Placental Pathologic Associations With Morbidly Adherent Placenta: Potential Insights Into Pathogenesis.

Research paper by Linda M LM Ernst, Rebecca L RL Linn, Lucy L Minturn, Emily S ES Miller

Indexed on: 16 Aug '17Published on: 16 Aug '17Published in: Pediatric and Developmental Pathology


Background The pathology that underlies morbidly adherent placenta (MAP) is poorly understood. The objective of this study was to describe the placental pathology, especially implantation site pathology, associated with MAP. Methods This was a single institution, retrospective case-control study design examining placentas of patients who delivered between January 2008 and September 2013. MAP cases were defined by the need for clinical intervention at delivery beyond spontaneous placental delivery or simple manual extraction of the placenta. Controls consisted of patients with placentas sent for examination due to a history of maternal malignancy with no clinical suspicion of accreta. Placental pathologic findings of maternal vascular underperfusion (MVU), acute inflammation, chronic inflammation, fetal vascular obstruction, and hemorrhage were recorded and compared using bivariable and multivariable analyses. Results Three categories of pathologic changes were seen more commonly in MAP placentas (N = 101) than control placentas (N = 110): chronic basal inflammation, villous changes of MVU, and retromembranous and subchorionic/intervillous hemorrhage. In multivariable analyses adjusted for confounders, basal chronic villitis (aOR 5.6, 1.73-18.18), plasma cell deciduitis (aOR 2.63, 1.08-6.39), increased syncytial knots (aOR 3.92, 1.57-9.75), villous agglutination (aOR 24.85, 2.78-221.75), increased perivillous fibrin (aOR 5.08, 1.49-17.34), and the presence of subchorionic/intervillous thrombi (aOR 4.01, 1.63-9.86) remained associated with MAP. Conclusions MAP is highly associated with evidence of intraparenchymal placental hemorrhage, villous changes of MVU, and a lymphoplasmacytic infiltrate at the implantation site. The contribution of this basal chronic inflammatory infiltrate to MAP requires further investigation.