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  1. Definition. Necrotizing enterocolitis (NEC) is an ischemic and inflammatory necrosis of the bowel primarily affecting premature neonates after the initiation of enteral feeding.

  2. Incidence. NEC is predominantly a disorder of preterm infants, with an incidence of 6–10% in infants weighing <1500g. Although 10% of all cases of NEC occur in term infants, the incidence is highest in premature infants. NEC has an overall mortality of 10–30%.

  3. Pathophysiology. A multifactorial theory has been suggested in which several risk factors including prematurity, formula feedings, ischemia, and bacterial colonization interact to initiate mucosal damage via a final common pathway involving activation of the inflammatory cascade. Mucosal damage results in an invasion of the bowel wall by gas producing bacteria, resulting in an intramural gas accumulation (pneumatosis intestinalis). This sequence of events may progress to transmural necrosis or gangrene of the bowel and finally to multiple sites of bowel perforation and peritonitis.

  4. Risk factors

      1. Prematurity. There is an inverse relationship between gestational age and a risk for developing NEC. This may involve immature mucosal barrier, mucosal enzymes, and various gastrointestinal hormones. Premature infants may have an imbalance between pro- and anti-inflammatory factors and thus have an increased activation of inflammatory mediators and a decreased inactivation of specific mediators like platelet-activating factor, which has been linked to NEC. An inability to autoregulate the intestinal microcirculation effectively and differences in bacterial colonization may also make preterm infants more susceptible to NEC.

      1. Enteral feedings. NEC is rare in unfed infants, and 90–95% infants with NEC have received at least one enteral feed. Enteral feeding provides necessary substrate for proliferation of enteric pathogens. Hyperosmolar formulas or medications may alter mucosal permeability and cause mucosal damage. Human milk, with the benefit of providing immunoprotective as well as local growth promoting factors, significantly lowers the risk for NEC. Moreover, enteral immunoglobulin A-immunoglobulin G (IgA-IgG) feeds also decreased the risk for NEC in preliminary clinical studies. Use of trophic phase of feeding followed by slow advancements of feeding volume decreases the incidence of NEC.

      1. Bacterial colonization and viral enteritis. Bacteria including Escherichia coli, Klebsiella species, Clostridia species, and Staphylococcus epidermidis are implicated in NEC. Blood cultures are positive in only 20–30% of cases. Alternatively, viral enteritis from viruses like enterovirus and rotavirus may compromise the mucosal barrier leading to secondary sepsis from enteric organisms. In some centers, rotavirus may be responsible for as many as 30% of all NEC cases.

      1. Hypoxic/ischemic events play a greater role in term and near-term infants, although bowels in preterm infants are also susceptible to ischemic events. During periods of circulatory stress, as in perinatal asphyxia, blood is diverted away from the splanchnic circulation (diving reflex). The resulting intestinal ischemia followed by reperfusion may lead to bowel damage. An imbalance between vasodilating (nitric oxide and others) and vasoconstricting molecules (endothelin 1, and others) in newborns may lead to a defective autoregulation of splanchnic blood flow. For example, infants with NEC have been shown by Doppler flow velocimetry to have a higher flow resistance in the superior mesenteric artery in the first day of life. Similarly, infants with congenital heart disease may have a compromised bowel perfusion, making them ...

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