The etiology of IUGR in most cases is unknown. To determine the frequencies of placental abnormalities in IUGR and their relationship to neonatal outcome, we retrospectively reviewed obstetrical and neonatal data for 87 infants with IUGR (BW<10%ile) admitted to UMMS NICU between 1/92-12/94 for whom placental pathology was available. IUGR cases with identified chromosomal abnormalities or confirmed congenital infection were excluded. All placental pathology was reviewed by a pediatric pathologist (C-C.J.S.). There were 64(74%) symmetric IUGR (HC<10%ile) and 23 (26%) asymmetric IUGR. They were similar for demographic, obstetrical and neonatal factors. Placental abnormalities were found in 54 (62%) placentas [30 (34.5%), 1 abnormality; 25(28.7%), ≥ 2 abnormalities]. Lesions causing placental insufficiency were the most common (44%) (infarction, N=33, 37.5%; placental vascular thrombosis, N=13, 14.7%). Other lesions were inflammatory lesions (26%) (chronic villitis, N=14, 16%; hemorrhagic endovasculitis, N=7, 8%; and chorioamnionitis, N=6, 6.8%), and gross lesions 12.5% (abruption, N=7, 8%; velamentous cord insertion, N=4, 4.6%; and circumvallate placenta, N=2, 2.3%). Sixty-three percent of subjects with placental insufficiency were white and 33% were African-American (p=0.005). Seventy-three percent with pregnancy-induced hypertension (p<0.001) and 57% with oligohydramnios (p=0.045) had placental insufficiency lesions. We conclude that chronic placental abnormalities are associated with IUGR and may be a major factor in the pathogenesis of abnormal fetal growth. We are currently studying the impact of these placental lesions on long term neurodevelopmental outcomes.