Neonatal hyperglycaemia in extremely preterm and extremely low birth weight infants: A report of a rare case and a review of the literature

Abstract

Neonatal hyperglycaemia poses risks, and the efficacy of insulin therapy is uncertain, warranting comprehensive research and guidelines. The present study reports the case of an extremely preterm neonate with an extremely low birth weight (ELBW; <1,000 g) admitted to the neonatal intensive care unit (NICU) due to recurrent hyperglycaemic episodes (peak level, 465 mg/dl) with transient hypoglycaemia on the first day of life. The mother, a 31-year-old primiparous woman, had gestational hypertension and preeclampsia, resulting in neonatal distress at birth and the need for positive pressure ventilation for stabilisation. The condition of the baby remained stable in the NICU following resuscitation. The case described herein details the management of a neonate facing multiple stresses and metabolic challenges, including grade IV hyaline membrane disease, grade II necrotising enterocolitis and a patent foramen ovale with good heart contractility. The initial laboratory findings revealed pancytopenia. At 1 h of life, the neonate experienced hypoglycaemia (33 mg/dl), treated with a 10% bolus dextrose infusion and continuous parenteral nutrition. Glucose infusion rate (GIR) adjustments followed local guidelines. Cardiovascular support with dobutamine and dopamine addressed the low blood pressure. Subsequently, the neonate developed hyperglycaemia, requiring insulin therapy and GIR adjustments. By close monitoring and promptly intervening, the authors were able to achieve stable blood glucose levels using insulin boluses (0.1 U) and adjusting the GIR to 10.9 mg/kg body weight (BW)/min. Stable glycaemia was attained by the 4th day prior to referral, with a GIR of 12.4 mg/kg BW/min. The case in the present study highlights the challenges of managing extremely preterm infants with ELBW and emphasises effective resuscitation and NICU interventions. It was hypothesised that her refractory hyperglycaemia was caused by her underlying extremely premature neonatal condition, including inadequate insulin response, gluconeogenesis, reduced glucose transporter levels, insufficient protein intake affecting insulin-like growth factor-1 release, immature pancreas development and stress-related hormonal responses.