Journal of pediatric surgery
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Previously, we have shown that supplementation of intestinal alkaline phosphatase (IAP) decreased severity of necrotizing enterocolitis (NEC)-associated intestinal injury. We hypothesized that IAP administration is protective of intestinal epithelial barrier function in a dose-dependent manner. ⋯ Early enteral supplemental IAP may reduce NEC-related injury and may be useful for preserving the intestinal epithelial barrier function.
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Review Comparative Study
Laparoscopic surgery in children with congenital heart disease.
The study aim was to determine outcomes of children with congenital heart disease who underwent laparoscopic procedures. ⋯ In this review, there were no major contraindications to performing laparoscopic procedures in children with congenital heart disease, and we conclude that it is reasonably safe to perform laparoscopic surgery on these children.
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The purpose of this study was to characterize epidemiologic trends and cost implications of hospital readmission after treatment of pediatric appendicitis. ⋯ In freestanding children's hospitals, readmission after treatment of pediatric appendicitis is a relatively common and costly occurrence. Collaborative efforts are needed to characterize patient, treatment, and hospital-related risk factors as a basis for developing preventative strategies.
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Massive small bowel resection (SBR) results in villus angiogenesis and a critical adaptation response within the remnant bowel. Previous ex vivo studies of intestinal blood flow after SBR are conflicting. We sought to determine the effect of SBR on intestinal hemodynamics using photoacoustic microscopy, a noninvasive, label-free, high-resolution in vivo hybrid imaging modality. ⋯ Massive SBR results in an immediate reduction in intestinal blood flow and increase in tissue oxygen utilization. These physiologic changes are observed throughout the remnant small intestine. The contribution of these early hemodynamic alterations may contribute to the induction of villus angiogenesis and the pathogenesis of normal intestinal adaptation responses.