Placental pathology: its impact on explaining prenatal and perinatal death

Abstract

This review considers six main situations in which pathologists are expected to report and interpret placental messages for obstetricians, neonatologists and, indirectly, parents: (1) abortion is the body's corrective response to the embryonic defect suggested by malformed chorionic villi; (2) infection causing chorionic villous inflammation is specific and haematogenous; pathogen identification is mandatory, in contrast to chorioamnionitis caused by increased local immunosuppression allowing indiscriminate bacterial entry; (3) prematurity and (4) intrauterine growth restriction are often associated with pregnancy-specific disease (pre-eclampsia) or preexisting maternal conditions (systemic lupus); parental studies may improve outcome in subsequent pregnancies; (5) intrauterine death near term is often due to placental dysmaturity featuring a severely reduced number of syncytiocapillary membranes; it accounts for the death in utero of 3 in 1000 pregnancies; detection helps to minimise recurrence in subsequent pregnancies; (6) twins are best confirmed as monozygous by the absence of chorionic tissue in the dividing membranes; most monochorionic twins have vascular connections whose detailed analysis is requested only if there are inter-twin differences in growth and colour. From a formal point of view, many more bits of pathology than discussed in this review can be found in placentas and, with the advances in ultrasonography, might even be seen prior to birth. The extent of such a disturbance might ultimately affect fetal growth, which is amenable to prenatal detection offering the chances for an appropriate management. In contrast, dysmaturity is a great challenge as no predictive tests are as yet available.

Hypoxic Patterns of Placental Injury: A Review

“…12 In this type of placental pathology in pregnancies of 35 weeks or longer, on average, 1 vasculosyncytial membrane per terminal villus was found as compared with, on average, 3 per chorionic villi normally seen. 68 Villous hypomaturity is responsible for 22.5% of intrauterine deaths 69 and has a 70-fold increased risk of associated fetal death, with a 10-fold risk for recurrence, compared with baseline. 70 The fetuses die because of hypoxia, 1 but they can be rescued by earlier delivery.…”

Placental Immaturity, Endocardial Fibroelastosis and Fetal Hypoxia

“…Defective placental maturation can currently not be clinically diagnosed [5,7] . It is not highlighted by slowing of the fetal growth curve, neither by abnormal fetal movements nor by abnormal Doppler flow velocity waveforms.…”

“…As the recurrent risk of stillbirth is tenfold over that of the baseline, awareness of this entity by obstetricians and pediatricians may help minimize the recurrence in a subsequent pregnancy. Recently, Stallmach and Hebisch [7] suggested that cesarean section at completed 37 weeks could be a valid option. The benefit must, however, be balanced against the risks of premature birth and respiratory distress syndrome [7] .…”

“…Recently, Stallmach and Hebisch [7] suggested that cesarean section at completed 37 weeks could be a valid option. The benefit must, however, be balanced against the risks of premature birth and respiratory distress syndrome [7] . As illustrated by the dramatic outcome of these 3 cases, we consider that this recommendation has to be discussed with parents.…”

Overexpression of the SK3 channel alters vascular remodeling during pregnancy, leading to fetal demise

“…These maternal complications and associated fetal complications include intrauterine growth restriction, preterm delivery, and fetal demise (23). Given that ϳ50% of conceptions end in miscarriages (15,27), understanding the relationship between cardiovascular maladaptation, remodeling, and pregnancy complications is central to assuring maternal and fetal health.…”