Case Report of Hyponatremic Seizures in a Term Neonate Attributed to Excessive Maternal Coconut Water Ingestion During Labor.

We report the case of a term neonate who was somnolent at birth with ventilatory distress and experienced 2 seizures shortly after delivery. Laboratory tests revealed the neonate had a serum sodium of 113 mmol/L. The seizures stopped after treatment with midazolam, and the sodium was corrected slowly with 3% hypertonic saline without further sequelae. The severe neonatal hyponatremia and seizures were attributed to maternal consumption of excessive amounts of coconut water during labor. This case demonstrates the importance of careful consideration of both fluid volume and fluid electrolyte composition during labor to prevent adverse maternal and neonatal outcomes.

Egr2-neurons control the adult respiratory response to hypercapnia.

`The early growth response 2 transcription factor, Egr2, establishes a population of brainstem neurons essential for normal breathing at birth. Egr2-null mice die perinatally of respiratory insufficiency characterized by subnormal respiratory rate and severe apneas. Here we bypass this lethality using a noninvasive pharmacogenetic approach to inducibly perturb neuron activity postnatally, and ask if Egr2-neurons control respiration in adult mice. We found that the normal ventilatory increase in response to elevated tissue CO2 was impaired, blunted by 63.1 ± 8.7% after neuron perturbation due to deficits in both respiratory amplitude and frequency. By contrast, room-air breathing was unaffected, suggesting that the drive for baseline breathing may not require those Egr2-neurons manipulated here. Of the multiple brainstem sites proposed to affect ventilation in response to hypercapnia, only the retrotrapezoid nucleus, a portion of the serotonergic raphé, and a portion of the A5 nucleus have a history of Egr2 expression. We recently showed that acute inhibition of serotonergic neurons en masse blunts the CO2 chemoreflex in adults, causing a difference in hypercapnic response of ∼50% after neuron perturbation through effects on respiratory amplitude only. The suppressed respiratory frequency upon perturbation of Egr2-neurons thus may stem from non-serotonergic neurons within the Egr2 domain. Perturbation of Egr2-neurons did not affect body temperature, even on exposure to ambient 4°C. These findings support a model in which Egr2-neurons are a critical component of the respiratory chemoreflex into adulthood. Methodologically, these results highlight how pharmacogenetic approaches allow neuron function to be queried in unanesthetized adult animals, reaching beyond the roadblocks of developmental lethality and compensation as well as the anatomical disturbances associated with invasive methods. This article is part of a Special Issue entitled Optogenetics (7th BRES).