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Review
. 2003 Dec;8(6):449-59.
doi: 10.1016/S1084-2756(03)00123-4.

Treatment and prevention of necrotizing enterocolitis

Affiliations
Review

Treatment and prevention of necrotizing enterocolitis

Jane S Lee et al. Semin Neonatol. 2003 Dec.

Abstract

Necrotizing enterocolitis (NEC) is the most common serious, acquired gastrointestinal disorder in the newborn infant. Although many variables are associated with development of NEC, only prematurity has been consistently identified in case-controlled studies. Traditionally, the diving seal reflex has been invoked as the mechanism responsible for ischaemic injury and necrosis. Intestinal ischaemia is likely to be the final common pathway in NEC; however, it is due to the release of vasoconstricting substances, such as platelet activating factor, rather than perinatal asphyxia. Bacteria and/or bacterial toxins are likely to have a key role in the pathogenesis of NEC by fostering production of inflammatory mediators. The role of feeding practices in the pathogenesis of NEC remains controversial. Treatment of infants with NEC generally includes a regimen of bowel rest, gastric decompression, systemic antibiotics and parenteral nutrition. Infants with perforation are generally operated upon; however, there has been recent interest in primary peritoneal drainage as an alternative. Prevention of NEC still remains elusive. Avoidance of preterm birth, use of antenatal steroids and breast-milk feeding are practices that offer the greatest potential benefits. Use of any other strategy should await further trials.

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Figures

Fig. 1
Fig. 1
Relative risk of confirmed necrotizing enterocolitis in infants randomized to donor human milk vs formula milk. Reproduced from Ref. , with permission.
Fig. 2
Fig. 2
Restricted vs liberal water intake for preventing necrotizing enterocolitis. Modified from Ref. .
Fig. 3
Fig. 3
Enteral antibiotics for preventing necrotizing enterocolitis. Modified from Ref. .
Fig. 4
Fig. 4
Enteral antibiotics for preventing necrotizing-enterocolitis-related deaths. Modified from Ref. .

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