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Patterns of placental pathology in preterm premature rupture of membranes

Published online by Cambridge University Press:  18 March 2013

J. Armstrong-Wells ,
M. D. Post ,
M. Donnelly ,
M. J. Manco-Johnson ,
B. M. Fisher  and
V. D. Winn
J. Armstrong-Wells*
Affiliation:
Department of Pediatrics (Neurology), University of Colorado Denver, Aurora, Colorado, USA Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
M. D. Post
Affiliation:
Department of Pathology, University of Colorado Denver, Aurora, Colorado, USA
M. Donnelly
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
M. J. Manco-Johnson
Affiliation:
Department of Hematology/Oncology/BMT, University of Colorado Denver, Aurora, Colorado, USA
B. M. Fisher
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
V. D. Winn
Affiliation:
Department of Obstetrics & Gynecology, University of Colorado Denver, Aurora, Colorado, USA
*
*Address for correspondence: Dr J. Armstrong-Wells, MD., MPH., Assistant Professor, Director, Perinatal and Hemorrhagic Stroke Programs, UCD Hemophilia and Thrombosis Center, 13199 E. Montview Blvd., Suite 100, Aurora, CO 80045, USA. Email [email protected]
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Abstract

Inflammation is associated with preterm premature rupture of membranes (PPROM) and adverse neonatal outcomes. Subchorionic thrombi, with or without inflammation, may also be a significant pathological finding in PPROM. Patterns of inflammation and thrombosis may give insight into mechanisms of adverse neonatal outcomes associated with PPROM. To characterize histologic findings of placentas from pregnancies complicated by PPROM at altitude, 44 placentas were evaluated for gross and histological indicators of inflammation and thrombosis. Student's t-test (or Mann–Whitney U-test), χ2 analysis (or Fisher's exact test), mean square contingency and logistic regression were used when appropriate. The prevalence of histologic acute chorioamnionitis (HCA) was 59%. Fetal-derived inflammation (funisitis and chorionic plate vasculitis) was seen at lower frequency (30% and 45%, respectively) and not always in association with HCA. There was a trend for Hispanic women to have higher odds of funisitis (OR = 5.9; P = 0.05). Subchorionic thrombi were seen in 34% of all placentas. The odds of subchorionic thrombi without HCA was 6.3 times greater that the odds of subchorionic thrombi with HCA (P = 0.02). There was no difference in gestational age or rupture-to-delivery interval, with the presence or absence of inflammatory or thrombotic lesions. These findings suggest that PPROM is caused by or can result in fetal inflammation, placental malperfusion, or both, independent of gestational age or rupture-to-delivery interval; maternal ethnicity and altitude may contribute to these findings. Future studies focused on this constellation of PPROM placental findings, genetic polymorphisms and neonatal outcomes are needed.

Keywords

altitude, chorioamnionitis, fetal inflammatory response, funisitis, subchorionic thrombi
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 4 , Issue 3 , June 2013 , pp. 249 - 255
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2013 

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