There is little to suggest that the course of preeclamsia can be substantia
lly affected by drug treatment. The vast majority of randomized studies do
not indicate beneficial effects of antihypertensive treatment on proteinuri
a, fetal heart rate abnormalities, abruptio placentae and the incidence of
preterm birth. There is also no definite effect on the development of super
imposed preeclampsia, HELLP syndrome, renal failure or eclampsia. Moreover,
blood pressure lowering agents fail to improve uteroplacental perfusion bu
t may have adverse effects on fetal growth. Antihypertensive treatment is o
nly indicated in severe hypertension (> 170/110 mm Hg) to reduce the risk o
f cerebral hemorrhage. Dihydralazine injections may result in reduced place
ntal blood flow and fetal distress. Oral nifedipine offers some advantages
in view of more potent vasodilator actions on uterine and fetoplacental ves
sels and a lower incidence of fetal distress. Increasing evidence suggests
that the mechanism of eclamptic seizure is cerebral vasoconstriction with r
esultant ischemia. Cerebral vessels are particularly sensitive to magnesium
, which works by reversing cerebral vasoconstriction with resultant improve
ment in blood flow. Controlled trials have shown magnesium to be superior t
o both placebo and phenytoin for the prevention of eclampsia. Furthermore,
magnesium has been found to be more effective than diazepam and phenytoin i
n preventing recurrence of seizures in women with eclampsia. Also the neona
tal outcome favors magnesium, which is now generally accepted as the drug o
f choice for the prevention and treatment of eclampsia.