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This perspective work by academic neonatal providers is written specifically for the audience of newborn care providers and neonatologists involved in neonatal hypoglycemia screening. Herein, we propose adding a screen for congenital hyperinsulinism (CHI) by measuring glucose and ketone (i.e., β-hydroxybutyrate (BOHB)) concentrations just prior to newborn hospital discharge and as close to 48 h after birth as possible, at the same time that the mandated state Newborn Dried Blood Spot Screen is obtained. In the proposed protocol, we do not recommend specific metabolite cutoffs, as our primary objective is to simply highlight the concept of screening for CHI in newborns to newborn caregivers. The premise for our proposed screen is based on the known effect of hyperinsulinism in suppressing ketogenesis, thereby limiting ketone production. We will briefly discuss genetic CHI, other forms of neonatal hypoglycemia, and their shared mechanisms; the mechanism of insulin regulation by functional pancreatic islet cell membrane KATP channels; adverse neurodevelopmental sequelae and brain injury due to missing or delaying the CHI diagnosis; the principles of a good screening test; how current neonatal hypoglycemia screening programs do not fulfill the criteria for being effective screening tests; and our proposed algorithm for screening for CHI in newborns. [ABSTRACT FROM AUTHOR]

Prolonged labor can lead to infection, fetal distress, asphyxia, and life-threatening harm to both the mother and the baby. Surfactant protein A (SP-A) was shown to contribute to the maintenance of pregnancy and timing of term labor. SP-A modulates the stoichiometric expression of the SP-R210L and SP-R210S isoforms of the SP-R210 receptor on alveolar macrophages (AMs). Lack of SP-R210L dysregulates macrophage inflammatory responses. We asked whether SP-A alters normal and inflammation-induced parturition through SP-R210 using SP-A- and SP-R210L-deficient mice. Labor and delivery of time-pregnant mice were monitored in real time using a time-lapse infrared camera. Intrauterine injection with either vehicle or Escherichia coli lipopolysaccharide (LPS) on embryonic (E) day 18.5 post coitus was used to assess the effect of gene disruption in chorioamnionitis-induced labor. We report that either lack of SP-A or disruption of SP-R210L delays parturition by 0.40 and 0.55 days compared with controls, respectively. LPS induced labor at 0.60, 1.01, 0.40, 1.00, and 1.31 days earlier than PBS controls in wild type (WT), SP-A-deficient, littermate controls, heterozygous, and homozygous SP-R210L-deficient mice, respectively. Lack of SP-A reduced litter size in PBS-treated mice, whereas the total number of pups delivered was similar in all LPS-treated mice. The number of live pups, however, was significantly reduced by 50%–70% in SP-A and SP-R210L-deficient mice compared with controls. Differences in gestational length were not associated with intrauterine growth restriction. The present findings support the novel concept that the SP-A/SP-R210 pathway modulates timely labor and delivery and supports fetal lung barrier integrity during fetal-to-neonatal transition in term pregnancy. NEW & NOTEWORTHY: To our knowledge, this study is the first to report that SP-A prevents delay of labor and inflammation-induced stillbirth through the receptor SP-R210L. [ABSTRACT FROM AUTHOR]

Background: Continuous positive airway pressure (CPAP) benefits preterm infants with respiratory distress, including reduced bronchopulmonary dysplasia (BPD) incidence, surfactant use, and extubation failure. Successful CPAP weaning also promotes oral feeding. However, there is no consensus on the optimal weaning of CPAP in neonates. This study aims to determine the effects of CPAP (CPAP) weaning guideline implementation on neonatal outcomes., Methods: CPAP gradual pressure weaning guidelines were implemented in the Penn State Children's Hospital NICU in 2020. We included baseline data from infants (Epoch1) before bubble CPAP implementation in 2018-19. We included infants (Epoch2) after implementing the guidelines during 2020-21. The inclusion criteria were infants <32 weeks gestation with CPAP support. Compliance with the CPAP weaning guidelines was the primary process measure. Primary outcome measures included successful CPAP wean on the first attempt. Balancing measures used were total days on respiratory support and length of hospital stay., Results: 195 infants were included in this study, 95 infants in Epoch 1 before bubble CPAP implementation and 100 infants in Epoch 2 after implementing guidelines. Infants in the two Epochs were similar in median gestational age at 29 vs 30 weeks (p=0.47) and were similar in median birth weight at 1190 vs 1130 grams (p=0.73). After implementing weaning guidelines, the successful weaning off CPAP improved from 9.5% to 54% (p<0.001). The total days needed to achieve full oral feeds decreased by 7 days (29 vs 22 median days, p<0.001). The BPD incidence was not significantly different between the two Epochs at 17% vs 16%, p= 0.87. There was no difference in total days of respiratory support, total length of stay, the number of infants discharged on home nasogastric feeding, and demographic variables., Conclusion: The implementation of the bubble CPAP weaning guideline improves the successful weaning of CPAP and promotes oral feeding in preterm infants., (Copyright © 2024 by Daedalus Enterprises.)

Prolonged labor can lead to infection, fetal distress, asphyxia, and life-threatening harm to both the mother and the baby. Surfactant protein A (SP-A) was shown to contribute to the maintenance of pregnancy and timing of term labor. SP-A modulates the stoichiometric expression of the SP-R210 L and SP-R210 S isoforms of the SP-R210 receptor on alveolar macrophages (AMs). Lack of SP-R210 L dysregulates macrophage inflammatory responses. We asked whether SP-A alters normal and inflammation-induced parturition through SP-R210 using SP-A- and SP-R210 L -deficient mice. Labor and delivery of time-pregnant mice were monitored in real time using a time-lapse infrared camera. Intrauterine injection with either vehicle or Escherichia coli lipopolysaccharide (LPS) on embryonic (E) day 18.5 post coitus was used to assess the effect of gene disruption in chorioamnionitis-induced labor. We report that either lack of SP-A or disruption of SP-R210 L delays parturition by 0.40 and 0.55 days compared with controls, respectively. LPS induced labor at 0.60, 1.01, 0.40, 1.00, and 1.31 days earlier than PBS controls in wild type (WT), SP-A-deficient, littermate controls, heterozygous, and homozygous SP-R210 L -deficient mice, respectively. Lack of SP-A reduced litter size in PBS-treated mice, whereas the total number of pups delivered was similar in all LPS-treated mice. The number of live pups, however, was significantly reduced by 50%-70% in SP-A and SP-R210 L -deficient mice compared with controls. Differences in gestational length were not associated with intrauterine growth restriction. The present findings support the novel concept that the SP-A/SP-R210 pathway modulates timely labor and delivery and supports fetal lung barrier integrity during fetal-to-neonatal transition in term pregnancy. NEW & NOTEWORTHY To our knowledge, this study is the first to report that SP-A prevents delay of labor and inflammation-induced stillbirth through the receptor SP-R210 L .