Pre-eclampsia Flashcards
What is PE?
PE is a disease of pregnancy:
only effective treatment is delivery
- Leading cause of iatrogenic prematurity for baby
- Immediate risks of eclampsia, stroke and heart failure
- Life long risk of CV disease for mother
PE risk factors
High risk: previous PE, chronic hypertension, autoimmune disease, DM, chronic kidney disease
Moderate risk: nulliparity, age>40, pregnancy interval >10yr, BMI>35, family hx PE, multiple pregnancy
PE pathophysiology
Originally thought to be a problem with a spiral artery remodelling
But now, thought to be more related to CVS
- results in systemic vasoconstriction and endothelial dysfunction
Failure of normal placentation: Normal placentation
Trophoblasts invade maternal vessels
Narrow spiral arteries remodelled
Wide-bore low-resistance vessels deliver large amounts of maternal blood
Nutrient + oxygen delivery to foetus
Failure of normal placentation: Normal placentation
Trophoblasts invade maternal vessels
Narrow spiral arteries remodelled
Wide-bore low-resistance vessels deliver large amounts of maternal blood
Nutrient + oxygen delivery to foetus
Failure of normal placentation: PE
Deficient TB invasion
SAs not remodelled
High-resistance placental bed
Poorly perfused hypoxic placenta
Deficient nutrient + oxygen delivery
Release of inflammatory cytokines (IL,TNF, etc)
Maternal endothelial dysfunction:
- increased vascular reactivity + vasospasm
- increased capillary permeability + reduced intravascular volume
Alternative hypothesis: CVS dysfunction
Thought that poor maternal cardiovascular reserve, poor adaption to pregnancy + XSive demands to meet that placenta= poor perfusion
Excessive demand-foetal macrosomia, twin pregnancy, prolonged pregnancy, excessive weight gain
Poor cardiac reserve- maternal age, obesity, ethnicity, diabetes, auto-immune diseasem chronic hypertension, chronic kidney disease
Common end pathway
Endothelial injury + vasoconstriction= end-organ damage follows:
- unsure of mechanism, but end result is confirmed
Effects of PE: Maternal
Cerebral oedema- eclampsia
Vasospasm- hypertension, renal failure
Endothelial injury- low platelets, disseminated intravascular coagulaopathy (DIC)
Albumin leakage- proteinuria, pulmonary oedema
- these women tend to be dry intravascularly to leakages, but can be dangerous
- traditionally given diuretics to get fluid out of the lungs
- but this can result in them being intravascularly depleted, but still having pulmonary oedema
Effects of PE: Foetal
Growth restriction
Prematurity
Placental abruption
Foetal death
Classification of hypertension in pregnancy:
<20/40 (before 20 weeks):
NO PROTEINURIA: pre-existing HTN
SIGNIFICANT PROTEINURIA: pre-existing HTN secondary to renal disease
> 20/40 (after 20 weeks):
NO PROTEINURIA: gestational HTN
SIGNIFICANT PROTEINURIA: PE
Signs and Symptoms
Can be asymptomatic
General symptoms: headaches, flashing lights, epigastric pain, nausea/vomiting, confusion, hypertension (use the right cuff and check for disappearance of sounds), proteinuria, brisk jerks
PE investigations:
24hr urinary protein / spot protein:creatinine ratio
Platelet count
LFT- liver enzymes (ALT)
U and E- creatinine
Clotting tests
sFlt-1:PlGF- VEGF and PlGF are usually involved in endothelial proliferation, and bind to membrane bound Flt-1 receptors to trigger these pathways. But when placenta becomes hypoxic, it releases soluble Flt-1 receptors, which still bind to VEGF and PlGF, but no endothelial proliferation
foetal assessment- US for growth and Dopplers (and possible check heartrate
sFlt1: PLGF ratio
The placenta releases GF- VEGF + PlGF- involved in promotion, proliferation + survival or vascular + endothelial cells
PlGF is a type of VEGF
Normal receptor is membrane bound Flt-1
Attached to the endothelium + when the VEGF + PlGF bind to it, promotes all the proliferative pathways + causes vasodilation- low resistance BF + optimum oxygen delivery
When the placenta becomes hypoxic, it starts to upregulate soluble Flt = sFlt-1
Therefore, VEGF + PlGF bind to sFlt-1 instead of membrane bound, so endothelium cannot promote vasodilation etc.,
- BVs become constricted
Results in vascular constriction + endothelial dysfunction
Ratio: High sFlt-1 + low PlGF = high ratio
Helps to correlate w severity of disease
BP management
Target BP = 130-140/80-90
1st line = labetalol (CI asthma, ischaemic heart disease,)
2nd line = nifedipine (CI aortic stenosis)
Consider = methyldopa (CI depression)
Point is not to prevent PE, but to reduce BP
