Aim: Severe neonatal hypoglycaemia (HG) leads to neurologic damage, mental retardation, epilepsy, impaired cardiac performance and muscle weakness. The aim was to assess the frequency and severity of HG in a population of newborns.
Patients and methods: We investigated 739 patients with neonatal hypoglycaemia (HG) (M:F=370:369) born at the University Clinic for Gynaecology and Obstetritics in Skopje in the period 2014-2016 and treated at the neonatal intensive care unit (NICU). 1416 babies were treated in the same period in NICU, and HG was observed in 52.18%. The birth weight was dominated by children with low birth weight: very low birth weight (VLBW)(<1500g) 253 children, (34,23%), low birth weight (1500-2500g) 402 (54.39%), appropriate for gestational age (AGA) 78(10.55%), and high birth weight (>4000g) 6 babies (0.81%). The gestational age was also dominated by children with low gestational age: gestational week (GW) 20-25 four children (0.54%), 26-30 GW 133 babies (17.99%), 31-35 GW472 (63.87%), and 36-40 GW130 neonates (17.59 %).
241 mothers (32.61%) have had an infection during pregnancy, 82 preeclampsia or eclampsia (11.09%), 20 diabetes mellitus (2.70%), 78 placental situations (placenta previa, abruption) (10.55%). In this study 47 babies (6.35%) with HG and co-morbidities died.
There was a significant positive correlation between HG birth weight (p<0.01), gestational age (p<0.05), and the lowest Apgar score (p<0.01). Neonatal deaths were significantly correlated with GA (р>0,01), co-morbidities of the mothers (р>0,05) but not with the birth weight (р>0,05). In contrast, a significant positive correlation was found between convulsions and body weight (р<0.05). The lowest Apgar score was positively correlated with the gestational age (0.01), but not with the birth weight (0.05).
Conclusion: Low birth weight, low gestational age, maternal risk factors, hypoxic-ischemic encephalopathy and neonatal infections are associated with HG and are a significant factor in overall neonatal mortality. Those results indicate that diminishing the frequency of the neonatal HG and the rates of neonatal mortality requires complex interaction of prenatal and postnatal interventions.
