INTRODUCTION: MSAF is less commonly found among neonates born prematurely. Recent data suggest that meconium in the amniotic fluid of term-gestation infants may itself CP by stimulating umbilical/placental vasoconstriction (OBSTET GYNECOL 1995;86:720). There are no data concerning long-term outcome of very premature neonates born through MSAF. From 1991-1994, we prospectively enrolled and followed a cohort of infants≤ 30 weeks gestational age for assessment of acute brain injury(intracranial hemorrhage [ICH] and large [> 5 mm] cystic periventricular leukomalacia [CPVL], as well as long-term development of CP.METHODS: Our population consisted of 118 ventilated preterm infants GA ≤ 30 weeks. Neurosonographic exams were performed weekly for ≥ 2 months in all infants. Survivors were followed in our high-risk clinic.RESULTS: 10/118 (8.4%) were born through MSAF. 85 of 100 (85%) survivors (including 7/10 born through MSAF) were followed long enough to have undergone adequate assessment for findings of CP. The occurrence of other potential causes of in-utero compromise (2nd or 3rd trimester bleeding, placental abruption, oligohydramnios, preterm PROM, toxemia, pregnancy-induced hypertension, gestational diabetes, ilicit drug use) were similar in the 2 groups. CONCLUSION: Preterm infants ≤30 wks GA born through MSAF have a trend for more CPVL as well as a significantly higher incidence of CP. These data support the concept of in-utero ischemic effect by meconium itself in causing fetal brain injury. Supported in part by NIH 5RO1 HD21453-06. Table

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