Pre-Eclampsia

Hypertension - a measured BP of >140/90mmHg on two occasions/4hrs apart

Chronic (essential) hypertension - BP >140/90mmhg at booking or before 20 weeks or already on anti-hypertensives

Gestational hypertension - sustained BP >140/90mmHg after 20 weeks gestation but without proteinuria in a previously normotensive patient

Pre-eclampsia

• Pre-eclampsia is a multi-system disorder of pregnancy
• It will develop in 25% of parturients with essential or gestational hypertension
• It is classically defined by a triad of:
1. Hypertension - new onset BP >140/90mmHg arising after 20 weeks gestation
2. Proteinuria - urine PCR >30mg/mmol, urinary protein >300mg/24hrs or 1+ proteinuria
3. Oedema - face, hands or feet


• Modern definitions recognise PET can be present without> proteinuria, but instead have other features of maternal or uteroplacental dysfunction (see below)

• Placental growth factor (PlGF)
• Decreased in PET, especially in severe PET
• Those <35 weeks with a PlGF <12pg/ml are likely to develop PET and require delivery within 14 days of testing
• Sensitivity 96%; NPV 98%


• Soluble fms-like tyrosine kinase 1 (sFlt-1)
• Increased in PET
• A high sFlt-1 - to - PlGF ratio indicates increased risk of PET
• This ratio has a sensitivity of 80% and a NPV of 99.3%


• Risk prediction models are recommended by NICE e.g. PREP-S (valid up to 34 weeks) or FullPIERS (at any gestational age)

• Healthy diet
• Regular aerobic exercise
• Aspirin 75 - 150mg daily from 12 weeks until delivery
• For women who have ≥2 moderate risk factors
• Reduces rates of pre-term PET (ASPRE trial)
• If dietary calcium is low, supplementation with >1g/day can lower chances of developing PET

• There's a maternal systemic inflammatory response which causes endothelial dysfunction
• There is a deficiency of the placentation process e.g. poor decidual invasion
• This leads to release of placental factors e.g. placental soluble factor
• There is placental ischaemia owing to this combination of restricted uteroplacental blood flow through abnormal arterial structure
• Uteroplacental hypoxia stimulates release of anti-angiogenic factors, which enter maternal bloodstream and injures maternal vasculature


• Endothelial dysfunction leads to:
• Vasospasm in the central retinal artery → visual disturbance
• Headache
• Glomerular disruption → proteinuria
• Vasoconstriction → hypertension

• Headache
• Visual disturbance e.g. flashing lights, blurred lights
• Altered mental state
• Papilloedema
• >3 beats clonus

• AKI - serum Cr >90μmol/L
• Urine protein-creatinine ratio >30

• Vomiting
• Subcostal pain
• RUQ tenderness
• Abnormal LFT's - ALT >70 iu/L or twice upper limit of normal

• Thrombocytopaenia <150 x10⁹/L
• HELLP syndrome (haemolysis, elevated liver enzymes and low platelets)
• Haemolysis demonstrated by LDH >600, bilirubin >20 or on a blood film
• Can lead to DIC

• Utero-placental dysfunction e.g. abnormal umbilical artery Dopplers, restricted foetal growth

• Target BP <135/85mmHg
• Blood pressure control is to reduce the risk of maternal intracranial haemorrhage (incidence 1.33/1000)


• Oral labetalol is first line treatment
• Oral nifedipine
• Oral methyldopa


• IV labetalol 20 - 50mg
• IV Hydralazine 5 - 10mg; can cause rapid decrease in SVR so consider fluid bolus alongside
• IV nifedipine 5 - 10mg


• IV magnesium is indicated to reduce the risk of progression to eclampsia (see below), although its panacea-like effects may help BP too

• This is more the domain of the obstetrician, but:
• Planned birth before 27 weeks if PET + severe features
• Birth initiated within 24 - 48hrs for those >37 weeks with onset of PET

• Restrict to 80ml/hr intake (up to 1ml/kg/hr)
• Ideally stop IV fluids; oral fluids only
• If IV fluids used, give through volumetric pump for accurate measurement
• Fluid balance monitoring, recording input and output accurately
• If urine output <0.5ml/kg/hr give a fluid challenge
• If no response to fluid challenge, consider invasive monitoring

• Patients are at risk of pulmonary oedema due to:
• Increased capillary endothelial leak
• Reduced plasma colloid oncotic pressure
• It is usually iatrogenic i.e. associated with fluid therapy
• Peak incidence is 48 - 72hrs post-partum


• Management involves:
• Fluid restriction (see above)
• Oxygen
• Furosemide 20 - 60mg
• Urgent delivery of foetus (if ante-partum)

• ABCDE
• Follow the magnesium infusion regime dervied from the Collaborative Eclampsia Trial protocol:
• 4g magnesium slow IV infusion over 5 - 15mins
• Followed by 1g/hr infusion which should be continued for 24hrs after the last fit
• Further 2g bolus if further fits
• Aim serum magnesium level 2 - 4mmol/L
• Diazepam, phenytoin and other anticonvulsants should not be used


• Urgent delivery of foetus should take place, but one should aim to stabilise the mother as much as possible prior to LSCS

• Urgent delivery of the foetus is indicated
• Require FBC within 2hr of attempted neuraxial anaesthesia as thrombocytopaenia may be rapidly progressive

• Prophylactic IV magnesium may be employed in severe PET as it reduces the risk of eclampsia by 50% (Magpie Trial, 2002)
• Dosing is the same as magnesium for eclampsia, namely 4g over 15mins followed by a 1g/hr infusion
• Maintain the infusion for 24 - 48hrs after delivery or last seizure, whichever comes later
• Aim serum magnesium level 2 - 4mmol/L

• ECG
• Saturations
• Heart rate
• Hourly non-invasive blood pressure (or arterial line)
• Fluid balance monitoring: fluid input & urine output
• Hourly reflexes/ankle clonus

• Clinical features include:
• Respiratory depression
• Cardiovascular depression
• Cardiac arrest
• Somnolence and drowsiness
• Muscle weakness or paralysis
• Loss of deep tendon reflexes
• Slurred speech
• Double vision
• Nausea and vomiting


• Management of toxicity includes stopping or reducing the rate of magnesium infusion, 10ml 10% calcium chloride IV over 10mins ± cardiovascular support ± respiratory support

• Neuraxial analgesia i.e. epidural is beneficial as it:
• Reduce sympathetic response to pain
• Facilitate cardiovascular stability i.e. reduce BP
• Improves uteroplacental fusion
• Facilitate top - up for operative intervention
• Ensure platelet count within 4hrs of attempted neuraxial intervention

• Neuraxial anaesthesia is preferential to GA owing to:
• Increased risk of airway difficulty; use smaller-than-expected ETT
• Increased pressor response to laryngoscopy risks intra-cerebral haemorrhage


• Ergometrine-containing uterotonics are contra-indicated owing to the risk of exacerbating hypertension
• One should continue existing MgSO₄ infusions but be aware they may prolong NMBA if GA technique used