Placental pathologic features of preterm preeclampsia

Our purpose was to compare the incidence and interrelationships of uteroplacental vasculopathy and chronic inflammatory and placental vasoocclusive lesions in preeclampsia and spontaneous delivery before 32 weeks' gestation.

Review of singleton live-born nonanomalous infants born at 22 to 32 weeks' gestation identified 76 cases of preeclampsia and 353 cases of spontaneous prematurity (spontaneous premature membrane rupture [n = 192], preterm labor, intact membranes [n = 161]). Histologic lesions were considered as belonging to one of five major pathophysiologic groups: (1) uteroplacental vascular lesions and related villous lesions, (2) chronic inflammatory lesions, (3) coagulation-related lesions, (4) acute inflammatory lesions, and (5) unclassified lesions. Contingency table analyses considered p < 0.05 significant. Factor analysis extracted combinations of related variables.

More frequent in preeclampsia versus spontaneous prematurity were chronic uteroplacental vasculitis (29% vs 20%, p < 0.05), chronic villitis (20% vs 3%, p < 0.001), avascular villi (39% vs 16%, p < 0.001), and "hemorrhagic endovasculitis" (9% vs 2.5%, p < 0.03). In the preeclampsia cases factor analysis extracted 13 categories of related lesions. Four categories contained uteroplacental vascular lesions. Five categories included lesions related to chronic inflammation, and eight included lesions related to coagulation. Four categories loaded lesions from one major pathophysiologic group only. Three categories loaded lesions from all three pathophysiologic groups. Unclassified lesions loaded into two factor categories that were unrelated to the other lesions.

Chronic inflammatory and placental vasoocclusive lesions are more common in preterm preeclampsia than in spontaneous prematurity. Immunopathologic processes and coagulation may be involved in the pathophysiologic mechanisms of preterm preeclampsia independent of uteroplacental vascular pathologic features.