

Whether to enter health insurance

Yes

Cooperation unit

Department of Gastroenterology, Beijing 304 Hospital

Treatment technique

Bioremediation therapy

Yersinia enterocolitica is the main pathogen of severe enterocolitis in humans. It is a gram-negative polymorphic microbacteria. Most of the strains are rod-shaped, and non-toxic strains are more common. When cultured at 25 ° C, there were peripheral flagella, which showed rolling motion, but when cultured at 37 ° C, there were few or no flagella. Low temperature resistance, can grow at 4 , but the optimal temperature is 20 28 , the optimal pH value is 7.6, it grows slowly on SS agar plate, it forms colorless (or off-white), transparent (or translucent) after 24h culture Smooth small colonies. There are O, H and K antigens. The bacteria cause intestinal infections mainly through invasiveness and enterotoxins.

The bacteria can be isolated from animals such as dogs, cats, and pigs. Oral infection mainly through contaminated food. The clinical manifestations of human infections are diverse, of which gastroenteritis (or enterocolitis) is the most common. This type occurs in infants and young children under 3 years old. The main symptoms are diarrhea, abdominal pain and fever. The basis for identification of this bacterium is dynamic positive, psychrophilic, urease positive, H 2 S positive when cultured at 25 ° C, and serological tests also have identification effect. Available with kanamycin, gentamicin and sulfa drugs.

The cause of necrotizing enterocolitis is unknown. It is believed that intestinal ischemic damage can destroy the intestine and produce mucus, making the intestine susceptible to bacteria. Once feeding is started, it provides sufficient substrate for the intestinal bacteria to multiply, and the bacteria can penetrate the intestinal wall, generate hydrogen and accumulate, and generate the characteristic intestinal wall gas on the X-ray. The gas can enter the portal vein and pass through the abdominal X Plain radiographs or B-ultrasonography of the liver reveal gas accumulation in the portal vein above the liver. As the disease progresses, it can lead to necrosis, perforation, peritonitis, sepsis and death of the entire intestinal wall.

Ischemic damage can be caused by mesenteric arterial spasm caused by primitive diving reflex triggered by hypoxic damage, leading to a significant reduction in intestinal blood flow; during blood exchange, during sepsis or when fed with high-tension formula, Reduced flow leads to intestinal ischemic damage. Similarly, congenital heart disease can reduce systemic blood flow, or decrease in arterial blood oxygen saturation, leading to hypoxia / ischemia in the intestine and necrotizing enterocolitis.

The claim that breastfeeding provides a protective effect has not been proven.

Intestinal necrosis starts from the mucosal layer and gradually affects the entire intestinal wall, leading to perforation, and 1/3 of neonates develop sepsis.

Infants can show bloating intestinal obstruction, gastric bile residues (after feeding) can gradually occur vomiting bile, or gross blood or microscopic stool, sepsis can be manifested as lethargy, unstable body temperature, increased apnea episodes, and metabolic acid Poisoning.

Occult blood screening or reductive examination of the stools of premature infants who have started feeding can help early diagnosis of necrotizing enterocolitis. Early X-ray examination was non-specific, showing only intestinal obstruction, but repeating X-ray examination, the fixed dilated bowel segment indicated the presence of necrotizing enterocolitis. X-ray diagnosis of necrotizing enterocolitis was gastrointestinal gas and portal vein. Gas accumulation and pneumoperitoneum suggest bowel perforation, which requires emergency surgery.

Pathological changes: In children with necrotizing enterocolitis, there are usually three factors in the small intestine: persistent intestinal ischemic damage, bacterial colonization, and substrates in the intestinal cavity (such as enteral feeding). NEC can affect the entire small intestine and colon, but the most common sites are in the distal ileum and proximal ascending colon. In mild cases, the necrotic bowel is only a few centimeters. In severe cases, it can extend to the jejunum and colon. intestinal. Bacteria can penetrate the intestinal wall, generate hydrogen and accumulate, and generate the characteristic intestinal gas accumulation on the X-ray. The gas can enter the portal vein. The abdominal vein accumulation on the liver can be seen through plain radiographs of the abdomen or liver B ultrasound. As the disease progresses, it can lead to necrosis, perforation, peritonitis, sepsis and death of the entire intestinal wall. The early lesions were mainly congestion, edema, hemorrhage, and necrosis of the intestinal mucosa and submucosa. The scope of the advanced lesions is enlarged, involving the muscular layer. In severe cases, intestinal wall necrosis can be complicated by intestinal perforation and peritonitis.

About 1/3 of the cases require surgery. Surgical indications are: intestinal perforation (pneumoperitoneum), signs of peritonitis (disappearance of bowel sounds, full abdominal muscles, tenderness, redness and swelling of the abdominal wall), or extraction of purulent material by abdominal puncture. For infants with necrotizing enterocolitis, surgical treatment should also be considered when clinical and laboratory conditions deteriorate after non-surgical treatment. During the operation, the necrotic intestinal segment is removed and reanastomized (if the residual intestinal segment shows no ischemia, the intestinal segment can be re-anastomized). With the improvement of sepsis and peritonitis, enteral nutrition can be re-established over a period of weeks or months. A small number of infants have intestinal strictures weeks or months after non-surgical treatment. The colon, usually at the spleen flexure, requires the removal of a narrow intestinal segment to restore the normal structure of the intestine.

About two-thirds of neonates with necrotizing enterocolitis survive, and prognosis can be improved through active supportive care and careful and timely surgical intervention. Non-surgical treatment is needed in about 70% of cases. If necrotizing enterocolitis is suspected, fasting should be performed immediately. Use a double-lumen nasogastric tube connected to an aspirator to reduce intestinal gas accumulation, and appropriate parenteral colloid and crystal liquid infusion To maintain circulation because extensive intestinal inflammation and peritonitis can cause considerable fluid loss in the third space. While intestinal repair, full parenteral nutrition needs 14 to 21 days. Systemic antibiotics should now include the - lactamase antibiotic (ampicillin, ticarcillin) and aminoglycosides. Further application of anti-anaerobic drugs (such as chloro Link vancomycin, metronidazole) should also be considered. Treatment should be continued on the 10th (dose see Table 260-6). The most important is the need to constantly re-evaluate infants (e.g., at least 6 hours) and continuous abdominal X-ray examination, complete blood count, platelet count and blood gas analysis.

For some infectious outbreaks, it is recommended that if the number of cases of necrotizing enterocolitis occurred in the short term, sick children should be isolated, and the rest in contact with the baby for evaluation.

For very small or sick premature child through the use of total parenteral nutrition delayed a few days or weeks of feeding, and then slowly increased enteral feeding within a few weeks, can reduce the incidence of necrotizing enterocolitis (NEC), and this is credible. However, while some studies found no benefit of this process.

Necrotizing enterocolitis can be centralized or sporadic outbreaks in the neonatal intensive care unit; Epidemiological studies have confirmed that some of the sporadic cases with special focus on pathogens (Staphylococcus bacteria such as Klebsiella, E. coli, coagulase-negative) about , but usually no special pathogens were found.