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Pathology - HELLP Syndrome
HELLP syndrome is a severe type of preeclampsia/eclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count. The pathogenesis is likely to entail inadequate invasion of maternal uterine arteries by the early trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that cause extensive endothelial injury in the mother. Platelet aggregation occurs at locations of endothelial damage, resulting in platelet depletion. Activation of platelets induces release of thromboxane A2 leading to vasospasm that is inadequately countered by endothelial relaxant factors and prostacyclin due to loss of endothelium. Deposition of fibrin also occurs in the lumens of tiny arteries, which increases shearing forces on red cells and promotes hemolysis (notice elevated LDH levels).
Obstruction of hepatic sinusoids with fibrinlike deposits accounts for local necrosis and hepatocellular damage (notice increased liver enzymes). Vascular obstruction within the liver creates a buildup of pressure and in this instance subcapsular hematoma is observed on ultrasonography; this process may even terminate in liver rupture. Treatment may include glucocorticoids to advance fetal lung maturation, although timely delivery of the fetus is necessary. Unlike preeclampsia syndrome, delivery may not result in immediate resolution of maternal symptoms after the HELLP syndrome has established.
HELLP syndrome is a severe type of preeclampsia/eclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count. The pathogenesis is likely to entail inadequate invasion of maternal uterine arteries by the early trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that cause extensive endothelial injury in the mother. Platelet aggregation occurs at locations of endothelial damage, resulting in platelet depletion. Activation of platelets induces release of thromboxane A2 leading to vasospasm that is inadequately countered by endothelial relaxant factors and prostacyclin due to loss of endothelium. Deposition of fibrin also occurs in the lumens of tiny arteries, which increases shearing forces on red cells and promotes hemolysis (notice elevated LDH levels).
Obstruction of hepatic sinusoids with fibrinlike deposits accounts for local necrosis and hepatocellular damage (notice increased liver enzymes). Vascular obstruction within the liver creates a buildup of pressure and in this instance subcapsular hematoma is observed on ultrasonography; this process may even terminate in liver rupture. Treatment may include glucocorticoids to advance fetal lung maturation, although timely delivery of the fetus is necessary. Unlike preeclampsia syndrome, delivery may not result in immediate resolution of maternal symptoms after the HELLP syndrome has established.
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