Improved Delivery of Enteral Nutrition May Prevent Post-Operative Organ Dysfunction and Sepsis Loss of intestinal EBF is linked to the pathophysiology of sepsis and MODS in murine models of ischemia-reperfusion injury and in critically ill adults after cardiopulmonary bypass (CPB). Intestinal enterocytes, or epithelial cells, and the apical tight junction complex, which connect these cells are the primary determinants of intestinal barrier function. The absence of EN results in impaired intestinal EBF in humans and animals, with loss of enterocyte integrity and increased paracellular permeability via apical tight junctions, leading to translocation of bacteria and bacterial products into the blood stream. When low dose EN is delivered in mice with ischemia-reperfusion injury intestinal barrier architecture, function, and downstream signaling are preserved and/or restored in a dose-response relationship. Delays in EN delivery may impact patient outcomes through effects on nutritional status and through the downstream negative effects of intestinal epithelial barrier dysfunction. Study investigators do not understand the extent to which post-operative ischemia-reperfusion injury after repair of left sided congenital cardiac defects interacts with hemodynamic, respiratory, and nutritional support to alter recovery of intestinal EBF. Further studies are needed to understand if intestinal EBF profile can be used to assess post-operative readiness for EN in infants with CHD, and if improvement of intestinal EBF will reduce post-operative sepsis and MODS. Plasma biomarkers of key elements of intestinal EBF (enterocyte integrity, turnover, functional enterocyte mass, and paracellular tight junction function) exist and are clinical relevant, but have not been systematically studied in children with CHD.