Necrotizing Enterocolitis in Full-Term or Near-Term Infants: Risk Factors

MartÍnez-tallo, Emilia; Claure, Nelson; Bancalari, Eduardo

doi:10.1159/000244428

Cited by 134 publications

(77 citation statements)

References 16 publications

(28 reference statements)

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“…10 A preponderance of reports have found FT NEC to be almost uniformly associated with some predisposing condition. 3,1,6,11,5 The identification of FT patients at a higher risk of NEC would aid in earlier clinical recognition and perhaps suggest possibilities for preventing NEC.…”

Section: Discussionmentioning

confidence: 99%

“…Approximately 90% of infants with NEC are premature. 1,2 Multiple factors including perinatal hypoxia, indomethacin treatment, multiple gestation, congenital heart disease, major congenital anomalies/disease, umbilical artery catheters, polycythemia, and pre-eclampsia have been associated with NEC. [3][4][5] The role of these factors in causing or predisposing to NEC is unclear, because prematurity itself may act as a "hidden variable," accounting for these correlations.…”

confidence: 99%

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Necrotizing enterocolitis in full-term infants

Ostlie¹,

Spilde²,

Peter³

et al. 2003

Journal of Pediatric Surgery

180

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Section: Discussionmentioning

confidence: 99%

Necrotizing enterocolitis in full-term infants

Ostlie¹,

Spilde²,

Peter³

et al. 2003

Journal of Pediatric Surgery

180

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“…In fact, since 1973, published reports have described over 150 term and near-term neonates with NEC. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] The prevalence of NEC among term neonates in the USA is not known, but Bolisetty et al 10 estimated that, in Australia, NEC occurs in one per 20 000 term births. As NEC is so rare among term neonates, it is challenging to develop and test prevention strategies.…”

Section: Introductionmentioning

confidence: 99%

“…We suspected that more cases of NEC in term infants would exist in the recent Intermountain Healthcare databases than in any of the published reports of this condition. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Our speculation was based on the fact that all but one of the previous reports of NEC in term neonates 10 were the experiences of individual hospitals. Thus, we undertook the present study, for two purposes; (1) to describe the cases of NEC of Bell's stage XII in term neonates cared for in the Intermountain Healthcare NICU system in recent years and (2) to contrast data from these patients with data from term neonates admitted to the same NICUs that did not develop NEC.…”

Section: Introductionmentioning

confidence: 99%

Necrotizing enterocolitis in term neonates: data from a multihospital health-care system

et al. 2007

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Objective: In the past 5½ years, 30 term or near-term neonates in the Intermountain Healthcare system developed necrotizing enterocolitis (NEC) Bell's stage XII. We sought to identify possible explanations for why these patients developed NEC, by comparing them with 5847 others that did not develop NEC, from the same hospitals and of the same gestational ages, cared for during the same 5½-year period.Study design: Data were collected from neonates admitted to any of the Intermountain Healthcare NICUs with a birth date from 1 January 2001 to 30 June 2006, and a gestational age >36 weeks. A variety of patient features and feeding practices were compared between those that did vs did not develop NEC.Result: Forty-one neonates >36 weeks gestation were listed in the discharge records as having NEC of Bell's stage II or higher. However, on review of these 41 medical records, 11 were seen to have had NEC of Bell's stage I, whereas the remaining 30 had radiographs and clinical courses indicative of Bell's stage XII. Those 30 formed the basis of this study. Twenty-eight of the 30 developed NEC after having been admitted to an NICU for some other reason; the other two developed NEC at home, within 2 days of being discharged from an NICU. The 30 that developed NEC were more likely than the 5847 that did not develop NEC, to have congenital heart disease (P ¼ 0.000), polycythemia (P ¼ 0.002), earlyonset bacterial sepsis (P ¼ 0.004) or hypotension (P ¼ 0.017). All 30 received enteral feedings before NEC developed; 29 were fed either artificial formula or a mixture of formula and breast milk. The one that was exclusively fed human milk was fed human milk with added fortifier (24 cal/oz). The 30 that developed NEC were more likely to be fed formula exclusively (P ¼ 0.000). Seven of the 30 had a laparotomy for NEC; two of the seven had total bowel necrosis and support was withdrawn. The other five had perforations and bowel resections. The mortality rate was 13% (4/30). Conclusion:In our series, NEC among term or near-term neonates was exclusively a complication developing among patients already admitted to a NICU for some other reason. We speculate that the combination of reduced mesenteric perfusion and feeding with artificial formula were factors predisposing them to develop NEC.

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“…Many risk factors have been identified as contributing to the pathogenesis of NEC, including prematurity, enteral feeding, hypothermia, bacterial colonization, and hypoxia [16][17][18][19][20][21][22][23]. Many believe NEC to be secondary to a deranged or uncontrolled inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Unexpected Macrophage Activity Alters the Inflammatory Process in Necrotizing Enterocolitis

Raque¹,

Matheson²,

Connolly³

et al. 2017

J Cytokine Biol

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Objective: Macrophages play a role in clearing bacteria from the gut in the initial stages of necrotizing enterocolitis (NEC). Macrophage Inflammatory Protein-1α (MIP-1α), also known as CCL3, is a chemokine produced by macrophages that enhances the immune response. It acts as both a recruiter of immune cells and a coactivator of other macrophages. Interleukin-12 (IL-12) is a pro-inflammatory chemotactant produced by several types of phagocytic cells such as dendritic cells and neutrophils, but primarily by macrophages. We hypothesized that the pro-inflammatory state associated with NEC pathophysiology would induce increased expression of MIP-1α and IL-12 that would be detectable in serum and intestinal tissue.Methods: Timed pregnant Sprague-Dawley rats were randomized by litter. Controls were delivered vaginally and dam-fed. NEC pup groups were delivered 12 h prematurely via Cesarean section, formula fed, given a single oral dose of lipopolysaccharide, and subjected to intermittent cold and hypoxia as part of a proven NEC rat model protocol. Animals were sacrificed at 0, 12, 24, 48, 72, and 96 h of life and serum and intestinal tissue samples were collected. Samples were analysed via western blot using antibodies with affinity to MIP-1α and IL-12 respectively.Results: Serum and ileal levels of MIP-1 alpha were increased from 48 to 72 h in NEC animals when compared with controls. Serum and ileal IL-12 was downregulated in NEC groups at 12 and 24 h compared to controls. Conclusion:Macrophage function plays an important role in the first 48 h of NEC pathophysiology. Downregulation of IL-12 in the setting of increased MIP-1α expression may represent deranged or inhibited macrophage function in the context of NEC pathogenesis. Further work to elucidate the significance of these findings is warranted.

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Necrotizing Enterocolitis in Full-Term or Near-Term Infants: Risk Factors

Cited by 134 publications

References 16 publications

Necrotizing enterocolitis in full-term infants

Necrotizing enterocolitis in full-term infants

Necrotizing enterocolitis in term neonates: data from a multihospital health-care system

Unexpected Macrophage Activity Alters the Inflammatory Process in Necrotizing Enterocolitis

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