Two selected retroplacental hematomas, each still in situ on its delivered placenta, were studied in microscopic sections. One was a self-limiting retroplacental hematoma from a case of eclampsia, the other an extensive hematoma from a case of clinically diagnosed abruptio placentae. Thus these represented an early and a late stage of progress of abruptio placentae. In each the basal plate which otherwise separates the hematoma from communication with the maternal lake was found to be lacerated. These spontaneous lacerations appeared to be the result of an expanding force from within the hematoma itself.It was inferred that at the time of spontaneous rupture of the basal plate blood from the hematoma may have returned through the laceration into the maternal lake, and thence back into the general circulation. It was further inferred that this provided a pathway for autoextraction of decidual tissue substances into the maternal circulation. A comparable mechansim of auto-extraction during placenta previa, marginal separation of the placenta, or marginal sinus rupture seems improbable because a pathway for appreciable return flow to the maternal circulation is lacking.The implications of the apparent decidual autoextraction, as an etiological factor in the acute maternal disorders of abruptio placentae, upon therapy are considered. It was reaffirmed that in abruptio placentae delivery usually should be accomplished promptly, even with resort to cesarean section if vaginal delivery is not imminent. This is to reduce the risk of further progress of the abruptio and of complications therefrom, including release of further activation of coagulation within the circulation. More importantly, whatever the obstetrical management, it becomes mandatory, once the clinical diagnosis of abruptio placentae is made, immediately to initiate “stand-by” preparations for restoration of the circulating coagulation mechanism (and blood loss). Need for this may become acutely manifest during delivery, if not before or after. This is because of the danger of defibrination secondary to intravascular coagulation, and failure thereby of hemostasis. Not to be prepared with large quantities of already cross-matched blood, or, lacking this, of other support of the circulating coagulation mechanism, is to run the risk of fatal hemorrhage from even minor lacerations of delivery or from the incisions of perineal or abdominal surgery for delivery. Because of the danger of extension of the premature placental separation, it is important that the restoration of the coagulation mechansim be simultaneous with, and not usually prior to, delivery.