Fetal Circulation

Figure 5.33. "Maternal floor infarction" is a recurring lesion is associated with growth retardation and death. In this process there is a layer of fibrin deposited at the base for 3 mm to 4 mm. Basal villi are entrapped and die, but it is not true infarction. This occurs in combination with some degree of diffuse perivillous fibrin deposition, as shown here. This placenta is from a live-born infant.

Fibrin Deposition Placenta
Figure 5.34. This more dramatic example of maternal floor infarction is from a 25 week stillborn.
Maternal Floor Infarction
Figure 5.35. This thin-walled cyst is located within a septum of a term placenta. Such cysts also occur on the surface (Figure 4.17). They develop within solid trophoblastic regions and are often adjacent to fibrin deposition. Cysts do not appear to be associated intrinsically with any pathology.

Avascular Villi

The presence of avascular vill (villous atrophy) implies interruption of the fetal blood supply. After fetal demise, the entire placenta undergoes this change if delivery does not occur. It does not infarct since maternal perfusion continues. Occlusion of part of the fetal circulation, as with thrombosis, will lead to zones of atrophic avascular villi, often recognizable grossly (Figure 5.36). Such change may reflect more diffuse fetal thrombotic processes in utero, with the potential for vascular disruptive lesions. Early microscopic change in villi includes vascular breakdown progressing to complete stromal fibrosis (avascular villi) (Figure 5.37). These histologic changes take days to weeks to develop.

Placenta Fibrosis

Figure 5.36. Fixed placenta with irregular pale area of atrophy. The light color comes from the lack of fetal blood and fibrosis within the affected villi. No gross thrombosis was noted, which is not unusual; however, fetal vascular thrombi are often found on histology. The tissue is not collapsed or hard and feels similar to adjacent villi.

Figure 5.36. Fixed placenta with irregular pale area of atrophy. The light color comes from the lack of fetal blood and fibrosis within the affected villi. No gross thrombosis was noted, which is not unusual; however, fetal vascular thrombi are often found on histology. The tissue is not collapsed or hard and feels similar to adjacent villi.

Histology Placental Lesions
Figure 5.37. Histology of avascular villi reveals a fibrotic stroma without blood vessels. The trophoblast on the surface is viable since it is still perfused by maternal blood. Change of this degree likely takes more than a week to evolve.

Chorangiomas

Chorangiomas are hemangiomas of the placenta and occur in about 1% of pregnancies. They are best designated as hamartomas. These lesions commonly occur under the chorionic plate (Figure 5.38) and have a variety of appearances, depending on vessel size, perfusion, and viability

Chorangioma
Figure 5.38. (A) The raised red, round solid lesion seen through the fetal surface is a chorangioma or hemangioma of the placenta. These are usually nodular, fleshy lesions connected to the chorionic plate.

Figure 5.38. (B) The lesion extends nearly to the maternal surface. The cut surface suggests there are large areas of infarction.

Figure 5.38. (B) The lesion extends nearly to the maternal surface. The cut surface suggests there are large areas of infarction.

Chorangioma

(Figure 5.39 to Figure 5.42). Chorangiomas are often confused with other gross lesions (Figure 5.42). Histology is that of a typical hemangioma, usually with small or medium sized vessels (Figure 5.43). Large choran-giomas may lead to fetal hydrops and platelet trapping. Rarely the infants have other hemangiomas.

Figure 5.39. Another chorangioma in a preterm placenta is much paler and irregularly lobulated. The size of the vessels, their congestion, and the presence of infarction will determine the characteristics of the mass. Large chorangiomas may be associated with nonimmune hydrops, possibly caused by fetal circulatory overload and shunting. Trapping of platelets and fetal thrombocytopenia may also occur.

Fetal Circulation

Figure 5.40. Chorangiomas are frequently multiple and may be pedunculated, as shown by the multiple berry-like lesions here.

Figure 5.41. The gelatinous ill-defined subchorionic region in this placenta was histologically a chorangioma.

Figure 5.41. The gelatinous ill-defined subchorionic region in this placenta was histologically a chorangioma.

Chorangioma Placenta

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Subchorionic Thrombus
Figure 5.42. Chorangiomas are often confused with other pathologic lesions, particularly if infracted. This thrombus-like mass was actually a chorangioma.
Trophoblast Mesenchymal
Figure 5.43. Microscopic view of a chorangioma reveals numerous small and a few larger blood vessels in lobulated areas resembling large villi. The vessels are congested. The surface of the chorangiomatous nodules is covered by trophoblast which, as usual, is somewhat hyperplastic (arrow).

Mesenchymal Dysplasia

This is a rare disorder of unknown etiology characterized by serpingi-nous surface blood vessels and large cystic villi, often resembling molar tissue. The most common association is with Beckwith-Weidemann syndrome (Figure 5.44).

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