Abstract
Sonographically detectable transient periventricular echodensities (PVED) are often observed in very-low-birth-weight (VLBW, <1500 gm) infants when screening for intraventricular hemorrhage (IVH); their impact on outcome remains unclear but recent studies have suggested an adverse neurodevelomental influence. Although hypoxia-ischemia has been considered a possible cause, clinically relevant risk factors and preventive treatments for this finding remain uncertain. We performed a retrospective matched case-control study of PVED and risk factors in all infants <1500 gm BW from 6/90-12/95, during which sonographic screening was routine. We studied antepartum, intrapartum, and postnatal factors, concentrating on epidemiologic, vascular, respiratory, and infectious factors, and on intrapartum magnesium sulfate (MAG) exposure, because of recent suggestions of a neuro-protective effect of this agent. We identified 1417 VLBW infants and 74 cases of transient PVED (inc. 5.2%) and matched 74 controls with normal sonograms (no IVH or PVL, latest at least 30d) for ±150 gm BW and date of birth. Controls and cases were similar in BW(994±242 vs 981±238 gm) and gestational age (28±2 wks). PVED cases were more likely to have placental funisitis (32%vs 3%) and patent ductus arteriosus (59% vs 38%) and less likely to have pre-eclampsia (4% vs 21%)(all P≤0.05). The proportions of any intrapartum MAG, tocolytic MAG, steroid use, SGA, RDS, and indomethacin were similar between groups. A logistic regression model (controlled for MAG use, chorioamnionitis, and indomethacin use) revealed predictors of PVED as shown in the Table. We conclude that intrapartum infection and PDA are risk factors for PVED in VLBW infants and that pre-eclampsia is more important than MAG use in reducing such neurologic findings.
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