What happens biologically during Pre-E

[caryn]

Not yet. Tests are in development.

It's thought that all pregnant women are very close to developing preeclampsia, and that all would develop it if their pregnancies lasted long enough, so it is difficult to pick out the women who will develop preeclampsia from the population as a whole.

[atvlady]

I am glad you said that Caryn. My high risk ob said there is some tests that are currently being researched as to detect preeclampsia developing in pregnancy but then he cut my water off when he said that still if preeclampsia is going to happen in pregnancy, the baby has to be delivered regardless. I am out of sorts with his response cause I have talked to other women who's pre-e was controled. I guess it depends on progression of pre-e???? I am confused by his answers and arrogancy with my last appt!!!!!

[caryn]

PE is a freaky weird disease, and so they describe it using words like "multifactorial" and "heterogeneous". Essentially that means that there are lots of ways to be predisposed to get it, and lots of ways for the symptoms to present.

There's no known therapy or treatment for preeclampsia apart from delivery, except possibly in women with underlying thrombophilias who might benefit from blood thinners. However, the data supporting the use of blood thinners has gotten weaker with time, rather than stronger, and that may just be an artifact of our older studies.

Some women are on blood pressure meds to keep their pressures down because that is thought to lower risk to them, and to pose risks to the baby that are manageable through careful oversight. (Bp meds are associated with smaller babies, possibly because lowering the maternal pressure lowers the perfusion of the placenta somewhat. That can be watched with extra ultrasounds and dosage can be tweaked accordingly.) But blood pressure meds are not thought to affect the time of onset of preeclampsia or the rate of progression of preeclampsia.

And bedrest is known not to work, either.

So we're stuck saying that the average time from diagnosis to delivery is around two weeks, and that some women go from 0-60 in four hours, and others crawl along for months.

[atvlady]

I agree Caryn. My high risk told me that I started to develop pre-e around my 16th week, about the time when my right foot swelled up so big I couldn't even wear flip flops. But when he said that I looked at him and said I saw you twice and why didn't you tell me then! I don't know what was going through my drs minds with my pregnancy but the saddest thing is it was at the cost of our daughter, and almost my life. I am deeply saddened by this but furious on the other hand. LUCKILY I am going to see a new MFM in November. On the other hand, my HELLP came on in about 2 weeks so yes when you say that 2 weeks is from diagnosis to delivery I can say that is very true. I find myself extremley verbal now in my care now and my future pregnancies. My new ob is very confident I can have a viable baby next time. But still in my mind my odds are 50/50.

How about the role of VEGF in pre-e??? Any imput on that??
And does lowering BP by means of medication do more harm then good?

PS Caryn...could we make this post a sticky????

[lharrison]

Great thread!! I have heard some of these explanations before but never all together in such a concise and understandable way. Thanks so much for the explanation!!

This post is in response to smb's post from 2/2009 - this may be a new development in predicting PE, but I am pregnant with my 2nd and being closely monitored after emergency c-section due to PE and HELLP at 35 weeks with 1st pregnancy. At my 18 week MFM appointment they checked a uterine arterial flow on both the left and right. MFM said that the pattern of the blood flow can be an indicator for developing PE later. A normal blood flow pattern would show as a sound wave with a peak and dip. In the cases that indicate PE, the wave pattern will have an extra notch or step as the arteries are trying to relax (after the peak). As explained above (and per my MFM) this has to do with your body trying extra hard to get the blood to the baby. He advised me that if the PE pattern shows up in the uterine arterial blood flow then your chances of developing PE are at 50%. Mine did show the PE blood flow pattern but I had already been advised that my chances of getting PE again are at 50% due to my last pregnancy. So, it did not change my chances but thought it might be helpful to share.

I wonder if this could be a test done on ALL pregnant women to possibly have an earlier marker for developing PE later in the pregnancy.

[rusah]

I'm not sure if this is active anymore, but I thought I'd add my thoughts

I'm just wondering if there's any relation between having a tilted/retroverted (not sure of the proper term!) uterus and getting preeclampsia. I was thinking that if what causes it is a not properly attached placenta (among other things!), could it be that having a tilted uterus increases your risk of the placenta not attaching properly?

I have a tilted uterus and I had preeclampsia with my other pregnancy, and am right on the verge of getting it with this one, which is why I'm wondering!

Thanks!

[miamibunnie]

Rusah good one...I also have been told that have a slightly tilted uterus, and wondered the same thing.

I'm not sure if this is active anymore, but I thought I'd add my thoughts

I'm just wondering if there's any relation between having a tilted/retroverted (not sure of the proper term!) uterus and getting preeclampsia. I was thinking that if what causes it is a not properly attached placenta (among other things!), could it be that having a tilted uterus increases your risk of the placenta not attaching properly?

I have a tilted uterus and I had preeclampsia with my other pregnancy, and am right on the verge of getting it with this one, which is why I'm wondering!

Thanks!

[caryn]

I don't know of any connection between retroverted uterus and preeclampsia, no. I don't think there would be one, because when implantation goes wrong in the way that predisposes to PE, it's not really because of gravity -- it's because of a biochemical miscommunication between paternal and maternal cells. Although I suppose if it's retroverted because of endometriosis, and endo lowers risk of PE, that might lower your risk of PE somewhat. (Only somewhat -- we have plenty of posters with endo histories!)

[veronica44]

To people's knowledge, is the mechanism for PE different for someone with chronic hypertension than for patients with normal or low blood pressure? It seems confusing that the chronic hypertensives have such a greater predisposition towards PE if the main explanation is implantation phenomena.

[caryn]

The research isn't specific to this point yet -- in other words, no one knows for certain -- but chronic hypertension is an immune characteristic as well, an activation of the innate immune response. Implantation could by dysregulated in chronic hypertensives because of their genetic tendency to hypertension. If that's true, my guess is that implantation can't proceed normally in chronics because other chemical responses unique to chronics are operating at the same time and interfere with a clean line of communication between the maternal and paternal cells -- like noisy crosstalk on a radio.

This is very difficult to study, but it's an ongoing, very intriguing, area of research. One thing that I find fascinating about it is that some chronics have babies who are *big* for gestational age, which might suggest that even though the placenta is shallowly implanted it's developing a decent blood supply anyway, or might suggest that implantation is deep enough to grow a big baby but at the same time the maternal immune response to it is creating hypoxia and triggering the same downstream effects that a shallow implantation would cause. There are multiple pathways operating here, multiple placental strategies for maximising bloodflow, so you could simultaneously have shallow implantation and then other strategies that compensated somewhat for that shallow implantation, like upregulation of maternal respiration rate and heart rate and appetite (so the little blood that does make it 'round to perfuse the placenta is still packed with supplies. (I think this is a useful way to explain tachycardia and breathlessness in some PE patients.)

The chemicals that are upregulated in PE, sFlt-1 and sEng, are upregulated in patients regardless of their predisposing underlying conditions, so hypoxia has to be a player in chronics, which suggests that chronics have shallow placentation going on, in some fashion.