Haemorrhage and necrosis are frequently observed in women that have died from eclampsia. This suggests reduced perfusion rather than mechanical damage from high blood pressure. Particularly affected are the brain, liver, heart, kidneys and the decidual vessels.
Current thinking is that reduced placental perfusion liberates blood borne materials which cause endothelial cell dysfunction and subsequent systemic disease. Endothelial injury produces an increased sensitivity to normally circulating pressor agents, particularly, angiotensin II, resulting in vasoconstriction and reduced perfusion. The activity of prostacyclin I2, a potent vasodilator and inhibitor of platelet aggregation is decreased, whilst that of thromboxane A2, a vasoconstrictor and promotor of platelet aggregation, is increased.
There is a loss of normal endothelial anticoagulant function and an increase in procoagulant production which activates the coagulation cascade. Clinically evident DIC may be present in 10% of women with severe pre-eclampsia but more sensitive indicators of activation of the coagulation cascade such as thrombocytopenia, low concentrations of antithrombin III and high concentrations of thrombin- antithrombin III may be more widely demonstrated.
Loss of fluid from the intravascular compartment accompanies the loss of endothelial integrity.
Vasospasm and microthrombi exacerbate the existing poor placental perfusion so further disturbing endothelial cell dysfunction and causing autoacceleration of the disease.
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