The role of ischemia in necrotizing enterocolitis

Initiation of Enteral Feeding After Necrotizing Enterocolitis

“…9 It is unlikely that these recurrences were caused by the early low volume feeding, but more likely associated with the large volume feeding achieved later. These data are in parallel with a previous report demonstrating that NEC tends to occur in premature infants on full enteral feeding, 11 although the reason for this remains unclear. Our recent studies suggest that premature infants have limited intestinal blood supply, which may not meet the increased oxygen demand after large amounts of enteral feeding and this results in hypoxia/ischemia injury in the mucosa, leading to subsequent bacterial translocation, inflammation, and NEC.…”

“…Our recent studies suggest that premature infants have limited intestinal blood supply, which may not meet the increased oxygen demand after large amounts of enteral feeding and this results in hypoxia/ischemia injury in the mucosa, leading to subsequent bacterial translocation, inflammation, and NEC. 11,12 Based on this hypothesis, early low volume enteral feeding may not exert a large stress to the premature intestine. In accordance, early minimal enteral feeding (MEF) has demonstrated a protective effect on the intestine by stimulating enteral hormone secretion and maturation of gut motor function.…”

Shifts in microbial transcription patterns prior to onset of Necrotizing enterocolitis may indicate low oxygen levels in the gut

“…Pig models have shown that fetuses and premature neonates have higher blood flow to the gut than in more developed gut systems (Nankervis et al, 2001), 1 7 2 and this may lead to more oxygenated conditions in the gut lumen. This is consistent with 1 7 3 previous observations showing that the gut of premature infants is initially colonized with 1 7 4 more aerobic organisms that later shifts to become more anaerobic communities (Brooks conditions have been observed in the gut tissue of many patients (Chen et al, 2016) and 1 7 7 histologic examination of removed dead tissue demonstrates coagulation necrosis, 1 7 8 evidence for ischemic injury (Ballance et al, 1990). Yet, hypoxia is highly disputed as a 1 7 9 primary controlling factor of NEC (Chen et al, 2016;Crissinger, 1994;Neu, 2005; 1 8 0 Nowicki and Nankervis, 1994;Young et al, 2011).…”

Current Research on the Epidemiology, Pathogenesis, and Management of Necrotizing Enterocolitis

“…Thirdly, several clinical studies have suggested that arginine and/or citrulline, amino acids, which are important in the production of nitric oxide and regulation of intestinal blood flow, are decreased in NEC and that the supplementation of infants with arginine may prevent NEC [69,70,71,72,73]. Finally, a recent histological study of resection tissue from infants with NEC showed that hypoxia markers, hypoxia-inducible factor 1α (HIF-1α) and glucose transporter 1 (GLUT1), were elevated in NEC but not in spontaneous intestinal perforation or where only a short segment of the bowel was affected [74]. …”