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Necrotizing enterocolitis is an acquired disease, primarily of preterm or sick neonates, characterized by mucosal or even deeper intestinal necrosis. It is the most common GI emergency among neonates. Symptoms and signs include feeding intolerance, lethargy, temperature instability, ileus, bloating, bilious emesis, hematochezia, reducing substances in the stool, apnea, and sometimes signs of sepsis. Diagnosis is clinical and is confirmed by imaging studies. Treatment is primarily supportive and includes nasogastric suction, parenteral fluids, TPN, antibiotics, isolation in cases of infection, and, often, surgery.
Over 85% of cases of necrotizing enterocolitis (NEC) occur in premature infants (see Premature Infant). It occurs in about 1 to 8% of neonatal ICU admissions.
General risk factors in addition to prematurity include
Prolonged rupture of the membranes (see Premature Rupture of Membranes (PROM)) with amnionitis
Small-for-gestational-age infants (see Small-for-Gestational-Age (SGA) Infant)
Congenital heart disease
Exchange transfusions (see Neonatal Hyperbilirubinemia : Exchange transfusion)
The incidence may also be higher in infants fed hypertonic formulas.
Three intestinal factors are usually present:
The exact etiology is not clear. It is believed that an ischemic insult damages the intestinal lining, leading to increased intestinal permeability and leaving the intestine susceptible to bacterial invasion. NEC rarely occurs before enteral feedings and is less common among breastfed infants. However, once feedings are begun, ample substrate is present for proliferation of luminal bacteria, which can penetrate the damaged intestinal wall, producing hydrogen gas. The gas may collect within the intestinal wall (pneumatosis intestinalis) or enter the portal veins.
The initial ischemic insult may result from vasospasm of the mesenteric arteries, which can be caused by an anoxic insult triggering the primitive diving reflex that markedly diminishes intestinal blood flow. Intestinal ischemia may also result from low blood flow during an exchange transfusion, during sepsis, or from the use of hyperosmolar formulas. Similarly, congenital heart disease with reduced systemic blood flow or arterial O2 desaturation may lead to intestinal hypoxia/ischemia and predispose to NEC.
NEC may occur as clusters of cases or as outbreaks in neonatal ICUs. Some clusters appear to be associated with specific organisms (eg, Klebsiella , Escherichia coli , coagulase-negative staphylococci), but often no specific pathogen is identified.
Necrosis begins in the mucosa and may progress to involve the full thickness of the intestinal wall, causing perforation with subsequent peritonitis and often free intra-abdominal air. Perforation occurs most commonly in the terminal ileum; the colon and the proximal small bowel are involved less frequently. Sepsis occurs in 33% of infants (see Neonatal Sepsis), and death may occur.
Infants may present with feeding difficulties and bloody or bilious gastric residuals (after feedings) that may progress to bilious emesis, ileus manifested by abdominal distention, or gross blood in stool. Sepsis may be manifested by lethargy, temperature instability, increased apneic spells, and metabolic acidosis.
Early x-rays may be nonspecific and reveal only ileus. However, a fixed, dilated intestinal loop that does not change on repeated x-rays indicates NEC. X-ray signs diagnostic of NEC are pneumatosis intestinalis and portal vein gas. Pneumoperitoneum indicates bowel perforation and an urgent need for surgery.
The mortality rate is 20 to 30%. Aggressive support and judicious timing of surgical intervention maximize the chance of survival.
Nonsurgical support is sufficient in over 75% of cases. Feedings must be stopped immediately if NEC is suspected, and the intestine should be decompressed with a double-lumen NGT attached to intermittent suction. Appropriate colloid and crystalloid parenteral fluids must be given to support circulation, because extensive intestinal inflammation and peritonitis may lead to considerable 3rd-space fluid loss. TPN is needed for 14 to 21 days while the intestine heals.
Systemic antibiotics should be started at once with a β-lactam antibiotic (eg, ampicillin, ticarcillin) and an aminoglycoside. Additional anaerobic coverage (eg, clindamycin, metronidazole) may also be considered and should continue for 10 days (for dosage, see Table: Recommended Dosages of Selected Parenteral Antibiotics for Neonates). Because some outbreaks may be infectious, patient isolation should be considered, particularly if several cases occur within a short time.
The infant requires close monitoring; frequent complete reevaluation (eg, at least every 12 h); and serial abdominal x-rays, CBCs, platelet counts, and blood gases. Intestinal strictures are the most common long-term complication of NEC, occurring in 10 to 36% of infants who survive the initial event. Strictures typically manifest within 2 to 3 mo of an NEC episode. Strictures are most commonly noted in the colon, especially on the left side. Resection of the stricture is then required.
Surgical intervention is needed in < 25% of infants. Absolute indications are intestinal perforation (pneumoperitoneum), signs of peritonitis (absent intestinal sounds and diffuse guarding and tenderness or erythema and edema of the abdominal wall), or aspiration of purulent material from the peritoneal cavity by paracentesis. Surgery should be considered for an infant with NEC whose clinical and laboratory condition worsens despite nonsurgical support. During surgery, gangrenous bowel is resected, and ostomies are created. (Primary reanastomosis may be done if the remaining intestine shows no signs of ischemia.) With resolution of sepsis and peritonitis, intestinal continuity can be reestablished several weeks or months later.
At-risk infants should be fed breast milk, and feedings should begin with small amounts that are gradually increased according to standardized protocols. (Preterm formula is an appropriate substitute if breast milk is not available.) Hypertonic formula, drugs, or contrast material should be avoided. Polycythemia should be treated promptly.
Probiotics (eg, Bifidus infantis , Lactobacillus acidophilus) help prevent NEC, but further studies to determine optimal dosing and appropriate strains are required.
NEC is intestinal necrosis of uncertain etiology; it occurs mainly in preterm or sick neonates after enteral feedings have begun.
Complications include intestinal perforation (most often in the terminal ileum) and peritonitis; sepsis occurs in 33%, and death may occur.
Initial manifestations are feeding difficulties and bloody or bilious gastric residuals (after feedings) followed by bilious emesis, abdominal distention, and/or gross blood in stool.
Diagnose using plain x-rays.
Supportive treatment using fluid resuscitation, nasogastric suction, broad-spectrum antibiotics, and TPN is effective in > 75% of cases.
Surgery to resect gangrenous bowel and treat perforation is needed in < 25% of infants.
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