Pre-eclampsia and eclampsia

10 min read Last updated April 8, 2026

Surgical approach (obstetric management context)

  • Definitive treatment is delivery of placenta (timing depends on maternal/fetal status and gestation)
    • Stabilise mother first (BP control, seizure prophylaxis, optimise oxygenation/volume status), then plan delivery
    • Mode of delivery: induction/assisted vaginal delivery if feasible; caesarean section if urgent maternal/fetal indication or unfavourable cervix
  • Common obstetric indications for urgent delivery
    • Eclampsia, uncontrolled severe hypertension, pulmonary oedema, HELLP, placental abruption, DIC, fetal compromise, severe growth restriction with abnormal Dopplers
  • Peri-delivery haemorrhage risk management
    • Abruption and coagulopathy increase PPH risk; anticipate blood products, uterotonics, possible cell salvage (local policy), and escalation to theatre/IR/hysterectomy if refractory

Anaesthetic management (typical scenarios: labour analgesia / CS / ICU)

  • Type of anaesthesia
    • Prefer regional (labour epidural; spinal/CSE for CS) if no contraindications (platelets/coagulation/neurology/raised ICP/airway concerns manageable)
    • GA if urgent delivery with contraindication to neuraxial, severe maternal compromise, or failed regional; anticipate difficult airway and hypertensive response to laryngoscopy
  • Airway device
    • GA: ETT (RSI). Avoid SGA as primary in obstetric GA except rescue per local guidance
  • Duration
    • CS typically ~45–90 min (variable with urgency/complexity); ongoing HDU/ICU care may be required post-delivery
  • How painful
    • Labour: severe visceral/somatic pain; neuraxial analgesia beneficial (also blunts catecholamine surges and assists BP control)
    • CS: major abdominal surgery; neuraxial anaesthesia provides excellent intra-op and early post-op analgesia; consider multimodal post-op (paracetamol ± opioids; NSAIDs only if renal function/platelets/BP allow)
  • Key anaesthetic aims
    • Prevent stroke/ICH (control severe BP), prevent seizures (magnesium), avoid hypoxia/hypercarbia, maintain uteroplacental perfusion, manage fluid carefully (avoid pulmonary oedema), anticipate coagulopathy and difficult airway

Definitions and diagnostic criteria

  • Pre-eclampsia: new-onset hypertension after 20 weeks’ gestation with maternal organ dysfunction and/or uteroplacental dysfunction
    • Hypertension: ≥140/90 mmHg on 2 occasions (or severe ≥160 systolic or ≥110 diastolic)
    • Proteinuria supports diagnosis but is not required if organ dysfunction present
  • Maternal organ dysfunction examples
    • Renal: creatinine rise/oliguria; Hepatic: transaminitis, RUQ/epigastric pain; Neurological: headache, visual symptoms, hyperreflexia, clonus; Haematological: thrombocytopenia, haemolysis; Pulmonary oedema
  • Uteroplacental dysfunction examples
    • Fetal growth restriction, abnormal umbilical artery Dopplers, placental abruption, stillbirth
  • Eclampsia: tonic–clonic seizures in a woman with pre-eclampsia (or with features suggestive of pre-eclampsia) not attributable to other causes
  • HELLP: Haemolysis, Elevated Liver enzymes, Low Platelets (variant/severe form of pre-eclampsia)

Epidemiology and risk factors

  • Incidence: pre-eclampsia ~2–8% pregnancies; eclampsia rarer in high-resource settings
  • Risk factors
    • Previous pre-eclampsia, chronic hypertension, CKD, diabetes, autoimmune disease (APS/SLE), multiple pregnancy, first pregnancy/new partner, obesity, advanced maternal age, assisted reproduction

Pathophysiology (high-yield)

  • Abnormal placentation → poor spiral artery remodelling → placental ischaemia
  • Release of anti-angiogenic/inflammatory mediators → endothelial dysfunction
    • ↑ SVR and vasospasm → hypertension, reduced organ perfusion
    • Capillary leak → oedema, pulmonary oedema, airway oedema
    • Coagulation activation/platelet consumption → thrombocytopenia, DIC risk
  • Intravascular volume often low/normal despite oedema; LV dysfunction may coexist
  • Cerebral effects: loss of autoregulation/vasogenic oedema (PRES) → headache, visual symptoms, seizures, intracranial haemorrhage

Clinical features and severity

  • Symptoms/signs suggesting severe disease
    • Severe headache, visual disturbance, RUQ/epigastric pain, dyspnoea/pulmonary oedema, reduced fetal movements, confusion, clonus
  • Complications
    • Maternal: stroke/ICH, eclampsia, pulmonary oedema, AKI, hepatic rupture, DIC, abruption, PPH, aspiration, difficult airway
    • Fetal: prematurity, growth restriction, hypoxia, stillbirth

Investigations and monitoring (perioperative focus)

  • Baseline bloods
    • FBC (platelets), U&E/creatinine, LFTs, coagulation profile (esp if platelets low/abruption/bleeding), group & save/crossmatch
  • Urine
    • Protein:creatinine ratio or 24h protein (diagnostic support); strict urine output monitoring (catheter if severe/operative/oliguria)
  • Maternal monitoring
    • Frequent BP (consider arterial line for severe/unstable BP, IV antihypertensives, GA, or major haemorrhage risk)
    • Continuous pulse oximetry; ECG; fluid balance; consider CXR/echo if pulmonary oedema or suspected cardiomyopathy
  • Fetal monitoring
    • CTG and obstetric ultrasound/Dopplers as indicated; coordinate timing with obstetrics/neonatology

Antihypertensive therapy (acute and perioperative)

  • Treat severe hypertension promptly to reduce stroke risk (local thresholds; commonly ≥160 systolic and/or ≥110 diastolic)
  • Common agents (UK practice)
    • IV labetalol (bolus/infusion) or oral labetalol; IV hydralazine; oral nifedipine (modified release commonly; immediate-release per protocol)
    • Avoid precipitous hypotension (maintain uteroplacental perfusion); titrate with close BP monitoring
  • Peri-intubation (if GA)
    • Blunt pressor response: opioids (balanced against neonatal depression), magnesium effect, short-acting agents per local practice; ensure deep anaesthesia before laryngoscopy

Seizure prophylaxis and treatment (magnesium sulphate)

  • Indications
    • Eclampsia (treatment), severe pre-eclampsia (prophylaxis), recurrent seizures, neurological symptoms/signs
  • Typical regimen (know principle; follow local protocol)
    • Loading dose IV over ~10–20 min then maintenance infusion for ~24 h (or 24 h after last seizure/delivery, depending on protocol)
  • Monitoring and toxicity
    • Monitor RR, SpO2, reflexes, urine output; toxicity: loss of reflexes → respiratory depression → cardiac arrest
    • Antidote: calcium gluconate IV (per protocol) and supportive care/ventilation
  • Anaesthetic interactions
    • Potentiates non-depolarising neuromuscular blockers; may reduce MAC; caution with opioids/sedatives and in renal impairment (reduced excretion)

Fluid management and pulmonary oedema

  • Principles
    • High risk of pulmonary oedema due to capillary leak, low oncotic pressure, LV dysfunction, iatrogenic overload
    • Aim euvolaemia; cautious crystalloid; avoid routine large preloads for neuraxial; use vasopressors judiciously
  • If pulmonary oedema
    • Oxygen/CPAP or ventilation, diuretics (e.g., furosemide), treat hypertension, consider echo and ICU; restrict fluids

Neuraxial anaesthesia/analgesia

  • Benefits
    • Avoids GA airway risks; attenuates stress response; epidural provides controllable block and excellent analgesia; facilitates operative delivery if needed
  • Key considerations
    • Platelets/coagulation: assess trend and clinical context (HELLP can deteriorate rapidly). Follow local neuraxial thresholds and senior decision-making
    • Hypotension may be less pronounced than normal pregnancy (high SVR), but still treat promptly to maintain uteroplacental perfusion
    • Vasopressors: phenylephrine or ephedrine per local obstetric practice; titrate carefully in severe hypertension
  • Spinal/CSE for CS
    • Consider lower intrathecal dose if haemodynamically fragile; CSE allows titration; invasive BP monitoring if severe disease

General anaesthesia for CS (when required)

  • Indications
    • Immediate threat to life of mother/baby, contraindication to neuraxial (coagulopathy/very low platelets/anticoagulation), failed neuraxial, severe maternal respiratory failure/raised ICP concerns
  • Preparation
    • Anticipate difficult airway (airway oedema): senior help, videolaryngoscope, smaller ETT, airway rescue plan, aspiration prophylaxis
    • Arterial line pre-induction if time; two large-bore IVs; blood available; magnesium running if indicated
  • Induction and maintenance
    • RSI with cricoid (local policy). Blunt hypertensive response (adequate depth; consider short-acting adjuncts per protocol). Avoid hypoxia/hypercarbia
    • After delivery: opioid/benzodiazepine as needed; uterotonics cautiously (oxytocin slow/infusion; avoid large bolus). Ergometrine can worsen hypertension; carboprost caution (bronchospasm/pulmonary HTN)
  • Extubation
    • Only when fully awake, haemodynamically stable, no pulmonary oedema; consider ICU ventilation if ongoing severe disease, oedema, or magnesium-related respiratory risk

Haematology: thrombocytopenia, HELLP, DIC and neuraxial decision-making

  • Thrombocytopenia may reflect severity and can fall rapidly (especially HELLP)
  • Assess bleeding risk holistically
    • Platelet count and trend, clinical bleeding, coagulation tests, liver dysfunction, abruption, anticoagulants, previous neuraxial puncture difficulty
    • Consider viscoelastic testing (TEG/ROTEM) where available to guide transfusion/haemostasis in haemorrhage/DIC
  • Blood product considerations
    • Platelets for active bleeding/operative delivery with significant thrombocytopenia per obstetric/haematology guidance; correct fibrinogen early in major obstetric haemorrhage

Postpartum care

  • Disease can worsen after delivery; continue close monitoring (BP, urine output, symptoms) and magnesium as indicated
  • Analgesia
    • Paracetamol ± opioids; NSAIDs only if renal function adequate, no significant thrombocytopenia/bleeding risk, and BP control acceptable (follow local guidance)
  • Thromboprophylaxis
    • Increased VTE risk; LMWH timing must consider neuraxial catheter removal and platelet count; follow obstetric VTE and neuraxial anticoagulation guidance
  • Critical care
    • HDU/ICU for severe hypertension, ongoing magnesium with respiratory risk, pulmonary oedema, AKI, HELLP/DIC, neurological symptoms, invasive monitoring needs
You are asked to anaesthetise a 32-year-old at 35 weeks with severe pre-eclampsia for category 2 caesarean section. Talk through your anaesthetic plan.

Structure: assess severity/complications → decide regional vs GA → monitoring/lines → BP/seizure control → fluid/haemostasis → postoperative destination.

  • Rapid assessment: symptoms (headache/visual/RUQ pain/dyspnoea), neuro signs (clonus), airway oedema, urine output, pulmonary oedema
  • Review investigations: platelets (trend), Hb, U&E/Cr, LFTs, coagulation; group & save/crossmatch
  • Optimise: treat severe BP with IV labetalol/hydralazine per protocol; magnesium if severe features/for prophylaxis; avoid fluid overload
  • Monitoring/lines: consider arterial line; 2 IV cannulae; urine catheter; left uterine displacement
  • Anaesthetic technique: regional preferred if coagulation acceptable—spinal/CSE with titration; manage hypotension with vasopressors carefully
  • If GA required: RSI with ETT; difficult airway plan; blunt pressor response; cautious uterotonics (avoid ergometrine if hypertensive)
  • Post-op: HDU/ICU if severe; continue BP control and magnesium; monitor for pulmonary oedema/bleeding/AKI
What are the anaesthetic implications of magnesium sulphate therapy?

Think: toxicity monitoring, drug interactions, and perioperative respiratory risk.

  • Potentiates non-depolarising neuromuscular blockade → use nerve stimulator; expect prolonged paralysis; adjust doses
  • Can cause hypotension/flushing; may reduce anaesthetic requirements
  • Toxicity: loss of reflexes → respiratory depression → cardiac arrest; higher risk with renal impairment
  • Monitoring: RR, SpO2, reflexes, urine output; have calcium gluconate available
Discuss neuraxial anaesthesia in pre-eclampsia, including thrombocytopenia.

Examiners want a balanced risk assessment: benefits of neuraxial vs risk of spinal/epidural haematoma and haemodynamic issues.

  • Benefits: avoids GA airway risk; improves analgesia; may improve BP control by reducing catecholamines; provides route for operative anaesthesia
  • Assess platelets and trend; HELLP can deteriorate quickly—repeat count close to procedure if concern
  • Consider overall coagulation/bleeding risk (coags, clinical bleeding, abruption, anticoagulants); use senior/haematology input and local thresholds
  • Haemodynamics: hypotension may be less than normal pregnancy but still treat promptly; avoid large fluid preloads; vasopressors titrated
A woman with eclampsia has a seizure on labour ward. What is your immediate management?

Use an ABC approach, treat the seizure, control BP, and plan delivery once stabilised.

  • Call for help: obstetrics, anaesthetics, senior midwife, neonatal team; prepare for transfer to theatre/ICU
  • ABC: left lateral tilt, high-flow oxygen, protect airway, suction, consider early intubation if recurrent seizures/low GCS/aspiration risk
  • Stop seizure: magnesium sulphate (load then infusion per protocol). If ongoing seizure despite Mg: benzodiazepine per protocol and secure airway/ventilate
  • Control severe hypertension with IV labetalol/hydralazine; avoid hypotension
  • Assess complications: hypoxia, aspiration, abruption, pulmonary oedema, stroke; send bloods incl FBC/LFT/U&E/coags; catheterise
  • Plan delivery once stabilised (often urgent); choose anaesthetic technique based on maternal status/coagulation/urgency
How does pre-eclampsia affect cardiovascular physiology and response to spinal anaesthesia?

Key concepts: high SVR, relative intravascular depletion, endothelial dysfunction, and variable cardiac function.

  • ↑ SVR and vasoconstriction; capillary leak with oedema but intravascular volume often low/normal
  • Spinal-induced sympathectomy may cause hypotension, but often less severe than in normotensive pregnancy; still treat promptly to protect uteroplacental perfusion
  • Some patients have LV dysfunction/diastolic impairment → sensitive to fluid loading; risk pulmonary oedema
What are the causes of pulmonary oedema in pre-eclampsia and how would you manage it perioperatively?

Think: Starling forces + cardiac function + iatrogenic factors.

  • Causes: capillary leak/endothelial dysfunction, low oncotic pressure, LV dysfunction, severe hypertension, fluid overload, tocolytics (if used)
  • Management: oxygen/CPAP, diuretics, restrict fluids, treat hypertension, consider echo/CXR, ICU involvement; ventilate if failing
  • Anaesthetic implications: avoid GA if possible; if GA needed, careful induction, PEEP, avoid excessive fluids; invasive monitoring may help
Describe the differential diagnosis of a seizure in pregnancy and how you would distinguish eclampsia.

Eclampsia is a diagnosis of exclusion but treat immediately if suspected.

  • Differentials: epilepsy, intracranial haemorrhage/stroke, cerebral venous sinus thrombosis, meningitis/encephalitis, hypoglycaemia, hyponatraemia, drug toxicity/withdrawal, amniotic fluid embolism (collapse), local anaesthetic toxicity
  • Suggestive of eclampsia: hypertension after 20 weeks, proteinuria/organ dysfunction, headache/visual symptoms, hyperreflexia/clonus, RUQ pain, thrombocytopenia/LFT derangement
  • Management principle: treat as eclampsia immediately (MgSO4, BP control, ABC) while investigating other causes
What are the key causes of maternal death in severe pre-eclampsia/eclampsia, and how does anaesthesia reduce risk?

Focus on preventable perioperative contributors: stroke, airway, aspiration, haemorrhage, pulmonary oedema.

  • Major threats: intracranial haemorrhage/stroke, pulmonary oedema/respiratory failure, aspiration, haemorrhage/DIC/abruption, multiorgan failure
  • Anaesthetic risk reduction: rapid BP control, magnesium therapy, early neuraxial where safe, difficult airway planning, cautious fluids, early ICU escalation, haemorrhage preparedness
You are called to a category 1 CS for fetal bradycardia in a woman with suspected HELLP. Platelets are 65 x10^9/L. What do you do?

This is a high-stakes decision: urgency vs neuraxial safety vs GA risk. Examiners want structured decision-making and escalation.

  • Immediate actions: call senior anaesthetist/consultant, obstetric consultant, haematology; activate major obstetric haemorrhage readiness; obtain current labs and trend if possible
  • Neuraxial: with platelets 65 and suspected HELLP (potential rapid fall), neuraxial is usually high risk—decision depends on local policy, trend, coagulation, urgency, and senior judgement
  • If GA chosen: prepare for difficult airway (oedema), RSI with ETT, arterial line if feasible without delaying, blunt pressor response, have blood products available
  • Transfusion: consider platelets if active bleeding/operative need per haematology; correct fibrinogen early if haemorrhage; use viscoelastic testing if available
  • Post-op: HDU/ICU; ongoing BP control, magnesium as indicated, monitor for DIC/bleeding/AKI

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