Enterocolitis necrotizante

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Necrotizing Enterocolitis: Relationship to Innate Immunity, Clinical Features, and Strategies for Prevention Nathan Jesse and Josef Neu NeoReviews 2006;7;e143-e150 DOI: 10.1542/neo.7-3-e143

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://neoreviews.aappublications.org/cgi/content/full/neoreviews;7/3/e143

NeoReviewsis the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 2000. NeoReviews is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2006 by the American Academy of Pediatrics. All rights reserved. Online ISSN: 1526-9906.Downloaded from http://neoreviews.aappublications.org by Carlos Aldana on September 2, 2010

Article gastroenterology

Necrotizing Enterocolitis:
Relationship to Innate Immunity, Clinical Features, and Strategies for Prevention
Nathan Jesse, MD,* Josef Neu, MD*


After completing this article, readers should be able to:

Author Disclosure Drs Jesse and Neu did not disclose anyfinancial relationships relevant to this article.

1. Define the pathophysiology of necrotizing enterocolitis (NEC). 2. Explain the relationship among minimal enteral nutrition, subsequent feedings, and NEC. 3. List the factors that render human milk enteral feedings protective against NEC. 4. Explain what measures should promote advances in mortality and morbidity associated with NEC in the nearfuture. 5. Describe the complications of NEC.

Necrotizing enterocolitis (NEC) is one of the most serious and devastating diseases encountered in the neonatal intensive care unit (NICU). It is the most common gastrointestinal malady in neonates. It affects 1% to 8% of all infants admitted to the NICU and has a mortality rate of 10% to 50%. NEC accounts for at least 1,000 deaths annuallyin the United States. The increased incidence of NEC over the past few decades may be attributable to advancements in perinatal care, which have allowed very preterm infants to survive long enough to develop NEC. The only consistently defined risk factor for NEC is prematurity; the incidence varies inversely with birthweight and gestational age. NEC strikes 4% to 13% of all very lowbirthweightbabies ( 1,500 g). Although NEC primarily affects preterm infants, 5% to 28% of cases occur in term and near-term babies. The disease is rare in older children. Asphyxia, congenital heart disease, polycythemia, umbilical catheterization, and the use of indomethacin and methylxanthines have been proposed as risk factors, although none has been shown to have a consistent association with NEC. The age ofonset of NEC also varies inversely with gestational age. In term infants, the median age at onset is 2 days; the preterm infant may develop the disease at several weeks of age. The risk remains high in preterm infants until they reach 35 to 36 weeks postconceptional age. The disparity in age of onset between term and preterm infants suggests that the condition in term infants may be due to adisease process different from that seen in preterm infants.

Clinical Presentation
The clinical presentation of NEC is highly variable, ranging from mild feeding intolerance or abdominal distention to fulminant shock and death. The classic description involves abdominal distention, microscopically-to-grossly bloody stools, gastric residuals, and possibly localizing abdominal signs. Laboratoryevaluation may reveal a normal-to-elevated white blood cell count with a shift to immature precursors, neutropenia, thrombocytopenia, and disseminated intravascular coagulation (DIC). Electrolyte abnormalities and metabolic acidosis are also common. Initial radiographic evaluation may reveal a fixed, dilated loop of bowel. The characteristic radiologic finding is pneumatosis intestinalis, which is...
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