Abstract
Low birthweight and decreased postnatal weight gain are known predictors of worse retinopathy of prematurity (ROP) but the role of prenatal growth patterns in ROP remains inconclusive. To distinguish small for gestational age (SGA) from intrauterine growth restriction (IUGR) as independent predictors of ROP, we performed a retrospective cohort study of patients who received ROP screening examinations at a level IV neonatal intensive care unit over a 7-year period. Data on IUGR and SGA status, worst stage of and need for treatment for ROP, and postnatal growth was obtained. 343 infants were included for analysis (mean gestational age = 28.6 weeks and birth weight = 1138.2 g). IUGR infants were more likely to have a worse stage of ROP and treatment-requiring ROP (both p < 0.0001) compared to non-IUGR infants. IUGR infants were more likely to be older at worst stage of ROP (p < 0.0001) and to develop postnatal growth failure (p = 0.01) than non-IUGR infants. Independent of postnatal growth failure status, IUGR infants had a 4–5 × increased risk of needing ROP treatment (p < 0.001) compared to non-IUGR infants. SGA versus appropriate for gestational age infants did not demonstrate differences in retinopathy outcomes, age at worst ROP stage, or postnatal growth failure. These findings emphasize the importance of prenatal growth on ROP development.
Highlights
Weight z-score change from birth to worst Retinopathy of prematurity (ROP) exam a appropriate for gestational age (AGA) (n = 300) SGA (n = 43) p value
While this study found an association between prenatal intrauterine growth restriction (IUGR) and worse ROP, it did not find an association between SGA and ROP
A recent meta-analysis found a positive association between SGA status and severe and treated ROP7, while another study found a relationship between poor postnatal weight gain and ROP, but no association with SGA and ROP11
Summary
Weight z-score change from birth to worst ROP exam a AGA (n = 300) SGA (n = 43) p value. IUGR status implies pathologic etiologies and oftentimes results from maternal conditions that impair blood flow and oxygen provision to the growing fetus (typically presenting as asymmetric growth restriction), such as maternal hypertensive disorders. IUGR may result from congenital infections and genetic disorders (typically presenting as symmetric growth restriction)[4]. IUGR is often utilized interchangeably with SGA in clinical practice, IUGR fetuses have been shown to have worse systemic o utcomes[8]. Our hypothesis was that IUGR, not SGA, is an independent risk factor for ROP treatment
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