consequences of poor placentation - pre-eclampsia Flashcards
Define pre-eclampsia(PE)
- characterized by hypertension
Why is pre- eclampsia important?
- MBRACE report
- 6th leading cause of direct maternal deaths in 2018
- commonest medical problem in pregnancy
- gestational hypertension (high BP)= 10% - no damage
-PE= 2-5% - damage - Severe PE = 1%
-Eclampsia (2% death rate)
leading cause of iatrogenic (inducing labour when there is danger) prematurity
-immediate risks of eclampsia, stroke and heart failure
-life long risk of CVS
pre-eclampsia and CVD
stress of pregnancy - stresses your CVS that it tips you into the pre- eclampsia
so does pre-eclapsia cause CVD or does pre-eclampsia trigger your predisposition and thats what can help predict you were going to have CVS in later life anyways
High risk factors of pre-eclampsia
- previous pre - eclampsia
-chronic hypertension
-diabetes mellitus
-chronic kidney disease
moderate risk factors of preeclampsia
- nulliparity - dk how pregnancy is gonna go bc never had a baby before
- age >40
-pregnancy interval 10 yr - you become older
-BMI >35 , heart is already in strain and pregnancy adds up
-family history pre - eclampsia - if your mum had pre-eclampsia then you are more likely to have it, when youre in a stress environment it turns on and off genes and also puts more stress on the heart
-multiple pregnancy - 2x more demand in CVS
pathophysiology of preclampsia
- placentation = placenta embeds into endometrium and transfers muscular placenta releases cytokines
HELP syndrome = multi organ disfunction - baby can be very small bc not getting enough nutrients
- to reverse preeclampsia you the placenta needs to come out so the baby has to come out
failure of normal placentation leads to preclampsia
Normal
* Trophoblasts invade maternal
vessels
* Narrow spiral arteries remodelled
* Wide-bore low-resistance vessels
deliver large amounts of maternal
blood
* Nutrient and oxygen delivery to
fetus
PE
Deficient trophoblast invasion
* Spiral arteries not remodelled - coiled and narrow
* High-resistance placental bed
* Poorly perfused hypoxic placenta
* Deficient nutrient and oxygen
delivery
* Release of inflammatory cytokines (IL,
TNF etc)
* Maternal endothelial dysfunction:
– Increased vascular reactivity and
vasospasm
– Increased capillary permeability
and reduced intravascular volume
Alternative hypothesis to placenta remodelling: CV dysfunction what causes pre- eclampsia
- maternal cardiovascular health is determined by :
cerebrovascular morbidity, chronic kidney disease, cardiovascular morbidity, ethnicity, lifestyle and genetics, diabetes, weight gain and stress of preganancy, prolonged pregnancy
using these factors we can predict pre- eclampsia
maternal effects of PE
– Cerebral oedema: eclampsia
– Vasospasm: hypertension,
renal failure
– Endothelial injury: low
platelets, disseminated
intravascular coagulopathy
(DIC)
– Albumin leakage: proteinuria,
pulmonary oedema
fetal effects
– Growthrestriction
– Prematurity
– Placentalabruption
– Fetal death
current screening and prevention program for PE
prevention is the best cure for PE
aspirin reduces systematic PE - reduces clotting
NICE 2019 guidlines
-1 high risk factor or 2 moderate risk factors use 75-150mg of aspirin from 12 weeks according to NICE 2019
problem with screeninga and predicting PE
does not have sensitivity - only 40% detection rate
so we use an algorithm of risk factors detection risk increases to 90%
Algorithm study to observe the effects of aspirin in high risk PE women
26, 491 women were screened
2,900 were detected to have high risk for pre term <37 weeks PE
800 were given aspirin and 800 were given placebo - some women out of 2900 dropped out bc they were on aspirin and it was unethical to not give aspirin.
The results showed women on aspirin had 62% reduction in pre term PE (<37 weeks) compared to 38% in placebo
and women in early term PE (<34w) had 82% reduction on aspirin compared to 18% placebo
++ RCT are strict conditions, and lots of scans and monitoring but this is not possible in the clinical setting in the real world due to NHS strain in resources and staff but at st georges hospital this trial findings were applied.
- 2 folds decrease in maternal risk 16% to 8%)
-two fold increase in PE detection (41% vs 76% )
-almost complete physician compliance with aspirin, to prevent missing out a PE which can cause miscarriage (29% vs 99%)
-reduction the prevalence of preterm PE (80%)
classification of pre-eclampsia
PE at <20 weeks and there is no protienuria then PE is due to pre- existing hypertension , if there is protein urea then it may be secondry renal disease caused hypertension
if PE happens at >20 weeks and there is no proteinuria then its gestational hypertension
but if at > 20 weeks and significant protein urea then it is pre-eclampsia
Diagnostic
algorithm based clinical diagnostic is emerging in hospitals
sFLt- 1 : PlGF ratio
PlGF is a vascular endothelial growth factor which is released and binds to the Flt-1 on receptors on endothelial cells to allow vasodilation and normal healthy proliferation.
in PE there are soluable free floating sFlit-1receptors which mop up the PlGF and prevent it from binding to the endothelial cells.
So high levels of sFLt- 1 and low levels of PlGF is important in predicting PE
cost analysis of sFlt-1: PIGF
quality adjusted life score
between 35- 37 weeks you don’t save much £174 whereas if you present at earlier weeks you save more £ 2488
