ESPE Abstracts (2019) 92 P1-204

Risk Factors for Brain Injury After Transient or Persistent Hyperinsulinemic Hypoglycemia in Neonates

Marcia Roeper1, Roschan Salimi Dafsari1, Sebastian Kummer1, Dirk Klee1, Ertan Mayatepek1, Hemmen Sabir2, Thomas Meissner1


1University Children's Hospital Duesseldorf, Duesseldorf, Germany. 2University of Bonn Children's Hospital, Bonn, Germany


Background: Aim of this study was to identify possible explanations why despite improved treatment options brain damage still occurs in neonates with transient or persistent hyperinsulinism. This study might serve as a basis for future research to improve the management of neonatal hypoglycemia reducing brain injury in these children.

Material and Methods: A retrospective medical chart review was conducted at the University Children's Hospital Duesseldorf, Germany. Out of 115 children with transient neonatal hyperinsulinism or persistent congential hyperinsulinism (CHI) n=11 patients with hypoglycemic brain damage were identified. Data was analyzed in terms of most likely etiologic hypoglycemic episodes and thereafter the associated cause of brain damage was investigated.

Results: In our cohort of 11 patients, 8 had neurodevelopmental delay, one of them severe. 7 had epilepsy, 3 had impaired vision and one patient had cerebral palsy. In 7 patients, magnetic resonance (MR) brain imaging showed signs of hypoglycemic brain injury. Remarkably, three children had transient hyperinsulinism achieving remission between 3 weeks to 3 months of life. The remaining 8 patients suffered from persistent CHI. Only 2 patients had risk factors for neonatal hypoglycemia and they both had persistent CHI. All patients had very low blood glucose levels <1,4 mmol/L (<25mg/dl; range 0,1-1,2 mmol/L; median 0,7 mmol/L) in at least one measurement. In 8 patients, the lowest known blood glucose concentration was recorded in the initial glucose control. All patients had symptomatic hypoglycemia and 8 patients had at least one episode of hypoglycemic seizure. In 7 patients, a delay of several hours up to 2 months was observed between first clinical symptoms, first blood glucose control and achieving appropriate glycemic stabilization.

Conclusion: Brain damage particularly occurred in newborns without risk factors for postnatal hypoglycemia as for these newborns blood glucose screenings are not standard procedure. Brain damage in transient hyperinsulinemic hypoglycemia was a frequent finding in our cohort. Inferior neurological outcome was notably associated with a delay between first clinical symptoms, diagnosis and initiation of adequate treatment. Additionally, hypoglycemic seizures and low blood glucose levels <1,4 mmol/L (<25mg/dl) were prevalent in those with brain damage. Further research is needed to improve early identification of patients with high risk for brain damage within the large group of neonates with physiological postnatal hypoglycemia.

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