Placental Transfer of Intravascular Coagulation between Mother and Fetus

Abstract

Extract: Pregnant sheep of 110–140 days' gestation were used to determine the effect of intravascular coagulation in the mother upon her fetus and the effect of intravascular coagulation in the fetus upon its mother. Because fetal lambs can be delivered and left attached to the mothers via the umbilical cord without placental separation, coagulation studies on a mother and her corresponding fetus could be done simultaneously. When intravascular coagulation was induced in the mothers by administering thromboplastin infusions intravenously, the attached fetal lambs also developed intravascular coagulation with decreased levels in platelets, fibrinogen, and factor V, and prolongation of prothrombin, thrombin, and partial thromboplastin times. When intravascular coagulation was induced in fetal lambs, the dam had a drop in platelet count, a minimal drop in fibrinogen levels, and the appearance of fibrin breakdown products in serum and urine. The factor or factors that crossed the placenta initiating this transfer of coagulation abnormalities are not known. It has been demonstrated that the transfer was not due to fibrin or fibrinogen breakdown products, nor to the infused thromboplastin, and that the trauma of surgery or hypoxia did not contribute to the coagulation abnormalities. The mothers consistently developed fibrin breakdown products in the serum and urine when intravascular coagulation was induced. This was in contrast to the results observed in fetal lambs, which, with one exception, did not show evidence of fibrin breakdown products in serum or urine under identical experimental conditions. These observations suggest the fibrinolytic system of the fetus is inefficient compared with that of the adult; this could be a considerable disadvantage in the presence of intravascular coagulation. Speculation: As a result of intravascular coagulation in the mother or the fetus a stimulus is produced on the opposite side of the placental barrier resulting in similar changes in the placental partner. This mechanism may be of significance in the etiology of fetal death in eclampsia.