Eun Jung Jung1, Hwa Jin Cho2, Jung Mi Byun3, Dae Hoon Jeong3, Kyung Bok Lee3, Moon Su Sung3, Ki Tae Kim3, Young Nam Kim4. 1. Department of Obstetrics and Gynecology, Inje University Busan Paik Hospital, Busan, South Korea. 2. Department of Pathology, Inje University Busan Paik Hospital, Busan, South Korea. 3. Department of Obstetrics and Gynecology, Inje University Busan Paik Hospital, Busan, South Korea; Paik Institute for Clinical Research, Inje University Busan Paik Hospital, Busan, South Korea. 4. Department of Obstetrics and Gynecology, Inje University Busan Paik Hospital, Busan, South Korea; Paik Institute for Clinical Research, Inje University Busan Paik Hospital, Busan, South Korea. Electronic address: 103090@paik.ac.kr.
Abstract
INTRODUCTION: Placenta previa is a condition in which the placenta implants in the poorly vascularized lower uterine segment, which may result in inadequate uteroplacental perfusion, in turn, adversely affect the neonatal outcome. Abnormal placentation may also lead to severe postpartum hemorrhage as placenta separation proceeds. We aimed to evaluate the differences in placental histopathology and perinatal outcomes in pregnancies complicated with placenta previa and controls. METHOD: We undertook a retrospective case-control study of 93 pregnancies with placenta previa and 81 controls between 2011 and 2017. RESULTS: Gross findings of the placenta showed that the placentas in placenta previa had significantly higher mean large chorionic plate diameters (18.5 ± 3.2 vs 17.5 ± 2.6 cm, P = .0298), chorionic plate areas (218.4 ± 62.9 cm2 vs 198.7 ± 56.0 cm2, P = .0344), and marginal cord insertion (19.8% vs 8.6%, P = .0411) than control groups. Placental histopathological findings showed that placentas in placenta previa was significantly associated with maternal underperfusion, including villous infarction (50.5% vs 25.9%, P = .0009) and increased intervillous fibrin deposition (38.7% vs 7.4%, P < .0001). Also, women in the placenta previa group had a higher rate of abnormally invasive placenta and severe postpartum hemorrhage. However, placenta previa was not associated with the increased risk of neonatal mortality and morbidity. DISCUSSION: Abnormal placentation into the poorly vascularized lower uterine segment induces compensatory placental growth and increased surface area in response to reduced placental perfusion, which was consistent with the histopathological findings of coagulative necrosis of chorionic villi and fibrin deposition in the intervillous space. The morphological changes occurring in placenta previa may have important roles in maintaining adequate uteroplacental-fetal perfusion, which may prevent adverse neonatal outcomes.
INTRODUCTION: Placenta previa is a condition in which the placenta implants in the poorly vascularized lower uterine segment, which may result in inadequate uteroplacental perfusion, in turn, adversely affect the neonatal outcome. Abnormal placentation may also lead to severe postpartum hemorrhage as placenta separation proceeds. We aimed to evaluate the differences in placental histopathology and perinatal outcomes in pregnancies complicated with placenta previa and controls. METHOD: We undertook a retrospective case-control study of 93 pregnancies with placenta previa and 81 controls between 2011 and 2017. RESULTS: Gross findings of the placenta showed that the placentas in placenta previa had significantly higher mean large chorionic plate diameters (18.5 ± 3.2 vs 17.5 ± 2.6 cm, P = .0298), chorionic plate areas (218.4 ± 62.9 cm2 vs 198.7 ± 56.0 cm2, P = .0344), and marginal cord insertion (19.8% vs 8.6%, P = .0411) than control groups. Placental histopathological findings showed that placentas in placenta previa was significantly associated with maternal underperfusion, including villous infarction (50.5% vs 25.9%, P = .0009) and increased intervillous fibrin deposition (38.7% vs 7.4%, P < .0001). Also, women in the placenta previa group had a higher rate of abnormally invasive placenta and severe postpartum hemorrhage. However, placenta previa was not associated with the increased risk of neonatal mortality and morbidity. DISCUSSION: Abnormal placentation into the poorly vascularized lower uterine segment induces compensatory placental growth and increased surface area in response to reduced placental perfusion, which was consistent with the histopathological findings of coagulative necrosis of chorionic villi and fibrin deposition in the intervillous space. The morphological changes occurring in placenta previa may have important roles in maintaining adequate uteroplacental-fetal perfusion, which may prevent adverse neonatal outcomes.
Authors: Elisa T Zhang; Roberta L Hannibal; Keyla M Badillo Rivera; Janet H T Song; Kelly McGowan; Xiaowei Zhu; Gudrun Meinhardt; Martin Knöfler; Jürgen Pollheimer; Alexander E Urban; Ann K Folkins; Deirdre J Lyell; Julie C Baker Journal: Biol Reprod Date: 2021-07-02 Impact factor: 4.285