Background: Withholding enteral feedings during hypothermia lacks supporting evidence.
Objectives: We aimed to determine if minimal enteral nutrition (MEN) during hypothermia in patients with hypoxic-ischemic encephalopathy was associated with a reduced duration of parenteral nutrition, time to full oral feeds, and length of stay, but would not be associated with increased systemic inflammation or feeding complications.
Methods: We performed a pilot, retrospective, matched case-control study within the Florida Neonatal Neurologic Network from December 2012 to May 2016 of patients who received MEN during hypothermia (n = 17) versus those who were not fed (n = 17). Length of stay, feeding-related outcomes, and brain injury identified by MRI were compared. Serum inflammatory mediators were measured at 0-6, 24, and 96 h of life by multiplex assay. MRI were scored using the Barkovich system.
Results: MEN subjects had a reduced length of hospital stay (mean 15 ± 11 vs. 24 ± 19 days, p < 0.05), days receiving parenteral nutrition (7 ± 2 vs. 11 ± 6, p < 0.05), and time to full oral feeds (8 ± 5 vs. 18 ± 18, p < 0.05). MEN was associated with a significantly reduced serum IL-12p70 at 24 and 96 h (p < 0.05). Brain MRI scores were not significantly different between groups.
Conclusion: MEN during hypothermia was associated with a reduced length of stay and time to full feeds, but did not increase feeding complications or systemic inflammation.
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http://dx.doi.org/10.1159/000487848 | DOI Listing |
Antioxid Redox Signal
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.
View Article and Find Full Text PDFJ Perinatol
January 2025
University of California, San Diego, Rady Children's Hospital of San Diego, La Jolla, CA, USA.
Objective: Evaluate the changes in management and outcomes of Californian infants with hypoxic ischemic encephalopathy (HIE).
Study Design: Infants with HIE were identified from a California administrative birth cohort using ICD codes and divided into two epochs, Epoch 1 (2010-2015) and Epoch 2 (2016-2019). Risk ratios (RR) for induced hypothermia (IH) in each epoch and their outcomes were calculated using log-linear regression.
Ischemic stroke can cause damage to neurons, resulting in neurological dysfunction. The main treatments in the acute phase include intravenous thrombolysis, endovascular stent-assisted vascular thrombectomy and antiplatelet therapy. Due to the limitations of the time window and the risk of early intracranial hemorrhage, finding active treatment plans is crucial for improving therapy.
View Article and Find Full Text PDFJ Pediatr
January 2025
Department of Pediatrics, McGill University; Montreal Children's Hospital.
Objective: To assess variability among data elements collected among existing neonatal hypoxic-ischemic encephalopathy (HIE) data registries worldwide and to determine the need for future harmonization of standard common data elements.
Study Design: This was a cross-sectional study of data elements collected from current or recently employed HIE registry data forms. Registries were identified by literature search and email inquiries to investigators worldwide.
Pediatr Neurol
January 2025
Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Background: To explore the utility of general movements assessment as a predictive tool of the neurological outcome in term-born infants with hypoxic-ischemic encephalopathy (HIE) at ages six and 12 months.
Methods: This prospective observational study was conducted for 18 months (August 2018 to December 2019). Term-born newborns with HIE were included.
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