Placental, renal, vascular and hepatic changes in pre-eclampsia
THE CONTEXT
Pre-eclampsia and eclampsia produce pathological changes in the uteroplacental circulation and several maternal organs.
Placental and spiral artery changes
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Red and white infarcts may be visible on the maternal surface of the placenta.
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Villous changes include syncytial degeneration, increased syncytial knots, cytotrophoblast proliferation, basement layer thickening and proliferative endarteritis.
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Endovascular cytotrophoblast invasion of spiral arteries fails to extend beyond the decidua–myometrial junction. The myometrial musculoelastic media therefore remains responsive to vasoconstrictor stimuli, decreasing blood flow.
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Acute atherosis can obliterate spiral artery lumina.
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Intervillous blood flow is impaired by about one-third because of maternal vascular changes. The resulting anatomical and functional placental changes contribute to fetal jeopardy.
Renal changes
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Glomerular enlargement is described as glomerular endotheliosis. Endothelial swelling, fibrin-like basement membrane deposits and interstitial cell proliferation may occlude capillary lumina.
Renal blood flow and glomerular filtration rate decrease, while tubular reabsorption or secretion is impaired. Recovery is likely to be complete after delivery.
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In severe cases, intense anoxia can cause extensive arterial thrombosis and bilateral renal cortical necrosis.
Vascular and hepatic changes
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Intense vasospasm occurs. Impaired circulation through the vasa vasorum damages vascular walls and endothelial integrity.
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Hepatic arteriolar thrombosis causes periportal hemorrhagic necrosis, beginning at the lobular periphery.
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Subcapsular hematoma may progress to liver rupture in severe cases. Right upper quadrant pain results from stretching of Glisson's capsule.
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Liver function tests are particularly abnormal in HELLP syndrome. HELLP denotes hemolysis, elevated liver enzymes and a low platelet count below 100,000/mm³.