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Objective The aim of this study was to determine which late-preterm (35–36 weeks' gestational age [GA]) and term neonates with early-onset hypoglycemia in the first 72 hours postnatal required a continuous glucose infusion to achieve and successfully maintain euglycemia. Study Design This is a retrospective cohort study of late preterm and term neonates born in 2010–2014 and admitted to the Mother-Baby Unit at Parkland Hospital who had laboratory-proven blood glucose concentration < 40 mg/dL (2.2 mmol/L) during the first 72 hours of life. Among the subgroup needing intravenous (IV) glucose infusion, we analyzed which factors predicted a maximum glucose infusion rate (GIR) ≥ 10 mg/kg/min. The entire cohort was randomly divided into a derivation cohort (n = 1,288) and a validation cohort (n = 1,298). Results In multivariate analysis, the need for IV glucose infusion was associated with small size for GA, low initial glucose concentration, early-onset infection, and other perinatal variables in both cohorts. A GIR ≥ 10 mg/kg / min was required in 14% of neonates with blood glucose value < 20 mg/dL during the first 3 hours of observation. The likelihood of a GIR ≥ 10 mg/kg/min was associated with lower initial blood glucose value and lower umbilical arterial pH. Conclusion Need for IV glucose infusion was associated with small size for GA, low initial glucose concentration, early-onset infection, and variables associated with perinatal hypoxia–asphyxia. The likelihood of a maximum GIR ≥ 10 mg/kg/min was greater in neonates with lower blood glucose value during the first 3 hours of observation and lower umbilical arterial pH. Key Points We studied 51,973 neonates ≥ 35 weeks' GA. We established a model predicting the need for IV glucose. We also predicted the need for a high rate of IV glucose. [ABSTRACT FROM AUTHOR]

BACKGROUND: Hypoglycemia in neonates is common and contributes to 4.0–5.8% of neonatal intensive care unit (NICU) admissions. In utero nicotine exposure is underexplored as a potential contributor to neonatal hypoglycemia. Rat models have shown that in utero nicotine exposure can be associated with a reduction in pancreatic beta cell mass, leading to glucose dysregulation. The primary aim of this work is to study the risk of developing hypoglycemia after birth in a population of in utero nicotine-exposed neonates. METHODS: We conducted a retrospective matched cohort study that augmented an existing dataset of neonates admitted to a level IV NICU with household-based in utero nicotine exposure (N = 335). Neonates in the control group parents denied household smoking (N = 325), were born within a 6-month timeframe, and were within a birthweight of 50 grams of a nicotine-exposed neonate. Data reviewed included gestational age, growth parameters, maternal history of diabetes, and glucose levels within the first three hours of life per unit protocol. RESULTS: 660 neonates were included in the analysis. In utero nicotine exposure demonstrated a 94.3% posterior probability (PP) for greater hypoglycemia risk (RR = 1.185, 95% CrI = [0.953, 1.445]). A 94.6% PP was demonstrated when neonates who were small for gestational age, intrauterine growth-restricted, and born to diabetic mothers were excluded (n = 482; RR = 1.271, 95% CrI = [0.946, 1.669]). CONCLUSION: Nicotine exposure in utero was found to be a potential risk factor for developing hypoglycemia after birth. Mechanisms of action should be explored, and additional research on in utero nicotine exposure risks should follow. [ABSTRACT FROM AUTHOR]