Hepatic Lesion in Eclampsia (An Experimental Study)

Abstract

The hepatic lesion in Eclampsia in humans is peculiar in that it does not occur in any pregnant animal or in any other human disease. The lesion is essentially a thrombosis occurring in the capillaries of the portal vein in the periphery of the liver lobule with hemorrhage into the adjacent tissues, resulting in necrosis. It is our belief that whatever the substance is which causes this thrombosis, it must be in greater concentration in the portal system.

From clinical experience we know that curtailment of protein together with intestinal elimination will in almost all cases prevent Eclampsia. We also know that Eclampsia does not occur unless the woman is pregnant, that is, living chorionic villi must be present. The fetus may be dead for true Eclampsia has occurred with Hydatidiform Mole.

In late pregnancy placental fragments are constantly entering the blood stream. This placental tissue is rich in tissue fibrinogen, a blood coagulant found in tissue extracts, which must be neutralized or destroyed by substances in the blood.

Mills 1 has demonstrated that tissue fibrinogen, a cephalin-protein complex can pass through the intact intestinal wall and shorten the clotting time of the blood. If this is true it seemed to us that we could explain the production of the hepatic lesion of Eclampsia as follows: If too much of the neutralizing substance is used up by the placental tissue, it is conceivable that tissue fibrinogen from meat, by mouth, requiring the same detoxifying substance, could reach such a concentration in the portal system that thrombosis would occur.