Age + Dev - Pre-eclampsia in Preganancy

Question 1

What is the epidemiology of pre-eclampsia?

Answer 1

→ Occurs in around 2-4% of pregnancies in USA and Europe (incidence rising?)
→ More common in Africa and Asia (8% to as high as 16%?)
→ ~1/10 maternal deaths in Africa and up to 1/4 in South America are associated with gestational hypertensive disorders (including PE).
→ Estimated to cause 50,000-60,000 maternal deaths per year
→ Precise underlying causes remain a mystery

Question 2

What are the symptoms for pre-ecclampsia?

Answer 2

→ New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
→ Occurring after 20 weeks’ gestation
→ Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases
→ Oedema common but not discriminatory for PE
→ Headache (in around 40% of severe PE patients)
→ Abdominal pain (in around 15% of severe PE patients)
→ Visual disturbances, seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)

Question 3

What are the different main subtypes of PE?

Answer 3

→ early onset

→ late onset

Question 4

What are the features of early onset PE?

Answer 4

→ < 34 weeks
→ Associated with fetal and maternal symptoms
→ Changes in placental structure

Question 5

What are the features of late onset PE?

Answer 5

→ >34 weeks
→ More common (90%)
→ Mostly maternal symptoms
→ Foetus generally OK
→ Less overt/no placental changes

Question 6

What are the risk factors that predispose women to PE?

Answer 6

→ Previous pregnancy with pre-eclampsia
→ BMI >30 (esp >35)
→ Family history
→ Increased maternal age (>40, <20?)
→ Gestational hypertension or previous hypertension
→ Pre-existing conditions: diabetes, PCOS, renal disease, subfertility, autoimmune disease.
→ Non-natural cycle IVF?
→ multiple pregnancies
→ ethnicity : asian
→

Question 7

What are the main risks to the mother?

Answer 7

→ damage to kidneys, liver, brain and other organ systems
→ HELLP
→ Possible progression to eclampsia (seizures, loss of consciousness)
→ Placental abruption (separation of the placenta from the endometrium)

Question 8

What are the main risks for the foetus?

Answer 8

→ foetal growth restriction
→ reduced foetal growth
→ preterm birth
→ pregnancy loss or stillborn

Question 9

What is the normal progression of EVT invasion?

Answer 9

→ EVT invasion of maternal spiral arteries leads to endothelial and smooth muscle breakdown
→ EVT become endothelial EVT and spiral arteries become high capacity

Question 10

What is EVT invasion like in PE?

Answer 10

→ EVT invasion of maternal spiral arteries is limited to decidual layer
→ Spiral arteries are not extensively remodelled, thus placental perfusion is restricted

Question 11

What is PLGF?

Answer 11

→ placental growth factor

→ VEGF related, pro-angiogenic factor released in large amounts by the placenta

Question 12

What is Flt1?

Answer 12

→ soluble VEGFR1

→ soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailability

Question 13

What happens to Flt1 and PLGF in PE?

Answer 13

excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction

Question 14

How is PE picked up on?

Answer 14

regular checks in antenatal appointments :
→ blood pressure check
→ urine tests to check for protein in urine

Question 15

What can be used to predict onset of PE?

Answer 15

PLGR levels alone or Flt-1/PIGR ratio

Question 16

How is PLGR alone used to predict PE?

Answer 16

→ Triage test (rules out PE in next 14 days in women 20-36 weeks + 6 days)
→ PLGF < 100 = abnormal and high risk for preterm delivery
→ under 12 is highly abnormal

Question 17

How is sFlt-1/PLGR ratio used to predict PE?

Answer 17

→ ratio under 38 rules out PE

→ ratio over 38 = increased risk of pre-ecclampsia

Question 18

How is PE managed?

Answer 18

→ PE can only be resolved by delivery of the placenta
→ If <34 weeks, preferable to try and maintain the pregnancy if possible for benefit of the fetus
→If >37 weeks, delivery preferable
→ Anti-hypertensive therapies
→ Corticosteroids for <34 weeks to promote fetal lung development before delivery.

Question 19

How can PE be prevented?

Answer 19

→ Weight loss (esp if BMI >35)
→ Exercise throughout pregnancy (seems to work independent of BMI)
→ Low-dose asprin (from 11-14 weeks) for high risk groups – but may only prevent early onset

Question 20

What are the long-term impacts of PE on maternal health?

Answer 20

→ Elevated risk of cardiovascular disease, type 2 diabetes and renal disease after PE
→ Roughly 1/8 risk of having pre-eclampsia in next pregnancy (greater if early onset)