Necrotizing ulcerative enterocolitis.

Necrotizing 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 necrotizing ulcerative enterocolitis include poor feeding tolerance, lethargy, unstable body temperature, ileus, abdominal distension, bilious vomiting, bloody stools, apnea, and sometimes signs of sepsis. Diagnosis is clinical and confirmed by radiographic examination. Treatment of necrotizing ulcerative enterocolitis is supportive, including temporary gastric emptying via a nasogastric tube, intravenous fluids, total parenteral nutrition, antibiotic therapy, isolation if infection occurs, and often surgery.

75% of cases of necrotizing ulcerative enterocolitis (NUEC) occur in premature infants, especially if prolonged rupture of membranes or fetal asphyxia were observed during delivery. The incidence of necrotizing ulcerative enterocolitis is higher in infants fed hypertonic formulas, in infants small for the gestational age, in infants with congenital heart defects with cyanosis, and in infants who have received exchange blood transfusion.

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What causes necrotizing ulcerative enterocolitis?

Children who develop necrotizing ulcerative enterocolitis usually have 3 intestinal factors: previous ischemic insult, bacterial colonization, and luminal substrate (i.e., enteral nutrition).

The etiology remains unclear. It is believed that ischemic stroke damages the intestinal mucosa, making it more permeable and susceptible to bacterial invasion. When the child begins to feed, the intestinal lumen becomes filled with a sufficient amount of substrate for the proliferation of bacteria, which can penetrate the damaged intestinal wall and produce hydrogen. Gas can accumulate in the intestinal wall (pneumatosis intestinalis) or penetrate into the portal venous system.

Ischemic stroke may develop due to spasm of the mesenteric arteries during hypoxia. In this case, the blood supply to the intestine is significantly reduced. Intestinal ischemia may also develop as a result of decreased blood flow during exchange transfusion, sepsis, and the use of hyperosmolar formulas when feeding a child. Similarly, congenital heart disease with decreased systemic blood flow or decreased oxygen saturation in arterial blood can lead to intestinal hypoxia/ischemia and be predisposing factors for the development of necrotizing ulcerative enterocolitis.

Necrosis begins in the mucosa and may increase to involve the entire thickness of the intestinal wall, causing intestinal perforation with subsequent 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 proximal small intestine are affected much less frequently. Sepsis develops in 1/3 of children and can be fatal.

Necrotizing ulcerative enterocolitis may occur as clusters or outbreaks in neonatal intensive care units (NICUs). Some outbreaks appear to be associated with a specific organism (eg, Klebsiella, E. coli, Staphylococcus), but often no specific pathogen can be identified.

Symptoms of necrotizing ulcerative enterocolitis

The child may have ileus, which is manifested by an enlarged abdomen, retention of gastric contents mixed with bile after feeding, up to the appearance of vomiting of bile, or the appearance of blood in the stool (determined visually or by laboratory testing). Sepsis may manifest itself as lethargy, unstable body temperature, frequent attacks of apnea, and metabolic acidosis.

Diagnosis of necrotizing ulcerative enterocolitis

Screening of all enterally fed preterm infants for fecal occult blood may aid in early detection of necrotizing ulcerative enterocolitis. Early plain abdominal radiography may reveal signs of ileus. A weighted arrangement of distended bowel loops that does not change with repeat imaging suggests necrotizing ulcerative enterocolitis. Radiographic signs of necrotizing ulcerative enterocolitis include pneumatization of the bowel and gas in the portal venous system. Pneumoperitoneum indicates bowel perforation and is an indication for emergency surgery.

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Treatment of necrotizing 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 necrotizing ulcerative enterocolitis is suspected, feeding the child should be stopped immediately, and the intestine should be decompressed by intermittent suction of the contents using a double-lumen nasogastric tube. Sufficient amounts of colloid and crystalloid solutions should be administered parenterally to maintain the BCC, since enterocolitis and peritonitis can lead to significant fluid losses. Total parenteral nutrition is necessary for 14-21 days until the intestinal condition is normalized. Systemic antibiotics should be administered from the very beginning, the starting drug is beta-lactam antibiotics (ampicillin, ticarcillin) and aminoglycosides. Additional drugs effective against anaerobic flora (eg, clindamycin, metronidazole) can also be prescribed for 10 days. Because some outbreaks may be infectious, isolation of patients should be considered, especially if several cases occur within a short period of time.

The newborn should be under dynamic observation: examination at least every 6 hours, repeated abdominal imaging, complete blood count with platelet count, acid-base balance. The most common late complication of necrotizing ulcerative enterocolitis is intestinal strictures, which develop in 10-36% of children who have had the disease. Strictures are most often found in the large intestine, especially in its left part. Subsequently, stricture resection is required.

Surgery is needed in less than one third of children. Absolute indications include bowel perforation (pneumoperitoneum), signs of peritonitis (absence of intestinal peristalsis and diffuse tension and tenderness or hyperemia of the skin and pastosity of the abdominal wall), or aspiration of purulent contents from the abdominal cavity during paracentesis. Surgery should be considered in children with necrotizing ulcerative enterocolitis whose condition and laboratory data deteriorate despite conservative therapy. During surgery, the gangrenous bowel is resected and stomas are created. (A primary anastomosis can be created if there is no evidence of ischemia of the remaining bowel.) If sepsis and peritonitis resolve after several weeks or months, a second stage of surgery can be performed and bowel patency restored.

The risk of developing necrotizing ulcerative enterocolitis can be reduced by delaying feeding for several days or weeks in very small or sick preterm infants and giving total parenteral nutrition; enteral feedings are increased slowly over weeks. However, some studies have shown that this approach has no benefit. The suggestion that breast milk has a protective effect is not proven. Recent studies suggest that probiotic use may be effective in preventing necrotizing ulcerative enterocolitis, but further studies are needed before this can be routinely recommended.