Placental contribution to neonatal encephalopathy

Abstract

Placental assessment, although currently underused, can inform our understanding of the etiology and timing of Neonatal Encephalopathy (NE). We review our current understanding of the links between placental dysfunction and NE and how this information may inform clinical decisions, now and in the future, emphasizing the four major placental lesions associated with NE. In addition, we discuss maternal and fetal factors that are hypothesized to contribute to specific placental pathologies, especially innate or acquired thrombophilias. We outline the importance of assessing placenta across trimesters and after delivery. As this field continues to evolve, currently available placental histopathological examination methods may need to be combined with advanced prenatal molecular and imaging assessments of placenta and be applied in well-designed studies in large representative populations to better define the links between placental dysfunction and NE.

Keywords: Chorioamnionitis; Chronic villitis; Fetal vascular malperfusion; Histopathology; Maternal vascular malperfusion; Neonatal encephalopathy; Perinatal brain injury; Placenta; Villitis of unknown etiology.

Figure 1.

Four major patterns of placental injury. (a) Maternal vascular malperfusion is characterized by villous crowding (center) with increased syncytial knots and villous agglutination combined with surrounding relative paucity of branching villi (4X, H&E stain). (b) Fetal vascular malperfusion (fetal thrombotic vasculopathy) shows uniformly hyalinized avascular terminal villi branching off a stem villus with stem vessel luminal obliteration (4X, H&E stain). (c) Acute chorioamnionitis with a severe grade 2 fetal inflammatory response in chorionic vessels as indicated by confluent neutrophilic infiltration of the fetal vessel walls on the side facing the amniotic fluid cavity (4X, H&E stain). (d) Chronic villitis, high grade, with stem vessel obliteration (obliterative fetal vasculopathy) shows a lymphohistiocytic infiltrate of maternally derived immune cells in the fetal connective tissue stroma of stem and terminal villi resulting in secondary occlusion of stem villous arteries (10X. H&E stain).