Early Path Medical Consultation Services

Early Path Medical Consultation Services
Pathology Services Working for Safer Pregnancies

Placental Pathology - Medical Student Lecture 2001
Carolyn M. Salafia, MD
Professor of Pathology and Pediatrics

CONTENTS

1. OVERVIEW

2. INTRODUCTION

3. PREECLAMPSIA

4. FETAL GROWTH

5. INTRAUTERINE INFECTION

6. MULTIFETAL PREGNANCY

PREECLAMPSIA

Preeclampsia, a common clinical condition that leads to pregnancy complications

Identify the most common and typical placental features of preeclampsia, and how it contributes to the maternal and fetal/neonatal complications.

Preeclampsia is a disorder of pregnancy recognized by Hippocrates as having a single cure (placental delivery, not delivery of the baby); today, the single cure for this potentially lethal syndrome of maternal hypertension, proteinuria, and edema remains delivery of the placenta. The primary affected maternal cell appears to be the endothelium; endothelial activation appears to mediate most if not all of the maternal disease process. Recently Redman and his group at Oxford University have proposed that preeclampsia is an extreme maternal endothelial response to syncytiotrophoblast repair, a process necessary to healthy pregnancy. Think about a newly delivered infant. The vernix caseosa that covers a newborn is the total desquamated squamous debris of fetal skin and amnion accumulated throughout pregnancy. Desquamated epithelium, having no place else to go, accumulates in amniotic fluid. Epithelial repair and replenishment must also take place in the villous placenta, but that senescent debris can be deposited- straight into the mother's blood stream! Trophoblast detritus has been shown to activate maternal inflammatory cells and maternal endothelium. Redman has proposed that either a lowered threshold of the maternal endothelium (so that a normal volume of placental debris elicits an exaggerated maternal endothelial activation response) or excessive placental injury can trigger the maternal disease of preeclampsia.

Maternal factors that can influence endothelial responsivity include hereditable thrombophilias, and preexisting medical diseases involving endothelium or inflammatory activation such as diabetes mellitus or lupus erythematosus. The classic placental pathology of "excessive placental debris production" in preeclampsia is abnormal, incomplete or failed trophoblast conversion of the vascular bed (see above). The abnormal retention of muscular and elastic elements within the uteroplacental vessels results in abnormal increased maternal/uteroplacental vascular resistance, reduced vascular capacitance, decreased total maternal/uteroplacental vascular flow and often dramatically reduced nutrient and oxygen presentation to the placenta. Isotope studies in the human suggest that the decrease in uteroplacental flow associated with the vascular lesions of preeclampsia may be from 50-70% of normal, providing an obvious mechanism for the often associated intrauterine growth retardation. Flow may also be at a greater pressure, and be more turbulent. Reduced flow or flow at an abnormal high pressure may affect the developing placental capillary bed. Abnormal decidual vascular conversion may result in increased intravascular pressure, and increased risk of "decidual vascular accidents" such as placental infarcts or abruption. An infarct is basically an ischemic maternal/uteroplacental vascular accident (Figure 8) while an abruption is a hemorrhagic uteroplacental vascular accident. In an infarct, the first event is occlusion of a maternal/uteroplacental vessel. Intervillous flow ceases, the intervillous space collapses, villi become compressed and undergo ischemic necrosis. In an abruption, the first event may also be occlusion of a maternal/uteroplacental artery. However, in abruption, the maternal artery ruptures after occlusion, causing a retroplacental hemorrhage. When there is retroplacental hemorrhage, the blood clot compresses, or squeezes, the overlying placenta. A squeezed, compressed placenta is harder to pump blood into. This increased placental resistance causes increased fetal heart work. At the same time, there is decreased fetal oxygen delivery (due to reduced placenta available for oxygen and nutrient exchange). Finally, extra placental blood, squeezed out of the placental blood vessels by the retroplacental clot, can be forced back up the umbilical cord, causing fetal vascular congestion. Abruptions are very worrisome conditions that may be lethal or may be damaging to the fetus, by oxygen deprivation, cardiac compromise, or diffuse visceral hemorrhage in hypoxic and volume-overloaded visceral (and CNS) capillary beds. Small abruptions, or abruptions at the margin/edge of the placenta may not be harmful to the fetus.

Scarred, shrunken, fibrotic and hypovascular villi, with reduced number and/or caliber of placental capillaries, are common in maternal/uteroplacental vascular insufficiency and represent destruction of normally forming placental vasculature. Capillary damage caused by abnormal force or turbulence of intervillous flow can produce fetomaternal hemorrhages which, in the midtrimester, are more frequent in hypertensive pregnancies Chronic maternal/uteroplacental vascular insufficiency may cause decreased placental vascularity by restricting nutrient transfer and levels of growth promoting factors. Reduced villous capillary number leads to fewer vasculosyncytial membranes, and reduced placental exchange efficiency, and may lead to fetal growth restriction or fetal intolerance of what might appear to be clinically "normal" labor. (Figure 9)