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Treatment and prevention of necrotizing enterocolitis

Open access
Lee, Jane S, Polin, Richard A·2003·Seminars in Neonatology

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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Metadata

Authors
Lee, J. S., & Polin, R. A.
Venue
Seminars in Neonatology
Publisher
Elsevier BV
Published
2003-12
Volume
8
Issue
6
Pages
449-459
ISSN
1084-2756 (ISSN-L)
OpenAlex
W2157716742
Cited by
304
References
0
FWCI
7.63
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Treatment and prevention of necrotizing enterocolitis. https://app.cochat.ai/papers/10.1016/s1084-2756(03)00123-4
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Lee, J. S., & Polin, R. A. (2003). Treatment and prevention of necrotizing enterocolitis. Seminars in Neonatology. https://doi.org/10.1016/s1084-2756(03)00123-4

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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