Stasis of maternal blood flow around an individual villus also results in fibrin deposition and can lead to diminished villous oxygenation and necrosis of syncytiotrophoblast (Fig. 6-3). These small yellow-white placental nodules are grossly visible within the parenchyma of a sectioned placenta. Within limits, these relect normal placental aging.
Maternal Floor Infarction. his extreme variant of perivillous fibrin deposition is a dense ibrinoid layer within the placental basal plate and is erroneously termed an infarction. Maternal loor inarction has a thick, yellow or white, irm corrugated surface that impedes normal maternal blood low into the intervillous space. In specific cases that extend beyond the basal plate to entrap villi and obliterate the intervillous space, the term massive perivillous ibrin deposition is used. The etiopathogenesis is unclear, but maternal auto-or alloimmunity appears contributory (Faye-Peterson, 2017; Romero, 2013). Antiphospholipid antibody syndrome and angiogenic factors involved with preeclampsia have also been implicated (Sebire, 2002, 2003; Whitten, 2013).
These lesions are not reliably imaged with prenatal sonography, but they may create a thicker basal plate. Afected pregnancies are associated with miscarriage, fetal-growth restriction, preterm delivery, and stillbirth (Andres, 1990; Mandsager, 1994). Importantly, these adverse outcomes can recur in subsequent pregnancies.
This is a collection of coagulated maternal blood normally found in the intervillous space mixed with fetal blood from a break in a villus. Grossly, these round or oval collections vary in size up to several centimeters. hey appear red if recent or white-yellow if older, and they develop at any placental depth. Intervillous thrombi are common and typically not associated with adverse fetal sequelae. Because there is potential for a communication between maternal and fetal circulations, large lesions can cause elevated maternal serum alpha-fetoprotein levels (Salaia, 1988).
Chorionic villi themselves receive oxygen solely from maternal circulation supplied to the intervillous space. Any uteroplacental disease that diminishes or obstructs this supply can result in infarction of an individual villus. These are common lesions in mature placentas and are benign in limited numbers. If numerous, however, placental insuiciency can develop. When they are thick, centrally located, and randomly distributed, they may be associated with preeclampsia or lupus anticoagulant.
As depicted in Figure 6-3, the maternal-placental-fetal unit can develop several hematoma types. These include: (1) retroplacental hematoma-between the placenta and its adjacent decidua; (2) marginal hematoma-between the chorion and
FIGURE 6-3 Potential sites of maternally and fetally related placental circulatory disturbances. (Adapted from Faye-Petersen, 2006.) decidua at the placental periphery-known clinically as sub chorionic hemorrhage; (3) subamnionic hematoma-these are of fetal vessel origin and found beneath the amnion but above the chorionic plate, and (4) subchorial thrombus along the roof of the intervillous space and beneath the chorionic plate. With this last type, massive subchorionic hematomas are also known as a Breus mole.