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Necrotizing ulcerative enterocolitis
Last reviewed: 23.04.2024
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Necrotic ulcerative enterocolitis is an acquired disease, primarily in premature and sick newborns, which is characterized by necrosis of the intestinal mucosa or even deeper layers.
Symptoms of necrotic ulcerative enterocolitis include a violation of food tolerance, lethargy, unstable body temperature, ileus, bloating, vomiting of bile, stool with blood, apnea, and sometimes signs of sepsis. The diagnosis is made on the basis of clinical data and is confirmed by X-ray examination. Treatment of necrotic ulcerative enterocolitis supporting, includes its temporary emptying of the stomach through the nasogastric tube, infusion therapy, complete parenteral nutrition, antibacterial therapy, isolation in case of infection and often surgical intervention.
75% of cases of necrotic ulcerative enterocolitis (NNAC) occurs in premature newborns, especially if there was a prolonged rupture of fetal membranes or fetal asphyxia during labor. The frequency of development of necrotic ulcerative enterocolitis is higher in infants fed with hypertonic mixtures, in small to the gestation period of infants, in children with congenital heart diseases with cyanosis, and in children who received a replacement blood transfusion.
What causes necrotic ulcerative enterocolitis?
In children who developed necrotic ulcerative enterocolitis, there are usually 3 factors on the part of the intestine: a previous ischemic stroke, colonization by bacteria, a substrate in the lumen of the intestine (ie, enteral nutrition).
Eitology remains unclear. It is believed that with ischemic stroke affects the intestinal mucosa, which leads to its increased permeability and sensitivity to bacterial invasion. When the baby begins to be fed, a sufficient amount of substrate appears in the lumen of the intestine for the reproduction of bacteria that can penetrate into the damaged intestinal wall and produce hydrogen. Gas can accumulate in the intestinal wall (intestinal pneumatosis) or penetrate into the portal vein system.
Ischemic stroke can develop due to spasm of mesenteric arteries during hypoxia. This significantly reduces the blood supply of the intestine. Also, bowel ischemia can develop as a result of a decrease in blood flow with replacement blood transfusions, sepsis, the use of hyperosmolar mixtures in feeding the baby. Similarly, congenital heart disease with a decrease in systemic blood flow or a decrease in oxygen saturation in the arterial blood can lead to hypoxia / ischemia of the intestine and may be predisposing factors for the development of necrotic ulcerative enterocolitis.
Necrosis starts in the mucosa and can increase, covering the entire thickness of the intestinal wall, causing perforation of the intestine, followed by the development of peritonitis and the appearance of free air in the abdominal cavity. Perforation most often occurs in the terminal ileum; The large intestine and the proximal parts of the small intestine are much less affected. Sepsis develops in 1/3 of the children, a fatal outcome may occur.
Necrotic ulcerative enterocolitis can occur as a group case or outbreak in intensive care and neonatal intensive care units. Some outbreaks are associated with a particular microorganism (eg, Klebsiella, Escherichia coli, Staphylococcus), but often it is not possible to identify a particular pathogen.
Symptoms of necrotizing ulcerative enterocolitis
The child may experience ileus, manifested by an enlarged abdomen, a delay in gastric contents with an admixture of bile after feeding, until the vomiting of bile, or the appearance of blood in the feces (determined visually or in a laboratory study). Sepsis can be manifested by lethargy, unstable body temperature, frequent attacks of apnea and metabolic acidosis.
Diagnosis of necrotic ulcerative enterocolitis
Screening of feces for latent blood in all preterm infants on enteral feeding can help early detection of necrotic ulcerative enterocolitis. Early visualization of the abdominal radiography can reveal signs of ileus. The weighted arrangement of the inflated intestinal loops, which does not change during repeated studies, indicates necrotic ulcerative enterocolitis. X-ray signs of necrotic ulcerative enterocolitis are pneumatization of the intestine and gas in the portal vein system. Pneumoperitoneum indicates perforation of the intestine and is an indication for an emergency operation.
Treatment of necrotic ulcerative enterocolitis
Mortality is 20-40%. Active conservative therapy and a reasonable approach to surgical treatment increase the chances of survival.
In 70% of cases, conservative treatment is sufficient. If suspicion of necrotic ulcerative enterocolitis is immediate, stop feeding the baby, perform intestinal decompression by intermittent suction of the contents with a double-lumen nasogastric tube. Sufficient colloidal and crystalloid solutions should be administered parenterally to maintain BCC, as enterocolitis and peritonitis can lead to significant fluid loss. Complete parenteral nutrition is necessary for 14-21 days, until the state of the intestines is normalized. Systemic administration of antibiotics should be carried out from the very beginning, the starting drug are beta-lactam antibiotics (ampicillin, ticarcillin) and aminoglycosides. Additional drugs effective against anaerobic flora (eg, clindamycin, metronidazole) may also be given within 10 days. Since some outbreaks may be contagious, one should think about isolating patients, especially if several cases occur within a short time.
The newborn should be under dynamic observation: examination at least every 6 hours, repeated shots of the abdominal cavity, a general blood test with counting the number of platelets, KHS. The most frequent late complication of necrotic ulcerative enterocolitis are intestinal strictures, which develop in 10-36% of children who have undergone the disease. Strictures are most often found in the large intestine, especially in the left part. In the future, stricture resection is required.
Operation is needed in less than a third of children. Absolute indications include intestinal perforation (pneumoperitoneum), signs of peritonitis (absence of intestinal peristalsis and diffuse stress and soreness or skin hyperemia and abdominal wall swelling), or aspiration of purulent contents from the abdominal cavity with paracentesis. About surgical intervention should be thought of in children with necrotic ulcerative enterocolitis, whose condition and laboratory data worsen, despite ongoing conservative therapy. During the operation, the gangrenous altered portion of the gut is resected and stoma is formed. (Primary anastomosis can be formed if there are no signs of ischemia of the remaining intestine.) With the resolution of sepsis and peritonitis, after a few weeks or months, the second stage of the operation can be performed and the intestinal patency is restored.
The risk of developing necrotic ulcerative enterocolitis can be reduced if the diet is postponed for several days or weeks in very small or sick preterm infants and full parenteral nutrition is provided; the volume of enteral feeding is increased slowly over a period of weeks. Nevertheless, some studies have shown that this approach has no advantages. The assumption that breast milk has a protective effect is not proven. Recent research suggests that the use of probiotics can effectively prevent necrotic ulcerative enterocolitis, but further research is needed to be included in routine recommendations.
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