HA! Once the science went the way of the sftball and vegee, it went completely over my head. Thank you guys for explaining it so well! Now, I'll only have to read it about 50 more times before I can comfortably explain it to someone else!

The thing about postpartum PE is that it's the same thing as regular PE, just later. The chemicals that trigger PE are produced later in the pregnancy, and perhaps most significantly during labor, instead of before labor, but the threshold gets crossed in either case.

Delivery is the cure, but the cure isn't immediate, because our bodies still have to repair the damage. Getting the placenta out stops production of the chemicals, but they can hang around in your bloodstream for quite a while until your body produces enough VEGF to bind to all the sFlt and pull it out of the circulation. A similar thing happens with sEng. So the symptoms don't appear until later, but the thing that creates the symptoms is still the placenta, in the long run.

Postpartum PE is easier to treat because they don't have to worry about dropping your pressures too low for the placenta to be supplied with blood. One reason pressures rise in PE is that the placenta *wants them to* -- so that it is adequately supplied with blood -- and turning down pressures might make matters worse. But if you've already delivered, that isn't a worry. The trick is just to diagnose postpartum cases in the first place; they are really dangerous because care providers don't tend to think, aha! a pregnancy disease has appeared in this not-pregnant person!

Good question, and the answer is probably more complicated than even this explanation. I'm kind of rusty on my explanations and I don't mind corrections, but let me give it a shot:

One of the things in a PE pregnancy that deprives the placenta of oxygen, releasing all those nasty factors into our bloodstreams, is that the spiral arteries that attach the placenta to the uterus don't get deep enough, and as the placenta gets bigger it demands more and more blood (because that's what feeds the placenta), but the spiral arteries aren't able to supply enough, so the placenta ends up getting more and more hypoxic (lack of oxygen) and we get more PE symptoms.

If I'm understanding right, that's one of the prime theories for what happens in early-onset (before 34 weeks) PE.

Late-onset PE (37 weeks+? what is it between 34-37weeks? I'll see if I can get a reference on that...) *might* be due to something other than problems with the spiral arteries. Same with post-partum PE.

The factors - sFlt-1 and sEng - are produced in every normal pregnancy, it's just that they are produced a lot *more* in PE pregnancies. So to get PE at all there is something going on, but it might be something different in early-onset vs late-onset or pp PE. The thing to remember, though, is that the disease is the same and it's just as dangerous no matter what causes it.

So is that completely different from preeclampsia before birth?

Yep, pretty much.

Your body always produces something called VEGF, which keeps your vasculature -- your blood vessels -- running. Labor makes lots of sFlt-1 and sEng, which bind to VEGF and take it out of circulation. Labor could make you produce enough to tip over the diagnostic edge into preeclampsia or HELLP. Getting the placenta out removes the primary source of sFlt-1 and sEng, and your body keeps making VEGF, and eventually all the other chemicals have been bound to and removed from circulation, and the amount of free VEGF rises enough to start to repair the vasculature again.

Does that make any sense?

Caryn has a technical explanation here
http://www.preeclampsia.org/forum/viewt ... up#p156937

If I'm understanding right, the placenta produces (at least) two factors that lead to the symptoms of PE. The placenta produces more of these factors when it is deprived of oxygen. Deprivation of oxygen happens quite a bit in labor or in a c-section, so lots of the factors are spilling out into your bloodstream. Your body does have a system to clean up those factors (it may even use one of the factors that the placenta produces to do it?) but it takes a little time.

Does anyone know why some people get PE post pard? I don't really understand it especially since the baby and placenta are out. I am sure it's probaby not completely understood, but is there any theories or ideas?