Objective To classify NICU interventions for parental distress and quantify their effectiveness. Study design We systematically reviewed controlled studies published before 2017 measuring NICU parental distress, defined broad intervention categories, and used random-effects meta-analysis to quantify treatment effectiveness. Results Among 1643 unique records, 58 eligible trials predominantly studied mothers of preterm infants. Interventions tested in 22 randomized trials decreased parental distress (p < 0.001) and demonstrated improvement beyond 6 months (p < 0.005). In subgroup analyses, complementary/alternative medicine and family-centered instruction interventions each decreased distress symptoms (p < 0.01), with fathers and mothers improving to similar extents. Most psychotherapy studies decreased distress individually but did not qualify for meta-analysis as a group. Conclusion NICU interventions modestly reduced parental distress. We identified family-centered instruction as a target for implementation and complementary/alternative medicine as a target for further study. Investigators must develop psychosocial interventions that serve NICU parents at large, including fathers and parents of full-term infants.
Background: Decreased intestinal perfusion may contribute to the development of necrotizing enterocolitis (NEC). Vascular endothelial growth factor (VEGF) is an angiogenic protein necessary for the development and maintenance of capillary networks. Whether VEGF is dysregulated in NEC remains unknown. Objectives: The objective of this study was to determine whether intestinal VEGF expression is altered in a neonatal mouse model of NEC and in human NEC patients. Methods: We first assessed changes of intestinal VEGF mRNA and protein in a neonatal mouse NEC model before significant injury occurs. We then examined whether exposure to formula feeding, bacterial inoculation, cold stress and/or intermittent hypoxia affected intestinal VEGF expression. Last, we visualized VEGF protein in intestinal tissues of murine and human NEC and control cases by immunohistochemistry. Results: Intestinal VEGF protein and mRNA were significantly decreased in pups exposed to the NEC protocol compared to controls. Hypoxia, cold stress and commensal bacteria, when administered together, significantly downregulated intestinal VEGF expression, while they had no significant effect when given alone. VEGF was localized to a few single intestinal epithelial cells and some cells of the lamina propria and myenteric plexus. VEGF staining was decreased in murine and human NEC intestines when compared to control tissues. Conclusion: Intestinal VEGF protein is reduced in human and experimental NEC. Decreased VEGF production might contribute to NEC pathogenesis.
OBJECTIVES: Timely multidisciplinary family meetings (TMFMs) promote shared decision-making. Despite guidelines that recommend meetings for all patients with serious illness, our NICU TMFM rate was 10%. In this study, we aimed to document a meeting within 5 days of hospitalization for 50% of all new NICU patients hospitalized for ≥5 days within 1 year of introducing interventions. METHODS: A multidisciplinary improvement team used the Model for Improvement to achieve the study aim by targeting key drivers of change. To make meetings easier, we introduced scheduling and documentation tools. To make meetings more customary, we provided education and reminders to professionals. We defined a TMFM as a documented discussion between a parent, a neonatologist, and a nonphysician professional, such as a nurse, within 5 days of hospitalization. We used statistical process control charts to assess the monthly proportion of new patients with a TMFM. In surveys and feedback sessions, family and clinician satisfaction with communication was assessed. RESULTS: TMFM documentation tripled during the intervention year when compared with the previous year (28 of 267 [10.5%] vs 70 of 224 [31.3%]; P < .001), revealing evidence of special cause variation on the statistical process control chart. Clinicians predominantly used ad hoc documentation instead of our scheduling and documentation tools. Parental satisfaction with care and communication did not vary significantly after interventions. Most physicians reported satisfaction with meetings. Nurses reported feeling empowered to request meetings. CONCLUSIONS: An academic, quaternary-care NICU tripled TMFM documentation after introducing a multifaceted intervention. This improvement may represent changes in professionals’ attitudes about providing and documenting family meetings.
Ischemic necrosis is a feature of necrotizing enterocolitis (NEC). We have previously found that VEGF is decreased in a neonatal mouse model of NEC. Here, we hypothesized that, in NEC, VEGF deficiency causes altered neonatal intestinal microvasculature and impaired microcirculation leading to NEC development. To test this hypothesis, neonatal pups were injected intraperitoneally with SU5416, a VEGF receptor kinase inhibitor prior to exposure to a NEC protocol. The intestinal mucosal microvasculature morphology was assessed by imaging after intracardiac dye injection. Endothelial (CD31+) cells were quantified by flow cytometry analysis following collagenase digestion of intestinal tissues. We found that: 1) Intestinal vascular networks were decreased in pups exposed to the NEC protocol for 48 hours compared to controls, and further decreased in pups treated with VEGF inhibitor; 2) The percentage of CD31+ cells in the CD45‐ Epcam‐ population was decreased in NEC small intestines (1.20%) vs. dam‐fed controls (4.64%), and further decreased when VEGF pathway was blocked (0.37%, p<0.05 vs dam‐fed). Pups exposed to the NEC protocol treated with VEGF inhibitor had increased incidence of severe NEC (score蠅2), compared to controls (18/29 vs 8/32, χ2=7.1, p<0.01) and had increased mortality. In conclusion, we found that inhibition of endogenous VEGF causes intestinal microcirculatory dysfunction and facilitates the development of neonatal NEC.. Grant Funding Source: Supported by a Thrasher Foundation Grant
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.