Maternal whole blood viscosity in pregnancy hypertension.

Hemoconcentration is prominent in preeclampsia. Concomitant changes in the flow properties of maternal blood, i.e. in whole blood viscosity (WBV), might be related to the occurrence of fetal or maternal complications. To test this hypothesis, WBV was estimated in 228 pregnancies. Patients were assigned to one of four groups according to maximum diastolic blood pressure. Significantly higher WBV values were found in the more hypertensive groups throughout pregnancy. WBV data, obtained between 26 and 36 weeks of amenorrhea, contributed significantly, independently of hypertension, to the prediction of fetal outcome. With regard to maternal complications, no significant contribution of WBV data could be established independently of blood pressure. The results support the hypothesis that WBV is a determining factor in the efficacy of placental perfusion.

Longitudinal changes in blood viscosity are correlated with fetal outcome.

The importance of longitudinal changes in maternal Whole Blood Viscosity (WBV) for fetal well-being was investigated. Consecutive WBV data were available, obtained from 44 pregnancies before 36 0/7 weeks. An increase in WBV was found to be associated with an unfavorable fetal outcome. This result might be considered as clinical evidence supporting the hypothesis that maternal WBV contains information on the efficacy of placental perfusion.

The influence of maternal whole blood viscosity on fetal growth.

To explore the relevance of the rheological properties of maternal blood in pregnancy to fetal growth a study of whole blood viscosity (WBV) was conducted in the early third trimester of 138 pregnancies. A significant negative correlation was found between WBV at low shear rate and birthweight centile. As the rheological parameters were found to be negatively correlated with the placenta coefficient, an independent role for maternal WBV seems likely. When WBV, placental weight and degree of infarction accounted for significant contributions in a logistic regression model, diastolic blood pressure data did not assist in the correct prediction of occurrence of a low birthweight centile (less than 10th). A simplified model is proposed, to explain the mechanisms by which some clinical variables may express their influence on fetal growth. In conclusion, it is suggested that WBV might be considered one of the factors which determine the efficacy of placental perfusion on the maternal side. However, as this variation in efficacy of placental perfusion is only weakly reflected in variations in birthweight, the influence of WBV on fetal growth cannot be very important.

Blood coagulation in pregnancy induced hypertension.

Decreased plasma levels of antithrombin III (AT III) are observed in women with severe pregnancy-induced or aggravated hypertension. Low AT III levels correlate with the platelet count and with symptoms of maternal and foetal morbidity. Therefore, in clinical practice both the platelet count and the plasma AT III levels provide significant information regarding the clotting disturbances in toxemic patients. Established AT III deficiency may explain the enhanced post-partum thrombosis risk in these patients. Primary prophylaxis in patients undergoing caesarean section with oral anticoagulants is preferred because of an observed enhanced bleeding tendency upon heparin prophylaxis.

Antithrombin III levels in preeclampsia correlate with maternal and fetal morbidity.

In 57 patients with pregnancy-induced or aggravated hypertension, antithrombin III levels correlated inversely with maternal morbidity. Morbidity was determined by the maximal diastolic blood pressure, disturbance of renal and liver function, and thrombocytopenia. Antithrombin III levels and platelet counts correlated inversely with the degree of placental infarction. Proteinuria (grams per 24 hours) was most predictive of fetal outcome, which was considered to be either favorable if a healthy baby could be discharged with its mother or unfavorable in case of perinatal death or a prolonged stay in the neonatal intensive care unit. Plasma antithrombin III and serum glutamic oxaloacetic transaminase levels, in that order, augmented the number of correct predictions. Antithrombin III inhibits blood coagulation by forming irreversible complexes with activated clotting enzymes, notably with factor Xa and thrombin. Evidence is presented which suggests that antithrombin III levels in preeclampsia are depressed as a result of increased consumption in the maternal vascular tree, rather than decreased synthesis or increased urinary loss.

Plasma antithrombin III levels in pre-eclampsia.

In a prospective study plasma AT III was determined in 2423 samples obtained from 653 women during pregnancy and post partum. The women were allocated to groups, according to the highest diastolic blood pressure, in the third trimester. AT III levels were normal throughout pregnancy, during labour and after vaginal delivery, except in 57 women with pregnancy induced or aggravated hypertension. We present evidence that AT III depression in pre-eclampsia is caused by increased consumption. AT III levels correlate with maternal morbidity as revealed by hepatorenal damage. A weak but significant correlation of AT III and platelets with placental infarction was demonstrated. Proteinuria was the best predictor of fetal outcome. AT III plasma levels increased the number of correct predictions. Following vaginal delivery AT III plasma levels rapidly returned to normal values.