Necrotizing Enterocolitis

Necrotizing enterocolitis is a disease entity that affects the asphyxiated or stressed premature infant of less than 2000-g weight. Full-term newborns with polycythemia or congenital heart disease and those who have had umbilical arterial or venous catheters in situ have been reported to also be at risk for necrotizing enterocolitis.

The exact cause of necrotizing enterocolitis remains unknown, and it is likely that there are multiple factors that ultimately lead to stasis, ischemia, and infection of the bowel wall. The risk factors include hypertonic feeding solutions producing damage to mucosal epithelium of the intestine, patent ductus arteriosus and episodes of apnea diverting blood flow away from the gastrointestinal tract, ischemia following exchange transfusions, and infections with Escherichia coli, Klebsiella pseudomonas, Clostridium species, coronavirus, rotavirus, and other enteroviruses.

The signs and symptoms, seen in decreasing frequency, are abdominal distention, gastric distention, retention of gastric feeds, apnea, gastrointestinal bleeding, and lethargy. Other signs are abdominal tenderness, redness of abdominal wall, and the presence of reducing substances in the stool.

A supine anteroposterior and cross-table lateral and upright view will aid in the radiographic diagnosis. Nonspecific findings are distention, air-fluid levels, and separation of intestinal loops, suggesting mural edema. Pneumatosis intestinalis is the radiographic hallmark, and its presence indicates gas in the bowel wall. Portal venous gas is an ominous sign, and pneumoperitoneum indicates perforation of the bowel.

The medical management consists of bowel rest, with the infant receiving nothing by mouth, and gastric decompression with a nasogastric tube. Cultures of blood, urine, and cerebrospinal fluid should be obtained. Ampicillin and cefotaxime 100 mg/kg q 8 to 12 h should be administered. The blood pressure and hydration status should be maintained with liberal use of crystalloids and Plasmanate. Fluid intake may have to be increased to 200 (mL/kg)/24 h and inotropic agents used if needed. Thrombocytopenia, neutropenia, and disseminated intravascular coagulopathy are often seen in neonates who are deteriorating, and platelet transfusions should be administered if there is evidence of systemic or gastrointestinal bleeding. Respiratory support may be required, and any acidosis should be corrected. Patients with early necrotizing enterocolitis should have close clinical observations and serial x-rays to look for signs of gangrene or intestinal perforation. The medical treatment includes bowel rest for 2 weeks and nutritional support with parenteral alimentation. The complications of necrotizing enterocolitis are bowel stricture, fistula, abscess, malabsorption, and failure to thrive.

Pneumoperitoneum related to signs of necrotizing enterocolitis is an absolute indication for surgical repair. Recent data indicate that paracentesis indicative of intestinal gangrene prior to intestinal perforation may be an indication for surgery. Persistent acidosis, oliguria, abdominal wall erythema, and portal vein air are associated with advanced disease. The surgical repair consists of removal of the segment of involved bowel and an enterostomy. Reanastomosis is usually performed after 4 to 6 weeks of bowel rest.

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