[Pathology of the placenta. IX. Intrauterine fetal death. Regression. Edema and fibrosis of the villous stroma].

Intra-uterine fetal death along with discontinuation of fetal circulation is followed by intraplacental processes which result in the following pathologico-anatomic pattern: Fetal vessels in terminal villi are doomed to collapse, with the major arteries being occluded due to proliferation. This is followed by substantial proliferation of connective tissue in peripheral villi, and by total disappearance of capillaries in terminal villi. Possible remnants of cytotrophoblast are lost from trophoblast epithelium, with the syncytiotrophoblast undergoing proliferation. Multiple syncytial proliferations were recorded from cases in which some time had passed from the event of intra-uterine fetal death. Stromal fibrosis is introduced by transient activation of mesenchyma of the terminal villi. Complete regression with totally fibrosed (collagenized) villi, vascular occlusion of stem villi, numerous spots of syncytial proliferation, and increased deposition of intervillous fibrin ist the morphological equivalent of missed abortion. Stromal fibrosis of terminal villi is a consequence of regression after intra-uterine fetal death or may possibly result from impairment of placental circulation of different causative background. Certain forms of fibrosis may possibly develop via stromatic edema (e.g. diabetes mellitus, blood group incompatibility, immunological disorders) together with edema-activated mesenchymal proliferation. Edema of villous stroma may be of diffuse or focal manifestation in the terminal villi and in advanced cases may affect all parts of the placenta. It is usually linked to diseases in which the entire fetoplacental unit is prone to edematization (maternal diabetes mellitus). Severe stromatic edema leads to formation of so-called stromatic ducts in which edema liquid is accumulated but is incapable of flowing out for absence of lymphatic drainage of the placenta.