- This can only occur in the second half (mainly 3rd trimester) of pregnancy
Definition
A pregnancy specific multi-system disorder with unpredictable, variable and widespread manifestations.
- Triad of signs
- Hypertension
- Proteinuria
- +/- Oedema
- Note that patients may be completely asymptomatic
Risk factors
- Maternal age (>40 doubles risk)
- Maternal BMI (>30 doubles risk)
- FHx (20-25% if mother; up to 40% if sibling)
- Parity
- Nulliparous women are 2-3 x more likely BUT
- Women who have had it in previous pregnancies are at a much higher risk than even nulliparous women (7- fold increase)
- Other PMHx e.g. renal disease/ DM/ connective tissue disease/ thrombophilia/ pre-existing hypertension
- Multiple pregnancy (twins doubles risk)
- Genetic abnormalities (triploidy) or Molar pregnancies
Pathophysiology
- A patient is at a much higher risk of developing pre-eclampsia if
- a family member has had it (there is a genetic predisposition)
- she has had it before
- Caused by a diffuse vascular endothelial dysfunction
- via release of angiogenic and angiolytic factors
- This causes widespread circulatory disturbanc to the liver; kidneys; CVS; CNS; placenta etc
- There are different stages of pre-eclampsia:
- Abnormal placental perfusion
- The pathophysiology of this is better known than the second stage:
- There is abnormal placentation and trophoblast invasion of the endometrium in which there is a failure of vascular remodelling of the spiral arteries
- This means the spiral arteries fail to become high-capacitance, low-resistance vessels
- The result is placental hypoxia and ischaemia
- The pathophysiology of this is better known than the second stage:
- Maternal syndrome
- The mechanism by which placental ischaemia causes widespread endothelial dysfunction is poorly understood:
- It is possible that oxidative stress mechanisms / PGI2/TXA2 (prostaglandin) imbalance / the role of Nitrogen compounds (NO) etc cause endothelial activation
- This increases capillary permeability; increases expression of cell adhesion molecule (CAM); increases the amount of pro-thrombotic factors; increases platelet aggregation; causes vasoconstriction (NB norm is vasodilation)
- This has multisystem effects (see below)
- The mechanism by which placental ischaemia causes widespread endothelial dysfunction is poorly understood:
- Abnormal placental perfusion
Multisystem effects:
Signs/Symptoms
- Headache, visual disturbance, epigastric/RUQ pain, nausea/vomiting, rapidly progressive oedema
- Raised BP; proteinuria; oedema; abdominal tenderness; disorientation/confusion; small for gestational age uterus; IUD; hyper-reflexia/clonus/involuntary movements
- Features of severe pre-eclampsia include
- Severe hypertension >170/110mmHg and proteinuria ++/+++
- Headache
- Visual disturbance
- Papilloedema
- RUQ/Epigastric pain
- Hyperreflexia
- Platelet count <100 (x10^6/l); abnormal liver enzymes (HELLP syndrome- haemolysis/elevated liver enzymes/low platelet count)
HELLP syndrome is usually in conjunction with pre-eclampsia and is managed in the same way (BP control; ultimately, delivery; may require blood products where clinically indicated; steroids for the foetal lung development)
Investigations
- U&Es
- Raised Creat, K, urea
- Also request serum uric acid (urate)- raised
- LFTs
- Abnormal liver enzymes
- FBC
- Coagulation screen
- USS (biometry / AFI / doppler)
Management
- Assess risk at booking and in first trimester
- If BP rises in first trimester, assess for other causes
- Antenatal screening:
- BP; urine; Maternal uterine artery doppler (MUAD)
When to refer?
- Day case referral if any of the 3 major signs or concerning symptoms e.g. persistent headache
- Admission require if:
- BP>170/110 (alone) or >140/90 + proteinuria
- Significant symptoms e.g. headache, visual sx or RUQ pain
- Abnormal biochemistry
- Significant proteinuria (>300mg/day)
- Need for antihypertensive treatment
- Signs of foetal compromise
Inpatient assessment
- BP 4 hourly; Daily urinalysis; Fluid balance chart +/- urine collection for protein; regular bloods
- Foetal surveillance
- Foetal movements
- CTG
- USS
- biometry; amniotic fluid index (AFI)
- Umbilical artery doppler
Treatment
- Advise women at high risk of pre-eclampsia to take 75 mg of aspirin* daily from 12 weeks until the birth of the baby. Women at high risk are those with any of the following:
- hypertensive disease during a previous pregnancy
- chronic kidney disease
- autoimmune disease such as systemic lupus erythematosis or antiphospholipid syndrome
- type 1 or type 2 diabetes
- chronic hypertension.
- Advise women with more than one moderate risk factor for pre-eclampsia to take 75 mg of aspirin* daily from 12 weeks until the birth of the baby. Factors indicating moderate risk are:
- first pregnancy
- age 40 years or older
- pregnancy interval of more than 10 years
- body mass index (BMI) of 35 kg/m2 or more at first visit
- family history of pre-eclampsia
- multiple pregnancy.
Pharmacological treatment- acute
Delivery
- Delivery is the only ‘cure’
- Mother must be stabilised beforehand
- Offer induction in patients < 34 weeks if they have severe hypertension refractory to treatment or other complications necessitating delivery
- Offer induction in patients 34-36+6 weeks if they have mild-moderate hypertension, depending on maternal and foetal condition, risk factors and services
- Recommend immediate induction (within 24-48 hours) for patients >37 weeks