Doppler sonographic findings for hypertension in pregnancy and HELLP syndrome

Abstract

Doppler examinations of the umbilical artery, both uterine arteries, and the fetal middle cerebral artery were performed in the third trimester in 18 patients with pregnancy induced hypertension, 52 patients with preeclampsia, and 32 patients with HELLP syndrome and the results were correlated with the parameters fetal outcome. For 74% of the patients this was the first pregnancy, in 93% of the cases a cesarean section was necessary; 66% of the newborn babies were dystrophic and 90% of them were born prematurely. The blood flow in one uterine artery was restricted in 95% of all 102 pregnant women, only 5% did not show any pathological findings. A pathological blood flow was observed on Doppler sonography in the umbilical artery in 70% of the group and 39% showed a pathologically increased perfusion of the fetal middle cerebral artery. The average birth weights and gestational ages in the study group were markedly reduced in comparison with healthy pregnant women (pregnancy induced hypertension: 1620 g/35 weeks; preeclampsia: 1660 g/34 weeks; HELLP syndrome: 1160 g/31 weeks, respectively). The lowest values for average birth weight and gestational age occurred when all four investigated blood vessels showed pathological Doppler findings: 1180 g/31 weeks (0 to 1 pathological vascular findings: 2780 g/38 weeks; 2 pathological vascular findings: 1845 g/34.5 weeks; 3 pathological vascular findings: 1330 g/31 weeks). This Doppler study underlines the importance of examining four blood vessels: the uterine, the umbilical, and the fetal middle cerebral arteries for a complete analysis of the fetoplacental hemodynamics. On account of the severely impaired hemodynamics observed in the placentas of our patients with hypertensive diseases in pregnancy or HELLP syndrome, we believe the early diagnosis of these disorders by Doppler sonography and an early start of therapy to be essential.

Doppler measurements in fetal descending aorta and umbilical artery can predict borderline oxygenation in pre-eclampsia and HELLP syndrome

“…Treatment requires premature termination of pregnancy, either by caesarean section or vaginal delivery if cervical conditions are optimal. Many studies have associated preeclampsia with increased perinatal (25%) and maternal (3% -5%) morbidity and mortality [10][11][12][13], decreased neonatal birth weights and higher incidence of premature delivery [12,14,15]. The low birth rates recorded in our study for pre-eclamptic patients with or without HELLP syndrome are thus in agreement with previous reports 12, 14,15].…”

“…Many studies have associated preeclampsia with increased perinatal (25%) and maternal (3% -5%) morbidity and mortality [10][11][12][13], decreased neonatal birth weights and higher incidence of premature delivery [12,14,15]. The low birth rates recorded in our study for pre-eclamptic patients with or without HELLP syndrome are thus in agreement with previous reports 12, 14,15]. In this study, IUGR was associated with a decrease in end-diastolic flow velocities in the descend-ing aorta before changes in umbilical artery were detected.…”

Fetal middle cerebral to uterine artery pulsatility index ratios in normal and pre‐eclamptic pregnancies

“…One of the widely accepted theories regarding the development of pre‐eclampsia is that an immunologically mediated deficiency in the trophoblastic invasion of the placental bed spiral arteries leads to a poorly perfused fetoplacental unit3. Since the first report of Campbell et al 4 in 1983, there have been numerous clinical studies showing a strong correlation between elevated uterine artery resistance and unfavorable pregnancy outcome5–7. There have been several reports of the association between abnormal uterine artery velocimetry at mid gestation and pre‐eclampsia, which frequently is complicated by preterm delivery and intrauterine growth restriction (IUGR)8–12.…”

A Model for the HELLP Syndrome: The Maternal Experience

“…This syndrome is a disease of endothelial dysfunction that occurs at implantation, creating activation of intravascular coagulation with incomplete trophoblast invasion and incomplete maternal spiral artery transformation. This leads to vascular ischemia and fibrin deposits, resulting in cyclic vasospasms and clotting cascade activation (Davies, 1992;Joern, Funk, & Rath, 1999;Portis et al, 1997). The exact etiology remains unknown.…”