A Perinatal Pathology View of Preterm Labor

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Villous and Uteroplacental Vascular Pathology

In addition to cellular evidence of acute and chronic inflammation, placental histopathology can reveal vascular pathologic changes to the placenta that can severely impair the appropriate growth of the fetus and the ability of the uterine environment to maintain pregnancy to term. There are 3 vascular spaces unique to pregnancy: the maternal vasculature in the decidua and myometrium of the uterus remodeled by invasive trophoblast (the extra embryonic layer of epithelium that forms around the blastocyst and attaches the embryo to the uterus wall), the intervillous blood space (an extravascular space bounded by the villous syncytiotrophoblast epithelium), and the fetoplacental vasculature.

The uterine vasculature of a successful pregnancy reflects a remarkable adaptation of mature arteries to accommodate massive increases in flow volume, which is executed principally but not exclusively by the invasive endovascular cytotrophoblast. Lesions of the uteroplacental vasculature include absent or incomplete vascular conversion (identified by persistence of vascular media), failed passive vascular dilatation, presence of fibrinoid necrosis or atherosis, persistence of endovascular trophoblast, infarction, and chronic vasculitis. Maternal vascular remodeling finally extends to the destruction of intima, media, and elastica of the vessel wall and their replacement by an amorphous "fibrinoid" material, laid down at least in part by the semiallogeneic trophoblast. Maternal re-endothelialization of this foreign material completes the remodeling process. If this vascular adaptation does not take place to a sufficient extent, the vessels retain high-resistance/low capacitance properties, and blood flow from the uterus to the placenta is severely restricted. Combinations of these lesions may result in overall uteroplacental insufficiency and result in a number of obstetric complications, including fetal growth restriction, late fetal death, and prematurity.

The intervillous space has also recently been shown to be a dynamic and frequently remodeled vascular space; the perivillous fibrin/fibrinoid, often dismissed as a result of normal aging changes, has been proposed to play a role in adapting the intervillous space to optimize uteroplacental perfusion.[17] Thus, the feto-placental vasculature is a remarkably dynamic system, extending both as a macrovascular and a microvascular structure within the fetus and placenta during pregnancy.

Villous lesions considered to be related to uteroplacental vascular pathologic features include abruptio placentae, villous infarcts, terminal villous fibrosis, increased syncytiotrophoblast knotting, cytotrophoblast proliferation, and villous hypovascularity. The diagnosis of abruptio placentae is made grossly by the presence of a retroplacental hematoma with subjacent placental infarct or more commonly by microscopic evidence of placental villous infarct with decidual destruction and indentation with decidual and parabasal hemorrhage. Histologic diagnosis is considered to be consistent with (but not diagnostic of) abruptio placentae when focal regions show decidual destruction and hemorrhage and an increase in syncytiotrophoblast knotting, often with villous stromal hemorrhage.

Coagulation-related lesions in the vascular circulation include uteroplacental vascular thrombosis and intervillous thrombosis. A diagnosis of excessive perivillous fibrin deposition indicates the presence of more than 10% of villi encased in perivillous fibrin. Coagulation-related lesions within the placental circulation include chorionic and fetal stem vessel thrombi, "hemorrhagic endovasculitis," and avascular terminal villi, an indication of fetal microcirculatory vaso-occlusion.


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