ABSTRACT
The neonatal gastrointestinal (GI) tract can be vulnerable to injury from hypoxic respiratory failure and birth asphyxia. However, hypoxic-ischemic intestinal injury is rare, except when associated with congenital heart defects or other problems that can decrease blood flow to the descending aorta and cause a lack of perfusion to the mesenteric arteries, causing ischemia and necrosis.
Hypoxic-ischemic intestinal injury is not the same as classic necrotizing enterocolitis (NEC). Classic NEC is seen in preterm infants without history of a perinatal hypoxic-ischemic event. It is multifactorial, strongly associated with intestinal immaturity and likely related to an excessive inflammatory response and dysbiosis. In contrast, hypoxic-ischemic intestinal injury is more common in term infants with congenital heart defects without a clear link to inflammation or dysbiosis.
The lumen of the GI tract is a hypoxic environment essential for normal barrier function, survival of commensal bacteria, and expression of hypoxia-inducible factor (HIF). HIF is a major regulator of the cellular response to hypoxia and ischemia, a regulator of inflammation within the intestine, and a regulator vascular endothelial growth factor (VEGF) to stimulate angiogenesis and inhibit apoptosis. Dysregulation of oxygen gradients and/or disruptions of the HIF mechanism can lead to inflammation and intestinal injury.
