The scientific basis of our work, to expand. Our own publications follow directly below.
Placentation: the common origin
In the first weeks of pregnancy, cells of the placenta (trophoblast) migrate into the uterine wall and remodel the maternal spiral arteries into wide, low-resistance vessels. If this remodelling remains incomplete, the placenta is undersupplied. Depending on the extent, the pregnancy ends early, or the consequences appear later as pre-eclampsia, HELLP syndrome, growth restriction, placental abruption or preterm birth. In 2011 Brosens and colleagues grouped these conditions as disorders of deep placentation (“Great Obstetrical Syndromes”).
Immunology of pregnancy
Half of the embryo's characteristics come from the father. To prevent rejection, the maternal immune system has to adapt at the interface with the placenta: specialised immune cells of the uterine lining support vascular remodelling, regulatory cells dampen defence reactions. If this tolerance is insufficient, implantation and placental development can be impaired. Research on tests and treatments in this field is ongoing; the guidelines assess them cautiously.
Haemorheology: the flow properties of blood
The supply of the placenta depends not only on the vessels but also on how well the blood flows. Key factors include plasma viscosity, haematocrit, and the deformability and aggregation of red blood cells. In a normal pregnancy plasma volume increases, the blood is physiologically diluted and flows more easily in the smallest vessels. If this adaptation fails, studies show an increased risk of pre-eclampsia and growth restriction. We have published our own studies on the flow properties of blood in pregnancy and in complications.
Blood clotting in pregnancy
During pregnancy almost all clotting factors rise, some to three times their level. This protects against major blood loss at birth but increases the risk of thrombosis several-fold. Around 60% of all pregnancy-related thromboses are observed after delivery. Normalisation usually takes several weeks (up to about 6 weeks). In women with a known bleeding tendency, for example due to platelet disorders or a factor deficiency, this adaptation may be delayed. Whether this results in a bleeding risk in pregnancy or after birth must be assessed individually.
Recurrence risks after pre-eclampsia
There is no exact prediction of the individual risk. However, statistical data on the timing, severity and accompanying circumstances of the earlier disease allow a rough estimate.
The risk of recurrence depends mainly on when the disease first occurred:
| First onset | Risk of recurrence |
|---|
| up to week 28 | approx. 39% |
| weeks 29–32 | approx. 29% |
| weeks 33–36 | approx. 22% |
| from week 37 | approx. 3% |
After HELLP syndrome the risk of another HELLP syndrome is about 13%; after eclampsia the risk of pre-eclampsia is 22 to 35%. Gestational hypertension recurs in 16 to 47%.
Guidelines at a glance
For further reading: AWMF guideline Recurrent miscarriage, ESHRE Recurrent Pregnancy Loss (2022), AWMF guideline Diagnosis and therapy before assisted reproduction, AWMF guideline Hypertensive disorders in pregnancy, AWMF guideline Prevention of venous thromboembolism.