Obstructive sleep apnea (OSA) is a highly prevalent medical condition in obese children and is associated with significant neurocognitive, cardiovascular and metabolic derangements. Monogenic forms of obesity resulting from disruption of the leptin-melanocortin pathways have become more notable in recent years and distinguish between various obese phenotypes. However, the association of such disorders with OSA is not well established in children or adults. In this report, we describe a 23-month-old female with morbid obesity and OSA, who was found to carry a defect in the melanocortin-4 receptor (MC4R) pathway. This report emphasizes the genetic basis of obesity related to MC4R deficiency and OSA in children.

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Background Neonatal hypoglycemia has been associated with various forms of neurological impairment including developmental delay, seizures, visual processing problems, and cognitive difficulties [1]. Consensus guidelines have been created to expedite the identification and resolution of hypoglycemic episodes. Interventions, such oral dextrose gel, have been shown to quickly and effectively reverse episodes of severe hypoglycemia [2]. However, more research needs to be conducted to quantify potential effects of oral glucose gel pathways on prevention of hypoglycemia in the neonatal period. Objective We evaluated the effects of introducing a clinical pathway for improving hypoglycemia with oral dextrose gel. We hypothesized a decrease in the length of stay of neonates with hypoglycemia after the introduction of the clinical pathway. Design/Methods We conducted a retrospective chart review evaluating neonates born ≥ 35 weeks gestational age, who exhibited asymptomatic hypoglycemia within 48 hours of life (HOL) while receiving exclusive oral feeds. The primary outcome was overall length of hospital stay. We extracted data from charts of children born prior and after the implementation of this oral dextrose gel pathway in both the well-baby nursery and Neonatal Intensive Care Unit (NICU) of a single medical center over a one-year period. Results 385 total neonates who fit the aforementioned criteria were included, with 175 neonates representing the historical control group and 210 neonates in the intervention group receiving oral dextrose gel. Analysis demonstrated no significant difference in the overall length of stay, as well as the total episodes of hypoglycemia and number of days the neonate received intravenous fluid therapy with dextrose. Conclusion(s) Our study demonstrates that the introduction of oral dextrose gel pathway did not have a significant effecton the overall length of hospital stay, as well as the total episodes of hypoglycemia and number of days the neonate received intravenous fluid therapy with dextrose at our institution. Further research is needed to evaluate whether response to oral dextrose gel can be used as a predictor of severe hypoglycemia in the neonatal period. Presentation: No date and time listed

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