title: The very low birthweight infant: maternal complications leading to preterm birth, placental lesions, and intrauterine growth.
abstract: The placental lesions of the very low birthweight (VLBW) infant were investigated in relation to clinical complications leading to preterm birth and evidence of growth impairment. The 249 singleton gestations yielding infants less than 1500 g were grouped according to the clinical complications leading to preterm birth as premature membrane rupture (116/249, 47%) preterm labor (55/249, 22%), pregnancy-induced hypertension (PIH, 54/249, 22%), and normotensive abruption (ABR, 24/249, 10%). Specifically excluded from this data set were cases with greater than 2 weeks discordance, fetal congenital anomalies, placenta previa, and maternal medical or gestational diseases such as chronic hypertension and diabetes mellitus, and intrauterine growth retardation (IUGR) as a primary indication for delivery. Placental weight and lesions including decidual vasculopathy and related villous lesions, chronic villitis/intervillositis, and decidual plasmacytosis were considered as variables in analyses in which raw birthweight was the dependent variable and gestational age a confounder. Of the 195 VLBW, 79 (41%) infants from normotensive mothers had lesions of decidual vasculopathy or chronic inflammation. In the VLBW infants from hypertensive mothers, growth restriction was related to markers of decidual vasculopathy. In the absence of maternal hypertension the growth restriction was independently associated with chronic villitis. Decidual vasculopathy (characteristic of PIH) and chronic intrauterine inflammation underlie the complications of many normotensive VLBW infants. The placental lesions in VLBW-IUGR depend on the presence or absence of maternal hypertension. In the absence of maternal hypertension, VLBW-IUGR is associated with chronic inflammation and is independent of decidual vasculopathy. In the presence of maternal hypertension, VLBW-IUGR is directly related to decidual vasculopathy.
authors.affiliation: Department of Pathology, University of Connecticut School of Medicine, Farmington, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Salafia
authors.forename: L M
authors.initials: LM
authors.lastname: Ernst
authors.forename: J C
authors.initials: JC
authors.lastname: Pezzullo
authors.forename: E J
authors.initials: EJ
authors.lastname: Wolf
authors.forename: T S
authors.initials: TS
authors.lastname: Rosenkrantz
authors.forename: A M
authors.initials: AM
authors.lastname: Vintzileos
mesh_terms: D000037:Abruptio Placentae / Q000150:complications / Q000473:pathology; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000473:pathology*; D005322:Premature Rupture of Fetal Membranes / Q000209:etiology / Q000473:pathology; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007752:Obstetric Labor, Premature / Q000209:etiology / Q000473:pathology*; D010920:Placenta / Q000473:pathology*; D010922:Placenta Diseases / Q000150:complications / Q000473:pathology; D011225:Pre-Eclampsia / Q000473:pathology; D011247:Pregnancy