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
Why not deliver?
Complications of prematurity
Possibility of failed induction needing
Caesarean section
Attempts to prolong pregnancy
Severe uncontrolled PE needs delivery after stabilisation
Severe PE
Diastolic BP >110 mm x 2
Systolic BP >160 x 2
> ++ proteinuria
Signs or symptoms of imminent eclampsia:
Hyper-reflexia (neuronal irritability)
Frontal headache
Blurred vision (cerebral vasospasm)
Epigastric tenderness (tension on liver capsule)
Prevention of seizures
Magnesium sulphate to women w PE reduces the risk of an eclamptic seizure
Reduced risk of placental abruption too
Helps to reduce risk of eclamptic seizure + lowers maternal mortality
HYPIDAT conclusion
induction of labour is recommended for women w mild PE or mild gestational hypertension at a gestational age beyond 37+0 weeks
PHOENIX conclusion
between 34-36+6 weeks induction of labour should be considered for women w mild/moderate complications vs expectant to 37+0 weeks, but w higher change of NNU admission (due to prematurity)
POSTNATAL MANAGEMENT
Carefully assess women w signs/symptoms or PE:
- After birth, BP raises again, as no longer needs to be low resistance
- But, if BP already v high + increases further after pregnancy, then risk of eclampsia
- BP tends to spike 3-5 post-birth
Assess need to continue anti-hypertensives
Arrange appropriate follow-up
An assessment of BP and proteinuria by the GP at 6 weeks postnatal check is recommended
If hypertension/proteinuria persists, then further investigation is needed
If still hypertensive after 6 weeks, then classified as chronic hypertension
