Villi appear normal to the right while there is an abrupt transition to avascular villi to the left.

Contiguous terminal villi show absence of capillaries and contain hyalinized stroma. The intervillous space is devoid of RBCs.

Fibrin thrombi within capillaries (arrow) can be appreciated.

Fetal thrombotic vasculopathy (FTV) is characterized by the presence of avascular villi in a distribution consistent with vascular occlusion upstream in the fetal circulation. In 1/3 of cases, thrombi can be found in large chorionic or stem villi (Redline).

When avascular villi are extensive, the possibility of serious fetal complications becomes significant. In one study, extensive avascular villi were associated with intrauterine growth retardation, oligohydrfamnios, and thromboembolic disease in the fetus as well as an idiopathic decrease in fetal platelet count (Redline) and fetal cardiac anomalies (Saleemuddin). In one study, a threshold of greater than 15 affected villi per section of placenta is associated with an increased risk of cerebral palsy and other neurologic impairment (Redline).

The underlying etiology of fetal thrombotic vasculopathy remains elusive. Some predisposing factors may include maternal coagulation disorders such as antiphospholipid antibody (Kraus).

Fetal thrombotic vasculopathy (FTV) in the placenta is the presence of extensive avascular villi. This lesion usually is associated with demonstrable thrombi in the fetal circulation, either in the chorionic plate vessels, stem villous vessels or villous circulation.

The possibility of serious fetal complications becomes significant if there are extensive areas of avascular villi.