Recent aspects of hemostasis, hematology and hemorheology in preeclampsia-eclampsia.
Because intravascular fibrin deposition is found in the glomerular capillaries of patients who have died of eclampsia, it was long assumed that a chronic form of intravascular clotting represents the decisive cause of the condition. Fibrin deposition is also typically observed in the uteroplacental bloodstream. The occurrence of high levels of soluble fibrin and fibrin(ogen) degradation products, which in severe cases can also include fibrin oligomers, in combination with thrombocytopenia and factor VIII consumption were interpreted as additional evidence for the significance of intravascular clotting in the pathogenesis of EPH gestosis. The hemolysis of the microangiopathologic type, which occurs in severe cases, was attributed to the resulting impairment in microcirculation. Doubts regarding this theory arose when it was noted that the course of EPH gestosis is not altered by the use of heparin, and that even in severe cases of eclampsia with hemolysis and thrombocytopenia the plasmatic clotting system is involved only to a small extent and probably only secondarily. More recent investigations have yielded the first evidence of reduced prostacyclin synthesis in maternal and fetal vessels in patients with EPH gestosis. Since prostacyclins lower arterial resistance yet at the same time are strong inhibitors of thrombocyte aggregation, this prostacyclin deficiency could account for the hypertension and the occurrence of platelet thrombi in the placental bloodstream associated with EPH gestosis. The observation of a reduction in the number of thrombocytes as a consequence of increased platelet breakdown, which precedes a rise in the level of fibrin(ogen) degradation products, also points to the significance of an abnormal interrelation between platelets and endothelium. In addition to the plasmatic and thrombocytic hypercoagulability and impaired prostacyclin synthesis, hemoconcentration with increased microvascular permeability is also observed. Early detection of disturbances of the vessel wall and vessel contents may provide a means of prophylaxis.
D000328:Adult; D001775:Blood Circulation; D001777:Blood Coagulation; D001779:Blood Coagulation Factors / Q000502:physiology; D002199:Capillary Permeability; D011464:Epoprostenol / Q000096:biosynthesis; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006400:Hematocrit; D006461:Hemolysis; D006487:Hemostasis; D006801:Humans; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D012212:Rheology
D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D011464:Epoprostenol