Placental infarcts

Placental infarcts


A placental infarction is a localized area of ischemic tissue necrosis that is due to an obstruction of the villous blood supply. While an infarct may occur in any part of the placenta, they are more commonly peripherally located. A placental infarct characteristically begins at the basal plate and extends in a triangular or oval pattern toward the fetal surface of the placenta. Placental infarcts are detected in approximately 25% of term placentas; they occur more frequently in placentas of women with hypertension or pre-eclampsia. The prevalence of placental infarction is increased 5-fold with placental abruption. Infarction usually involves < 5% of the placenta and is therefore, not clinically significant. However, the degree of placental infarction varies from 33% with mild pre-eclampsia to 60% in cases of severe pre-eclampsia. The loss of over one-third of placental function due to infarction indicates a compromised utero-placental circulation and has been associated with intra-uterine growth restriction and fetal compromise. Maternal floor infarction is to be distinguished from placental infarction. The former process results from the deposition of fibrin in the decidua beneath the placenta and does not result from arterial occlusion and ischemic necrosis. The term maternal floor infarction is therefore, a misnomer. The fibrin in maternal floor infarctions extends into the intervillous spaces and results in villous atrophy. Naeye has reported that maternal floor infarcts are present in 1 of every 200 placentas examined pathologically. However, this figure is considered too high by other authorities. Naeye also reported a stillbirth rate of 17% with maternal floor infarction; intrauterine growth restriction is increased 2-fold. There is a 12% recurrence risk for maternal floor infarction in subsequent pregnancies.


Placental infarcts have a variable sonographic appearance. After a placental infarction, the structure of the villus is preserved. The non-viable trophoblast are acoustically similar to viable villi. With increased cellularity, a placental infarct becomes hyperechoic. The accumulation of acellular fibrin that makes a placental infarct so apparent on gross inspection is hypoechoic and difficult to distinguish from a decidual septal cyst or an intervillous thrombus. The sonographic transformation of a placental infarct from hyperechoic to hypoechoic may occur over a 4 day interval.

Differential Diagnosis

Localized placental infarctions are quite common. However, placental infarctions are only detected if they are hyperechoic (recent) or hypoechoic (filled in with debris). Most placental infarcts are isoechoic and, therefore, not visible sonographically. If a placental infarct is hypoechoic, it would be indistinguishable from a septal cyst or intervillous thrombosis.

Sonographic Features

Those placental infarcts that are visible sonographically contain hypoechoic or anechoic foci of hemorrhage.

Mature placental infarcts cannot be distinguished from normal placenta.

Occasionally, part of a placental infarct will calcify, resulting in acoustic shadowing.

Sonographic findings with maternal-floor infarction include: 1) fetal growth restriction; 2) oligohydramnios; and 3) irregular hyperechoic areas extending through the placenta.

Subchorionic cysts within or adjacent to the hyperechoic placental areas may also be visualized sonographically.

These placental abnormalities may be present in 1/3 of the cases of maternal floor infarction.

A thickened placenta in association with intrauterine growth restriction may represent the first indication of a maternal floor infarction.

Associated Syndromes