68 research outputs found
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Massive subcutaneous emphysema, pneumomediastinum, and pneumopericardium in children
Massive subcutaneous emphysema (SE), pneumomediastinum (PM), and pneumopericardium (PP) are rare conditions in the pediatric population. Air leak syndrome is a constellation of disorders that include SE, PM, PP, and pulmonary interstitial emphysema. In children, SE, PM, and PP are associated with obstructive airway disease most often in the case of asthma. Management may be conservative or involve invasive procedures that require surgical intervention. Here, we describe a case of massive SE, PM, and PP in a 10-year-old child after placement of a peripherally inserted central line and review the literature
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Pediatric Surgery (Seventh Edition) - Chapter 10 – Sepsis and Related Considerations
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Neonatal sepsis
This chapter examines the definition, epidemiology, pathophysiology, diagnosis, management, and outcome of neonatal sepsis. Sepsis was classically described in the adult patient with a Gram-negative infection who subsequently developed fever, hypotension with poor tissue perfusion, and ultimately multiple organ failure. Until recently, sepsis was defined as the presence of a systemic inflammatory response syndrome (SIRS) response coupled with a causative infection. Risk factors for neonatal sepsis can be divided into maternal and neonatal factors. Maternal contributors are more likely to be involved in early onset sepsis (EOS) than late onset sepsis (LOS) and have been divided into three categories: infection, colonization, and risk factors. Acute phase reactants and biomarkers can be measured in the evaluation of neonatal sepsis. Given the profound morbidity and mortality associated with neonatal sepsis, management should begin with prevention. The most significant prevention strategy has been the implementation of prenatal screening and administration of intrapartum antibiotics for group B Streptococcus (GBS) infection
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199. A WNT5A Model of Anorectal Malformation Demonstrates Up-Regulation of FGF10 But Not SHH During Hindgut Development
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Oral session: Thu 2/14 7:30 amPediatrics/developmental biology II: Development, regeneration, & cancer165. Intestinal Duplication As a Result of Inactivation of Wnt5a
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Necrotizing enterocolitis — bench to bedside: novel and emerging strategies
Necrotizing enterocolitis (NEC) is a devastating illness that predominantly affects premature neonates. The mortality associated with this disease has changed very little during the last two decades. Neonates with NEC fall into two categories: those who respond to medical management alone and those who require surgical treatment. The disease distribution may be focal, multifocal, or panintestinal. Surgical treatment should therefore be based on disease presentation. Recent studies have added significant insight into our understanding of the pathogenesis of NEC. Several groups have shown that upregulation of nitric oxide plays an integral role in the development of epithelial injury in NEC. As a result, some treatment strategies have been aimed at abrogating the toxic effects of nitric oxide. In addition, several investigators have reported the cytoprotective effect of epidermal growth factor, which is found in high levels in breast milk, on the intestinal epithelium. Thus, fortification of infant formula with specific growth factors could soon become a preferred strategy to accelerate intestinal maturation in the premature neonate to prevent the development of NEC. One of the most devastating complications of NEC is the development of short bowel syndrome (SBS). The current treatment of SBS involves intestinal lengthening procedures or bowel transplantation. A novel emerging method for treating SBS involves the use of tissue-engineered intestine. In laboratory animals, tissue-engineered small intestine has been shown to be successful in treating intestinal failure. This article examines recent data regarding surgical treatment options for NEC as well as emerging treatment modalities
Vascular Endothelial Growth Factor (VEGF) Bioavailability Regulates Angiogenesis and Intestinal Stem and Progenitor Cell Proliferation during Postnatal Small Intestinal Development.
BACKGROUND:Vascular endothelial growth factor (VEGF) is a highly conserved, master regulatory molecule required for endothelial cell proliferation, organization, migration and branching morphogenesis. Podocoryne carnea and drosophila, which lack endothelial cells and a vascular system, express VEGF homologs, indicating potential roles beyond angiogenesis and vasculogenesis. The role of VEGF in the development and homeostasis of the postnatal small intestine is unknown. We hypothesized regulating VEGF bioavailability in the postnatal small intestine would exhibit effects beyond the vasculature and influence epithelial cell stem/progenitor populations. METHODS:VEGF mutant mice were created that overexpressed VEGF in the brush border of epithelium via the villin promotor following doxycycline treatment. To decrease VEGF bioavailability, sFlt-1 mutant mice were generated that overexpressed the soluble VEGF receptor sFlt-1 upon doxycycline administration in the intestinal epithelium. Mice were analyzed after 21 days of doxycycline administration. RESULTS:Increased VEGF expression was confirmed by RT-qPCR and ELISA in the intestine of the VEGF mutants compared to littermates. The VEGF mutant duodenum demonstrated increased angiogenesis and vascular leak as compared to littermate controls. The VEGF mutant duodenum revealed taller villi and increased Ki-67-positive cells in the transit-amplifying zone with reduced Lgr5 expression. The duodenum of sFlt-1 mutants revealed shorter villi and longer crypts with reduced proliferation in the transit-amplifying zone, reduced expression of Dll1, Bmp4 and VE-cadherin, and increased expression of Sox9 and EphB2. CONCLUSIONS:Manipulating VEGF bioavailability leads to profound effects on not only the intestinal vasculature, but epithelial stem and progenitor cells in the intestinal crypt. Elucidation of the crosstalk between VEGF signaling in the vasculature, mesenchyme and epithelial stem/progenitor cell populations may direct future cell therapies for intestinal dysfunction or disease
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FGF-10 protects the intestinal epithelium from LPS-induced injury (902.14)
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