Background
Retinopathy of prematurity (ROP) is a proliferative vascular disease of the retina that primarily affects premature infants and is one of the leading causes of visual loss in children [1]. Premature infants that are born at low birth weight or at a lower gestational age are particularly vulnerable [2].
In addition to genetic risk factors that are associated with the development of ROP [3-5], there are well established environmental risk factors for ROP, including early oxygen exposure and extreme prematurity [6]. Hyperglycemia is a newly reported environmental risk factor for ROP. Hyperglycemia, commonly defined as whole blood glucose level greater than 125 mg/dl or plasma glucose level greater than 150 mg/dl, occurs frequently in premature infants. In a study by Dweck et al., it was found that 86% of infants with a birthweight less than 1100 grams were hyperglycemic, with the highest risk of being hyperglycemic occurring within the first 24 hours of birth [7]. Data from a cohort analyses of the NIRTURE study also demonstrated that 80% of very low birth weight infants had glucose levels > 8 mmol/L (>144 mg/dL) and 32% had glucose levels > 10 mmol/L (>180 mg/dL) >10% of the time in the first week of life [8].
Recent studies have shown an association between neonatal hyperglycemia and (1) increased risk of early death and morbidity in extremely low birth weight infants [9,10], (2) increased morbidity and mortality in premature infants with necrotizing enterocolitis [11], and (3) has also been shown to be a risk factor for death and white matter reduction in preterm infants [12]. In addition, previous studies have demonstrated an association between hyperglycemia and the development of ROP [13-15]. The purpose of this study was to evaluate the relationship between the duration of hyperglycemia and the development of ROP in a larger cohort of premature infants born at less than 32 weeks gestation.