Uteroplacental Vascular Pathology

In many types of complicated pregnancies - from preeclampsia to first trimester pregnancy loss to prematurity and late fetal growth restriction - "normal" uteroplacental vascular adaptation takes place only partially within any one vessel, and/or not to the maximum depth, and/or in a more limited total number of placental bed arteries. The wide variety of pregnancy compromise seen with poor uteroplacental vascular conversion most likely reflects different combinations of these potential problems, with different strengths of deleterious influences, and different times of onset in gestation. No uteroplacental arterial lesion distinguishes among the different clinical conditions associated with uteroplacental vascular pathology. Preeclampsia is classically considered to be related to defective or otherwise abnormal uteroplacental vascular modification during the early months of pregnancy, although the maternal disease (which can take a myriad of forms within a wide range of organ systems) presents weeks to months after the pathologic anatomy is established. Not surprisingly, chronic uteroplacental malperfusion is commonly accompanied by fetal growth restriction (which commonly parallels the degree of placental injury).

Many villous lesions are more common when there are also uteroplacental vascular lesions, including infarcts, abruption, and diffuse villous lesions which cannot be identified grossly. Scarred, shrunken, fibrotic and hypovascular villi, with reduced numbers and/or caliber of placental capillaries, may be the end result of destruction of growing villous capillaries by abnormal uteroplacental flow. While abnormal uteroplacental vascular conversion must date - especially in the endometrium - to the first and second trimesters, it is difficult to date the time of onset of other lesions. In some cases, placental growth can provide some measure of the chronicity of adequacy (or lack of same) of the uteroplacental vascular supply. The preservation of nuclear detail within infarcts and abruption can provide crude estimates of lesion age. Decidual hemosiderosis indicates bleeding at least 24-48 hours prior to delivery.

Finally, it should be emphasized that the conversion of the uteroplacental vasculature requires the normal interaction of maternal and placental tissues. While we can not discriminate now whether failed vascular conversion causes subsequent abnormal immune interaction (and development of chronic inflammatory lesions), or if failed immune interactions cause subsequent failure of uteroplacental vascular conversion, we do know that these processes (of vascular conversion and immune interaction) are intimately associated. Therefore it is not surprising that uteroplacental vascular and chronic inflammatory lesions are common found together in placentas from compromised pregnancies. Aberrant uteroplacental vascular conversion is known to have a recurrence risk in subsequent pregnancies, as would, obviously, cell-mediated immune responses. It is common in cases with recurrent pregnancy compromise to see an "evolution" of the histologic abnormalities from a first to a third or fourth loss, with progressive manifestation of chronic inflammatory pathology, or changing uteroplacental vascular lesions.

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