INTRAUTERINE GROWTH RESTRICTION IN INFANTS OF LESS-THAN 32 WEEKS GESTATION - ASSOCIATED PLACENTAL PATHOLOGICAL FEATURES

OBJECTIVE: Our purpose was to describe placental lesions associated wi th normal and abnormal fetal growth in infants delivered for obstetric indications at < 32 weeks' gestation. STUDY DESIGN: Maternal and neon atal charts and placental tissues from 420 consecutive nonanomalous li ve-born singleton infants delivered at < 32 weeks' gestation with accu rate gestational dates were retrospectively studied. Excluded were cas es with maternal diabetes, chronic hypertension, hydrops fetalis, diag nosed congenital viral infection, and placenta previa, leaving four pr imary indications for delivery: preeclampsia, preterm labor, premature rupture of membranes, and nonhypertensive abruptio placentae. The pre sence and severity of placental lesions was scored by a pathologist bl inded to clinical data. Birth weight and length percentiles were calcu lated from published nomograms. Asymmetric intrauterine growth retarda tion (n = 32) was defined as birth weight < 10th percentile with lengt h > 10th percentile and symmetric intrauterine growth retardation (n = 48) as both weight and length < 10th percentile for gestational age, A ''growth restriction index'' was developed to express a continuum of growth in both length and weight. Contingency tables, analyses of var iance, and multiple regression analysis defined significance as p < 0. 05 (with corrections for multiple comparisons). RESULTS: A greater pro portion of cases with intrauterine growth retardation had lesions of u teroplacental insufficiency (p < 0.001) or chronic villitis (p < 0.02) than dib appropriately grown preterm infants. Cases with asymmetric i ntrauterine growth retardation tended to have more lesions than did ca ses with appropriate-for-gestational-age infants. Four multiple regres sion analyses used the growth restriction index as outcome and the his tologic lesions that had significant relationships to fetal growth as independent predictors in univariate analyses. Overall, uteroplacental fibrinoid necrosis, circulating nucleated erythrocytes, avascular ter minal villi, and villous infarct were significant independent predicto rs of fetal growth (adjusted R(2) = 0.312). With addition of preeclamp sia as a variable, villous fibrosis, avascular villi, infarct, and pre eclampsia were independent predictors of fetal growth (adjusted R(2) = 0.341). In the 65 preeclampsia cases no histologic lesion was an inde pendent predictor of fetal growth, whereas in the nonpreeclampsia case s, villous fibrosis and avascular villi were independent predictors of fetal growth (adjusted R(2) = 0.075). CONCLUSIONS: In nonanomalous pr eterm infants intrauterine growth retardation is most commonly symmetr ic and is primarily related to the cumulative number and severity of l esions reflecting abnormal uteroplacental or fetoplacental blood flow. The growth restriction index may contribute to the study of the biolo gic range of fetal growth. The statistical relationship of most placen tal lesions to intrauterine growth retardation depends on the presence or absence of preeclampsia.