Pre-eclampsia

  • 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
    1. Hypertension
    2. Proteinuria
    3. +/- 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:
    1. Abnormal placental perfusion
      1. The pathophysiology of this is better known than the second stage:
        1. There is abnormal placentation and trophoblast invasion of the endometrium in which there is a failure of vascular remodelling of the spiral arteries
        2. This means the spiral arteries fail to become high-capacitance, low-resistance vessels
        3. The result is placental hypoxia and ischaemia
    2. Maternal syndrome
      1. The mechanism by which placental ischaemia causes widespread endothelial dysfunction is poorly understood:
        1. It is possible that oxidative stress mechanisms / PGI2/TXA2 (prostaglandin) imbalance / the role of Nitrogen compounds (NO) etc cause endothelial activation
        2. 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)
        3. This has multisystem effects (see below)

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)
A is normal; B is abnormal with notching (arrow)- worrying sign 

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
Reduced / Absent flow is a marker of increased resistance to flow across the placenta.
Reversal of flow occurs when the pressure is so great as to push the flow back (worrying).

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

bp

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
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