Sam W Moore1, Marion Arnold, Colleen Wright. 1. Divisions of Pediatric Surgery, University of Stellenbosch, Tygerberg, Western Cape Tygerberg 7505, South Africa. swm@sun.ac.za
Abstract
AIM: Necrotizing enterocolitis (NEC) is the most common and severe acquired acute neonatal surgical condition, associated with premature neonates. Antenatal factors (e.g. vascular insufficiency and antenatal infections) may be important factors in "priming" the inflammatory cascade, thus predisposing to the disease. This study explores the role of placental pathology in predisposing to NEC pathogenesis. METHODS: 5338 placentas of high risk pregnancies were evaluated for placental insufficiency, infarction, and evidence of antenatal infection. Placentas of 72 premature infants developing surgical NEC (2007-2011) were identified as a separate study group and pathological placental features compared with unaffected infants. RESULTS: Placentas of 72 of the 134 infants with surgically treated NEC (>grade 2 Bells) were available for pathologic evaluation (the remainder having been referred from other delivery units). Placentas of surgical NEC cases had significantly more evidence of noteworthy vascular pathology (placental infarcts) than high risk cases [n=38 (54.5%) versus n=1122 (21%); P<0.01]. Evidence of placental infection/chorioamnionitis or villitis plus evidence of foetal inflammatory response was present in surgical NEC infants versus unaffected infants [n=22 (31.8%) versus n=647 (12%); P<0.01], suggesting a possible pathogenic role. CONCLUSION: This study suggests that exposure to antenatal placental infection may contribute to pathogenesis of NEC by modifying foetal vascular response and warrants further study.
AIM: Necrotizing enterocolitis (NEC) is the most common and severe acquired acute neonatal surgical condition, associated with premature neonates. Antenatal factors (e.g. vascular insufficiency and antenatal infections) may be important factors in "priming" the inflammatory cascade, thus predisposing to the disease. This study explores the role of placental pathology in predisposing to NEC pathogenesis. METHODS: 5338 placentas of high risk pregnancies were evaluated for placental insufficiency, infarction, and evidence of antenatal infection. Placentas of 72 premature infants developing surgical NEC (2007-2011) were identified as a separate study group and pathological placental features compared with unaffected infants. RESULTS: Placentas of 72 of the 134 infants with surgically treated NEC (>grade 2 Bells) were available for pathologic evaluation (the remainder having been referred from other delivery units). Placentas of surgical NEC cases had significantly more evidence of noteworthy vascular pathology (placental infarcts) than high risk cases [n=38 (54.5%) versus n=1122 (21%); P<0.01]. Evidence of placental infection/chorioamnionitis or villitis plus evidence of foetal inflammatory response was present in surgical NEC infants versus unaffected infants [n=22 (31.8%) versus n=647 (12%); P<0.01], suggesting a possible pathogenic role. CONCLUSION: This study suggests that exposure to antenatal placental infection may contribute to pathogenesis of NEC by modifying foetal vascular response and warrants further study.