Hospital and neurodevelopmental outcomes of extremely low-birth-weight infants with necrotizing enterocolitis and spontaneous intestinal perforation

Department of Pediatrics, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Journal of perinatology: official journal of the California Perinatal Association (Impact Factor: 2.07). 12/2011; 32(7):552-8. DOI: 10.1038/jp.2011.176
Source: PubMed


We sought to determine the incidence of necrotizing enterocolitis (NEC) and spontaneous intestinal perforation (SIP) in surviving extremely low-birth-weight (ELBW, <1000 g birth weight) infants and to establish the impact of NEC on outcomes by hospital discharge and at 18 to 22 months adjusted age in a large, contemporary, population-based practice.
Hospital outcome data for all ELBW infants born in the greater Cincinnati region from 1998 to 2009 were extracted from the National Institute of Child Health Neonatal Research Network Database. Neurodevelopmental outcome at 18 to 22 months was assessed using Bayley Scales of Infant Development-II scores for Mental Developmental Index and Psychomotor Developmental Index. Multivariable logistic regression was used and adjusted odds ratios reported to control for confounders.
From 1998 to 2009, ELBW infants accounted for 0.5% of the 352 176 live-born infants in greater Cincinnati. The incidence of NEC was 12%, with a 50% case-fatality rate. Death before discharge, morbid complications of prematurity and neurodevelopmental impairment were all increased among infants diagnosed with NEC. Infants with surgical NEC and SIP had a higher incidence of death, but long-term neurodevelopmental outcomes were not different comparing surviving ELBW infants with medical NEC, surgical NEC and SIP.
Although ELBW infants comprise a very small proportion of live-born infants, those who develop NEC and SIP are at an increased risk for death, morbid complications of prematurity and neurodevelopmental impairment. No significant differences in neurodevelopmental outcomes were observed between the medical and surgical NEC and SIP groups.

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    • "NEC is characterized by uncontrolled intestinal inflammation that can culminate in bowel necrosis [4]–[6]. Approximately 9,000 infants develop NEC in the United States each year, with reported mortality rates of 10–50% [7], [8]. "
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    ABSTRACT: Background Gastrointestinal barrier immaturity predisposes preterm infants to necrotizing enterocolitis (NEC). Intraepithelial lymphocytes (IEL) bearing the unconventional T cell receptor (TCR) γδ (γδ IEL) maintain intestinal integrity and prevent bacterial translocation in part through production of interleukin (IL) 17. Objective We sought to study the development of γδ IEL in the ileum of human infants and examine their role in NEC pathogenesis. We defined the ontogeny of γδ IEL proportions in murine and human intestine and subjected tcrδ−/− mice to experimental gut injury. In addition, we used polychromatic flow cytometry to calculate percentages of viable IEL (defined as CD3+ CD8+ CD103+ lymphocytes) and the fraction of γδ IEL in surgically resected tissue from infants with NEC and gestational age matched non-NEC surgical controls. Results In human preterm infants, the proportion of IEL was reduced by 66% in 11 NEC ileum resections compared to 30 non-NEC controls (p<0.001). While γδ IEL dominated over conventional αβ IEL early in gestation in mice and in humans, γδ IEL were preferential decreased in the ileum of surgical NEC patients compared to non-NEC controls (50% reduction, p<0.05). Loss of IEL in human NEC was associated with downregulation of the Th17 transcription factor retinoic acid-related orphan nuclear hormone receptor C (RORC, p<0.001). TCRδ-deficient mice showed increased severity of experimental gut injury (p<0.05) with higher TNFα expression but downregulation of IL17A. Conclusion Complimentary mouse and human data suggest a role of γδ IEL in IL17 production and intestinal barrier production early in life. Specific loss of the γδ IEL fraction may contribute to NEC pathogenesis. Nutritional or pharmacological interventions to support γδ IEL maintenance in the developing small intestine could serve as novel strategies for NEC prevention.
    Full-text · Article · Jun 2014 · PLoS ONE
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    • "During the last decade, a number of studies have documented that the MLS BAER is a valid method to improve the detection of neuropathology that involves the immature auditory brainstem (Jiang, 2012; Jiang et al., 2000, 2003, 2005, 2007, 2009a,b, 2010, 2012b,c; Wilkinson et al., 2007). Neonatal NEC occurs particularly frequently in babies who are born prematurely or preterm with less birth weight (Hintz et al., 2005; Martin et al., 2010; Rees et al., 2007; Schulzke et al., 2007; Shah et al., 2012; Stoll et al., 2004; Tarnow-Mordi et al., 2011). Since preterm birth per se could exert certain effect on the immature auditory brainstem, there is a need to exclude this possible confounding effect so that the effect of NEC on the BAER can be assessed more reliably and accurately. "
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    ABSTRACT: Necrotizing enterocolitis (NEC) is a devastating neonatal disease, often leading to long term neurodevelopmental impairment. The effect of NEC on the immature brain remains not fully understood. We test the hypothesis that NEC adversely affects functional integrity, particularly neural conduction, of the preterm brainstem. Thirty-two preterm NEC babies (30-36weeks gestation) were recruited at term age. Maximum length sequence brainstem auditory evoked response was recorded and analysed with click rates 91-910/s at term age. The results were compared with normal term babies and age-matched healthy preterm babies. Wave V latency, I-V and III-V intervals, and III-V/I-III interval ratio differed significantly among the three groups of babies at all click rates 91-910/s. Compared with normal term babies, preterm NEC babies showed significant increase in all these MLS BAER variables at all rates, with no apparent abnormalities in wave I and III latencies and I-III interval. All these abnormalities were more significant at higher than at lower click rates. No notable abnormalities were seen in wave amplitudes. Compared with age-matched healthy preterm babies, NEC babies showed similar abnormalities, although the abnormalities were relatively less significant. MLS BAER components that mainly reflect neural conduction in the more central regions of the auditory brainstem were abnormal in preterm NEC babies, although those components that mainly reflect peripheral function were generally normal. Neonatal NEC adversely affects myelination of the more rostral or central regions of the immature brainstem, resulting in delayed or impaired neural conduction, but spares the more peripheral regions.
    Full-text · Article · Mar 2014 · Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology
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    ABSTRACT: Aim: To examine brainstem auditory function and detect any abnormality at term in preterm infants after neonatal necrotizing enterocolitis (NEC). Methods: Brainstem auditory evoked response (BAER) was recorded at 21/sec and 60 dB nHL in 37 preterm infants who had NEC. The data obtained at term equivalent age were analyzed and compared with those in normal term infants. Results: The threshold of BAER in infants after NEC, though slightly elevated, did not differ significantly from that in the controls. The latencies of waves I and III were slightly longer than in the controls, without any statistical significance. However, wave V latency was prolonged and differed significantly from the controls (p < 0.01). I-V interpeak interval was also prolonged (p < 0.05). The data point distribution of wave V latency and I-V interval was higher in the infants after NEC than in the controls. The amplitudes of BAER wave components in the infants after NEC did not differ significantly from those in the controls. Conclusion: Preterm infants after NEC have no major abnormality in peripheral auditory function. However, neural conduction in the brainstem auditory pathway is abnormal, suggesting that NEC adversely affects brainstem auditory conduction.
    Full-text · Article · Aug 2012 · Acta Paediatrica
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