Placental Findings in Preterm and Term Preeclampsia: An Integrative Review of the Literature

Abstract

Introduction: 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.

Objective: 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.

Results: 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.

Conclusion: 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.

Fig. 1

Definition of preeclampsia and classification according to the moment of diagnosis

Fig. 2

Diagrammatic representation of the effects of spiral artery remodeling on the inflow of maternal blood into the intervillous space in normal and pathological pregnancies (poor placentation)

Fig. 3

Underlying conditions of placental insufficiency leading to preeclampsia and fetal growth restriction. Numerous factors are involved in the development of the placenta under physiological conditions: pro- and antiangiogenic factors, pro- and anti-inflammatory cytokines, and pro- and antiapoptotic factors. Under pathological conditions, the expression of many of these factors is altered Source: Courtesy of A. Antolini-Tavares, São Paulo, Brazil.

Fig. 4

Representative morphological findings in placentas at term and early onset preeclampsia (EOP) cases – Hematoxylin and Eosin (H/E) analysis. In A, we can observe the invasion of the trophoblast (*) to transform maternal vessels (mv) from high pressure to low pressure, with physiological formation of fibrin (f), at the beginning of pregnancy (HE, 20x objective). In B , it is possible to observe the vessels of the decidua (d) with an evident and thick (hypertrophic) smooth muscle layer, with small intramural deposits of fibrinoid material (fm) (HE, 20x objective). In C , we observe the decidual vessel with extensive destruction of the muscle layer (necrosis) and replacement with fibrinoid material (fm) (HE, 20x objective). In D , it is possible to observe the vessel with necrosis of the muscle layer and inflammatory recruitment of macrophages (foamy cytoplasm) (arrows) in the middle of fibrinoid material (fm), characterizing atherosis (HE, 20x objective). In E , we observed a normal placenta at term, without distal villous hypoplasia (HE, 2.5x objective). In F , a case of EOP, we have a panoramic view of thin and elongated chorionic villi, with small and miniaturized terminal villi (within the square), with fewer vessels inside (usually one or two), in relation to mature villi (about three vessels in each terminal villus), characterizing distal villous hypoplasia (HE, 4x objective). In G , a case of EOP, it is possible to observe infarction centrally located in the placental parenchyma, due to hypertension in the vascular bed of the intervillous space, associated with the interaction between trophoblast and deficient uterine vessels: it is observed that, on the right, the villi are agglutinated (decreasing the distance between them due to an abrupt decrease in blood in the intervillous space) and a more eosinophilic color (pink) with less distinction of cell morphology (necrosis), and that, in the lower left corner, the villi have a more mature pattern, as if there were a “penumbra” of hypoxia that was not able to cause ischemic cell death (HE, 4x objective). And in H , a case of EOP, we observed another feature of hypertensive placental infarction, this time associated with a hematoma inside (hematoma infarction) (HE, 10x objective).