Abstract

Preeclampsia (PE) is a pregnancy complication associated with increased maternal and perinatal morbidity and mortality. The disease presents with recent onset hypertension (after 20 weeks of gestation) and proteinuria, and can progress to multiple organ dysfunction, with worse outcomes among early onset preeclampsia (EOP) cases (< 34 weeks). The placenta is considered the root cause of PE; it represents the interface between the mother and the fetus, and acts as a macromembrane between the two circulations, due to its villous and vascular structures. Therefore, in pathological conditions, macroscopic and microscopic evaluation can provide clinically useful information that can confirm diagnosis and enlighten about outcomes and future therapeutic benefit. To perform an integrative review of the literature on pathological placental findings associated to preeclampsia (comparing EOP and late onset preeclampsia [LOP]) and its impacts on clinical manifestations. Cases of EOP presented worse maternal and perinatal outcomes, and pathophysiological and anatomopathological findings were different between EOP and LOP placentas, with less placental perfusion, greater placental pathological changes with less villous volume (villous hypoplasia), greater amount of trophoblastic debris, syncytial nodules, microcalcification, villous infarcts, decidual arteriolopathy in EOP placentas when compared with LOP placentas. Clinically, the use of low doses of aspirin has been shown to be effective in preventing PE, as well as magnesium sulfate in preventing seizures in cases of severe features. The anatomopathological characteristics between EOP and LOP are significantly different, with large morphological changes in cases of EOP, such as hypoxia, villous infarctions, and hypoplasia, among others, most likely as an attempt to ascertain adequate blood flow to the fetus. Therefore, a better understanding of the basic macroscopic examination and histological patterns of the injury is important to help justify outcomes and to determine cases more prone to recurrence and long-term consequences.

Highlights

  • Preeclampsia (PE) is a pregnancy complication associated with increased maternal and perinatal morbidity and mortality

  • To perform an integrative review of the literature on pathological placental findings associated to preeclampsia and its impacts on clinical manifestations

  • Cases of early onset preeclampsia (EOP) presented worse maternal and perinatal outcomes, and pathophysiological and anatomopathological findings were different between EOP and late onset preeclampsia (LOP) placentas, with less placental perfusion, greater placental pathological changes with less villous volume, greater amount of trophoblastic debris, syncytial nodules, microcalcification, villous infarcts, decidual arteriolopathy in EOP placentas when compared with LOP placentas

Read more

Summary

Introduction

Hypertensive disorders in pregnancy, and in particular preeclampsia (PE) and eclampsia, are one of the three main causes of maternal mortality and morbidity globally, and an important cause of fetal and perinatal complications, such as increased risk of stillbirth, neonatal death, intrauterine growth restriction, and preterm childbirth.[1]. In PE, greater systemic inflammation occurs.[34,35] Once an inflammatory process is established, it results in atherosis, lesions characterized by fibrinoid necrosis and accumulation of macrophages loaded with lipids (foam cells), which are not restricted to the placental bed Those lesions can appear virtually in any maternal blood vessel, and its clinical manifestation will be related to the most affected organ.[36] Unlike defective remodeling, atherosis can severely restrict the caliber of the uteroplacental vessels, causing secondary thrombosis lesions, limiting blood flow to the placenta, and causing infarctions with a risk of fetal death.[37] this process will contribute to the continuous release of free radicals formed after a sequence of ischemia-reperfusion processes.

Objective
Conclusion
Main Findings
12 ACOG Practice Bulletin No 202
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call