CAUSES
OF DECREASED MATERNAL CIRCULATION
Various pathologic conditions may impede the
maternal circulation to the placenta. They can be grouped as follows:
1. Diseases
of the uterine vessels: (a) acute atherosis, (b) arteriolar sclerosis associated with
essential hypertension, and (c) inflammation (angiitis) associated with
chorioamnionitis.
2. Premature
separation of the placenta associated with retroplacental hemorrhage or
inflammatory exudation.
3. Conditions
that may cause an increase in intra-uterine pressure: (a) multiple pregnancy,
(b) macrosomia, (c) polyhydramnios, and (d) hydatidiform mole.
4.
Extensive
thrombosis of the intervillous space or of the marginal sinus.
5.
Death
of the mother.
The most common cause of placental infarcts in cases of preeclampsia have been found to be acute atherosis of the decidual vessels. This lesion is manifested microscopically as a deposition of lipids, in the intima of decidual arterioles and endometrial arteriovenous lakes. Part of the material is doubly refractive under polarized light and occurs both extracellularly and inside lipophages. The lesions closely resemble acute fulminating atherosis in other settings. The process leads to marked intimal thickening and vascular occlusion. The lesions occur in the decidua vera, as well as in the basalis, but they do not involve to a comparable degree the vessels of the myometrium or other tissues in the body. Fat stains have not revealed the lesion in fetal vessels. Contiguous trophoblastic tissue seems to be a necessary factor in its pathogenesis. The lesions regress promptly after delivery. The cause of this condition is still unknown.
Although acute atherosis
may be found in about 50% of all cases of preeclampsia by the use of fat stains
on frozen sections of carefully selected decidua, the lesions have not been
found in all cases of preeclampsia and do not constitute the only cause of
maternal vascular obstruction. Another common cause of placental infarction is
premature separation with retroplacental hemorrhage, the etiology of which is
often undetermined. Moreover, inflammatory lesions associated with acute
intrauterine infection during gestation occasionally spread through the walls
of vessels and lead to thrombosis and occlusion. Furthermore, the blood flow to
the placenta may be impeded by conditions that cause marked increase in
intrauterine pressure, which, in turn, leads to overstretching of the uterine
wall and collapse of the thin-walled decidual vessels. Although the higher
incidence of preeclampsia in such cases lends support to the concept that
decreased blood flow through the decidual vessels is a causative factor in
preeclampsia, the actual proof of such diminished circulation has not yet been
submitted.
Likewise, it is
conceivable that extensive thrombosis of the intervillous space or of the
marginal sinus would prevent adequate oxygenation of the placenta, because
obstruction of the venous return elsewhere in the body frequently leads to infarction.
When a patient suffers
from hypertension before the onset of pregnancy, the arterioles in the uterus
and elsewhere in the body are usually hyalinized and have narrowed lumina. This
lesion in itself seems to be insufficient to produce placental infarction, but
it is an important contributing cause in those cases of essential hypertension
in which preeclampsia is superimposed. In fact, a combination of two or more of
the above conditions is the rule rather than the exception in cases of fatal
preeclampsia or eclampsia.
Maternal death is listed as a cause of impeded blood flow to the uterus in order to emphasize the fact that, during the few minutes of continued fetal circulation after sudden maternal death, the earliest stages of placental infarction become manifest. Such cases present nodular ischemia of the entire placenta. Usually, a few foci of beginning engorgement of villous capillaries with fetal blood appear in some of the nodules. This constitutes the preliminary phase of acute hemorrhagic infarction of the placenta.
