Pregnancy complicated by diffuse chorioamniotic hemosiderosis: Obstetric features and influence on respiratory diseases of the infant

Abstract

Long-term exposure to degenerating red blood cells is supposed to damage amnion, fetal alveolar epithelial cells and fetal pulmonary arteries, and may lead to dry lung syndrome and PPHN in the infant complicated by DCH.

Circumvallate Placenta: Associated Clinical Manifestations and Complications—A Retrospective Study

“…As to the association between circumvallate placenta and SGA, fetal growth restriction has been speculated to be caused by placental insufficiency due to a marginal infarct, hemorrhage, and hemosiderin deposition, in addition to a hypoplastic placenta [ 2 , 11 ]. It has also been suggested that prolonged vaginal bleeding during pregnancy causes hemosiderin deposition in the placenta and chorion, resulting in diffuse chorioamniotic hemosiderosis, and that the fetus may swallow bloody amniotic fluid and thereby develop CLD [ 12 , 13 ].…”

Amniotic epithelial cells damage by oxidative stress in cases of diffuse chorioamniotic hemosiderosis

“…Diffuse chorioamniotic hemosiderosis occurs when marginal or subchorionic placental hemorrhage migrates into the amniotic fluid, and iron, which is a component of hemoglobin, is diffusely deposited as hemosiderin in the chorionic plate or membrane . Although amniotic epithelial necrosis is known to occur with high frequency in CAOS, in which DCH is frequently observed, there has been no analysis of the relationship between the degree of DCH and amniotic epithelial necrosis. In this study, although we only had three cases, the severity of amniotic epithelial necrosis was associated with the increased deposition of hemosiderin.…”

Correlation of preterm infant illness severity with placental histology

“…Diffuse chorionic hemosiderosis, defined as hemosiderin-laden macrophages in the membranes and chorionic plate, is a chronic lesion associated with marginal placental abruption, recurrent maternal bleeding in earlier trimesters, and oligohydramnios [18]. This placental finding has been reported to be increased in infants with persistent pulmonary hypertension of the newborn, pulmonary hypoplasia, and chronic lung disease [41; 42]. Lung injury in these cases may be due to the effects of oligohydramnios on the developing lung as well as possible toxic effects of hemoglobin breakdown in the aspirated amniotic fluid.…”