Structured pre-delivery huddles enhance confidence in managing newborns with critical congenital heart disease in the delivery room.

Background: Newborns with critical congenital heart disease (CCHD) require specialized delivery room management, but varying experience and knowledge can reduce confidence and impact care.

Methods: A pre-delivery, structured huddle checklist was introduced, addressing team roles, expected physiology, and management plans. PDSA cycles incorporated guidelines and simulation-based education to improve confidence in specialized resuscitation strategies.

Acute Diffusion-Weighted Imaging Signaling Severe Periventricular Leukomalacia in Preterm Infants: Case Report and Review of Literature.

Periventricular leukomalacia occurs in up to 25% of very preterm infants resulting in adverse neurodevelopmental outcomes. In its acute phase, periventricular leukomalacia is clinically silent. Although ultrasonography is widely available, its sensitivity in the early detection of periventricular leukomalacia is low.

A quality improvement initiative to reduce acid-suppressing medication exposure in the NICU.

Background: Acid-suppressing medications (ASMs) are commonly prescribed in the neonatal intensive care unit (NICU), in particular among preterm infants, despite well-established adverse effects and little evidence to support efficacy.

Local Problem: We sought to develop an initiative to reduce ASM exposure in our predominantly inborn level III NICU. Our specific aim was to reduce the number of nonindicated ASM prescriptions by 50% within a 12-month period.

Protection of melatonin in experimental models of newborn hypoxic-ischemic brain injury through MT1 receptor.

The function of melatonin as a protective agent against newborn hypoxic-ischemic (H-I) brain injury is not yet well studied, and the mechanisms by which melatonin causes neuroprotection in neurological diseases are still evolving. This study was designed to investigate whether expression of MT1 receptors is reduced in newborn H-I brain injury and whether the protective action of melatonin is by alterations of the MT1 receptors. We demonstrated that there was significant reduction in MT1 receptors in ischemic brain of mouse pups in vivo following H-I brain injury and that melatonin offers neuroprotection through upregulation of MT1 receptors.

Bumetanide enhances phenobarbital efficacy in a rat model of hypoxic neonatal seizures.

Neonatal seizures can be refractory to conventional anticonvulsants, and this may in part be due to a developmental increase in expression of the neuronal Na(+)-K(+)-2 Cl(-) cotransporter, NKCC1, and consequent paradoxical excitatory actions of GABAA receptors in the perinatal period. The most common cause of neonatal seizures is hypoxic encephalopathy, and here we show in an established model of neonatal hypoxia-induced seizures that the NKCC1 inhibitor, bumetanide, in combination with phenobarbital is significantly more effective than phenobarbital alone. A sensitive mass spectrometry assay revealed that bumetanide concentrations in serum and brain were dose-dependent, and the expression of NKCC1 protein transiently increased in cortex and hippocampus after hypoxic seizures.

The clinically available NMDA receptor antagonist, memantine, exhibits relative safety in the developing rat brain.

The N-methyl-d-aspartate glutamate receptor (NMDAR) has been implicated in preterm brain injury (periventricular leukomalacia (PVL)) and represents a potential therapeutic target. However, the antagonist dizocilpine (MK-801) has been reported to increase constitutive neuronal apoptosis in the developing rat brain, limiting its clinical use in the developing brain. Memantine is another use-dependent NMDAR antagonist with shorter binding kinetics and has been demonstrated to be protective in a rat model of PVL, without effects on normal myelination or cortical growth.

NMDA receptor blockade with memantine attenuates white matter injury in a rat model of periventricular leukomalacia.

Hypoxia-ischemia (H/I) in the premature infant leads to white matter injury termed periventricular leukomalacia (PVL), the leading cause of subsequent neurological deficits. Glutamatergic excitotoxicity in white matter oligodendrocytes (OLs) mediated by cell surface glutamate receptors (GluRs) of the AMPA subtype has been demonstrated as one factor in this injury. Recently, it has been shown that rodent OLs also express functional NMDA GluRs (NMDARs), and overactivation of these receptors can mediate excitotoxic OL injury.