Placental Pathology of Idiopathic Intrauterine Growth Retardation at Term

Carolyn M. Salafia; Anthony M. Vintzileos; Lester Silberman; Kimberly F. Bantham; Cristine A. Vogel

doi:10.1055/s-2007-999316

American Journal of Perinatology, Table of Contents

Am J Perinatol 1992; 9(3): 179-184
DOI: 10.1055/s-2007-999316

ORIGINAL ARTICLE

Placental Pathology of Idiopathic Intrauterine Growth Retardation at Term

Carolyn M. Salafia, Anthony M. Vintzileos, Lester Silberman, Kimberly F. Bantham, Cristine A. Vogel

Departments of Laboratory Medicine and Obstetrics and Gynecology, Danbury Hospital, Danbury, Connecticut and the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Connecticut Health Center, Farmington, Connecticut

Abstract

ABSTRACT

Placental examination was carried out in 128 consecutive cases of idiopathic intrauterine growth retardation (IUGR) at term and the findings were compared with those of 179 gestational age-matched cases with normal growth. Mean pregnancy weight and mean maternal weight gain during pregnancy of IUGR cases were both significantly lower than for non-IUGR cases. There was a higher frequency of a history of previous growth-retarded infants between IUGR cases (18 of 128, or 14%) compared with non-IUGR cases (7 of 179, or 3.9%). The studied placental lesions were placental infarction, chronic villitis, hemorrhagic endovasculitis, and placental vascular thromboses. One or more of these lesions were present in 71 of 128 (55%) of IUGR cases, and ⁵⁸/₁₇₉ (32%) of non-IUGR cases. Thirty-eight of 72 (53%) cases with chronic villitis were IUGR (30% of all IUGR cases). Thirty-one of 49 cases (63%) with placental infarction were IUGR cases (24% of all IUGR cases). Nineteen of 32 cases (59%) with hemorrhagic endovasculitis were IUGR cases (15% of all IUGR cases). Twelve of 17 cases (71%) with placental vascular thromboses were IUGR (9% of all IUGR cases). Relationships of all placental lesions to IUGR were independent of each other. IUGR infants more frequently had multiple types of lesions in their placentas. Chronic villitis and hemorrhagic endovasculitis tended to occur in the same placentas. There were no significant relationships between maternal characteristics and placental lesions, except for an association between low pregravid weight and increased incidence of placental infarction. Decreased birth length was associated only with placental infarction (p <0.05). Cases with chronic villitis had lower ponderal indices than cases without chronic villitis, or with other placental lesions. Our data suggest that gross and microscopic placental lesions are significantly associated with growth impairment in a low-risk population. Different placental lesions show different patterns of related growth failure, suggesting different times of onset of intrauterine stress.

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