My guess is that the doc thinks you look like a chronic, and we often don't get anticoagulants and only get LDA about half the time.
I also had sudden severe onset at 33 weeks, with pressures of 220/116, and a 24-hour proteinuria of 17,000 (no, that is not a typo), and cerebral swelling bad enough to cause hallucinations. But my son was almost 5 pounds at that gestational age, which means he was getting an adequate supply of blood, and was *fine* - I was the one who was sick. He scored an 8/8 on my admission BPP and didn't drop to 4/8 until *after* they put me on bedrest and started a drug regimen designed to lower my pressures. He was delivered 2 days after admission in an emergent Caesarean because he had stopped bothering to move or practice breathe and started having big decels - probably because lowering my blood pressure down to 160/90 lowered the amount of blood flowing into the placental interchange and lowered his oxygen supply. (He's fine now, too.)
Babies just don't get that big when there's a long-term clotting problem of the kind Lovenox or heparin would treat. And preeclamptics who present like I did and take a long time to recover are what they call "superimposed PE" chronic hypertensives. My issue was hitting the point where my body couldn't handle the inflammation of pregnancy any more. There's no obvious way for either anticoagulants or LDA to affect that, although there is some ongoing research into the possibility that baby aspirin does something to the COX-1 pathway to improve vasculature functioning which might explain the very small benefit to a small number of people that keeps popping up in the big meta-analyses. So every doc I talked to about it said I simply wasn't a candidate for those meds, and I've read enough of the studies to agree with them.
In the aspirin metaanalysis Jasmin linked, the high-risk subgroup was women with a history of PE, and they were looking to see if aspirin might have had an effect on the development of the placenta if taken early in pregnancy. A 16 week cutoff will cover most of the early placental development.
The good news is that no research shows there's something that will definitely help because this isn't something that's under your control and isn't your fault - it's genetic and very much a consequence of placental development, and placentas are pretty unconcerned with a lot of things you could control. The bad news is that this isn't under your control, so you kinda have to white-knuckle the rest of this pregnancy. That's why we're here - there will be other women who have Been There Done That or who are doing it right now, a week ahead or a week behind you. These subsequent pregnancies are nervewracking.
We do try to discuss a lot of current studies either in Announcements and PE in the News or in our research blog on the main page. The monthly newsletter also has research articles in it - you can sign up on our main page!
The big NICHD studies are here: http://www.ncbi.nlm.nih.gov/pubmed/9494145
You'll notice that NICHD ran these studies a *long time ago* and have been trying to get OBs to adopt this information for years, with minimal success because anecdotes are very powerful. Several of the docs involved in these studies are members of the PF Medical Board or advise us. As I understand it they've pretty much thrown up their hands and said, well, there's a slight increase in abruption risk if we can trust the numbers, but there seems to be no other risk from LDA, so if they want to take it, let them. I am not a doc, though.
There's a big study going on right now into Lovenox to see if it works at all. When it concludes we'll know more. Folic acid is supplemented in early pregnancy to minimize rate of neural tube defects so all pregnant women are on it; some MFMs are looking at some very preliminary research like this and recommending it: http://www.ncbi.nlm.nih.gov/pubmed/21349824
But that recommendation makes me *reeeeeeaaaaaaly nervous*. The metaanalysis you linked at the bottom of your last post? It says Similarly, VCE did not reduce the incidence of pre-eclampsia in high-risk (VCE: 250/1744 - 14% vs placebo: 275/1741 - 16%; P=0.24; OR: 0.84; 95% CI: 0.63-1.12) and low-risk (VCE: 56/935 - 6% vs placebo 47/942 - 5%; P=0.57; OR: 1.20; 95% CI: 0.82-1.75) women. In high-risk women, other hypertensive disorders were more frequent in VCE (121/1692 - 7%) than placebo (79/1693 - 5%; P=0.002).
VCE stands for Vitamins C and E, which preeclamptics used to be told to supplement all the time. When I first posted to this board practically everyone was trying supplemental C and E on the advice of their MFMs who had read some preliminary studies. And the big study into it found that it didn't affect preeclampsia at all but made women who were supplementing it *sicker, quicker* - which this abstract describes as "other hypertensive disorders were more frequent in VCE". So even things that seem innocuous can harm - the population taking C and E ended up with higher pressures and earlier deliveries.
You know which population has a really low rate of preeclampsia? Recreational drug users. No one is going to recommend that we all run out and start taking recreational drugs to lower our risk of PE because recreational drug users have much higher rates of other pregnancy problems. So this is why I always say *no supplementing anything without talking to your docs about it*. No extra vitamin D or bedrest or folic acid unless your doc knows you're doing it. /Caryn's PSA over, thanks!