Ok - this intrigues me.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.)
Baby #1 - 8lbs1oz at 37 weeks. I had fewer growth scans, but I remember she was measuring a week ahead at 12 and 20 weeks (and I'm sure about my dates)
Baby #2 - EFW over 1 lb at 20 weeks; I forgot to ask percentiles, but I think I saw something on-screen about 95th percentile. Currently 22 weeks, so outcome is open. On Toprol this pregnancy but not with #1.
Everyone (my providers included) seems concerned about IUGR and blood flow to the fetus. But I wonder: If my history is that I manage to both have superimposed PE and grow a very nicely sized baby in the past, how should I apply that to my current pregnancy? Does it have any relevance at all?
It just seems so uncontrollable and unforeseeable.