Question of the month.   MAY  2001.
As soon as autopsy material was available in maternal deaths due to eclampsia, it was obvious that the most impressive lesions were usually located in the brain, the liver, the placenta, and the kidneys. They usually were parenchymatous hemorrhages many times leading to overt brain hemorrhages, liver hematomas, abruptio placenta, and bilateral renal cortical necrosis. Modern medical intervention has changed somewhat these fatal expressions of the eclamptic syndrome, but these four territories continue to be the main final targets of this disease.
Leaving the placenta aside for the sake of simplicity, what do the brain, the liver and the kidneys have in common that makes them the preferred targets of the advanced pathophysiology of eclampsia ? Why not the pancreas, the spleen or the bladder experience similar consequences qualitatively and quantitatively? If the intermediate mechanism of the disease is generalized endothelial dysfunction leading to endothelial damage and disruption, why is it not expressed equally in all territories?
Should we not consider that the early and late manifestations of a systemic endothelial involvement are subject to local or regional physical and hemodynamic peculiarities, in addition to potentially previously acquired handicaps? Just to mention one of these possible multiple factors; should not the existence of rigid poorly extensible fibrous capsules surrounding the brain, the liver and the kidneys intervene to magnify the conflicts generated by the vascular endothelium dysfunction in ways not seen in the absence of such rigid capsules? What about the organs' particular blood flows and the increased tissue and cellular pressure effects on its microcirculation due to a relatively inelastic compartment? What other explanation could we give?
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