abnormal trophoblast implantation in pre-eclampsia

Last reviewed 01/2018

Normally, by the 22nd week of pregnancy, the trophoblast has invaded the spiral arteries supplying the intervillous space. The diameter of the spiral arteries is increased to 4-6 times that in non-pregnant women, the endothelium is replaced by trophoblast, and the internal elastic lamina is replaced by trophoblast and a fibrin containing amorphous matrix. These vascular changes extend from the intervillous space to the inner third of the myometrium. Blood flows unimpeded into the intervillous space, and over the villous tree that contains the fetal vessels. Easy exchange of oxygen, nutrients and metabolic waste products is ensured.

In a pre-eclamptic pregnancy, trophoblastic implantation is frequently abnormal. The changes seen in the spiral arteries in a normal pregnancy do not occur or are limited to the decidual portion of the vessels. The myometrial segments maintain their smooth muscle coats which are sensitive to circulating pressor agents, particularly angiotensin II. The volume of trophoblast at the spiral arterioles is reduced to 40% of that in normal pregnancy. Perfusion is poor and associated with endothelial cell dysfunction. An imbalance in the prostacyclin-thromboxane system develops with a relative overproduction of thromboxane which encourages vasospasm of the spiral arterioles and local platelet aggregation.

The muscle coating and intima of the spiral arteries are damaged and become atherotic - a process comparable to accelerated arteriosclerosis in which the vessels become occluded by fibrinoid material and foamy macrophages accumulate in their necrotic wall. Their further narrowing results in a further increase in blood pressure. Perfusion of the intervillous space is further decreased and intrauterine growth retardation commonly results.

Similar changes are seen in allograft rejection suggesting that pre-eclampsia has an immunologic basis.