Pre-eclampsia and Eclampsia
Pre-eclampsia affects 2-8% of pregnancies globally and remains a leading cause of maternal mortality, accounting for 10-... CICM Fellowship Written, CICM Fellow
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Urgent signals
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- BP ≥160/110 mmHg (severe pre-eclampsia)
- New-onset seizure (eclampsia)
- Severe headache unresponsive to analgesia
- Visual disturbances (scotomata, blindness)
Exam focus
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- CICM Fellowship Written
- CICM Fellowship Viva
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- Hypertensive Emergency in ICU
- Seizure Management in ICU
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Pre-eclampsia affects 2-8% of pregnancies globally and remains a leading cause of maternal mortality, accounting for 10-... ACEM Fellowship Written, ACEM Fellow
Pre-eclampsia affects 2-8% of pregnancies globally and remains a leading cause of maternal mortality, accounting for 10-... CICM Fellowship Written, CICM Fellow
Quick Answer
One-liner: Pre-eclampsia is new-onset hypertension (≥140/90 mmHg) with proteinuria or end-organ dysfunction after 20 weeks gestation; eclampsia is the occurrence of seizures in this context. ICU management focuses on BP control, seizure prophylaxis with magnesium sulfate, and supportive care for multi-organ dysfunction until delivery.
Pre-eclampsia affects 2-8% of pregnancies globally and remains a leading cause of maternal mortality, accounting for 10-15% of maternal deaths worldwide [1]. Aboriginal and Torres Strait Islander women and Māori women experience 2-3× higher maternal mortality rates from hypertensive disorders [2]. ICU priorities are rapid blood pressure control (target below 160/110 mmHg, then 130-150/80-100), seizure prophylaxis with magnesium sulfate (4g loading, then 1g/hour), and supportive organ failure management. The definitive treatment is delivery of the placenta. ICU mortality ranges from 1-3% for severe pre-eclampsia, up to 10% for HELLP syndrome with complications.
CICM Exam Focus
Primary Exam Relevance
- Physiology: Angiogenic factor balance (sFlt-1, PlGF, VEGF), endothelial dysfunction, renin-angiotensin-aldosterone changes in pregnancy, uteroplacental circulation
- Pharmacology: Magnesium sulfate (NMDA antagonism, calcium channel blockade), labetalol pharmacokinetics in pregnancy, hydralazine metabolism, calcium gluconate as antidote
- Pathology: Glomerular endotheliosis, hepatic periportal necrosis in HELLP, cerebral white matter oedema in PRES
Fellowship Exam Relevance
- Written: Diagnostic criteria, ICU admission criteria, magnesium dosing and toxicity, antihypertensive selection, BP targets (CHIPS trial), HELLP management, delivery timing, postpartum complications
- Viva: Eclamptic seizure in ICU, HELLP with hepatic complications, pulmonary oedema management, PRES recognition, postpartum pre-eclampsia requiring ICU, ethical considerations in periviable delivery
- Key domains tested: Medical Expert, Communicator, Collaborator, Leader, Health Advocate
Key Points
The 10 things you MUST know for CICM exams:
- Definition: BP ≥140/90 mmHg + proteinuria OR end-organ dysfunction after 20 weeks
- Severe features: BP ≥160/110, HELLP, headache, visual changes, epigastric pain, AKI, altered GCS
- Magnesium sulfate: 4g IV loading over 20 min, then 1g/hour - prevents and treats seizures (MAGPIE trial)
- BP targets: CHIPS trial - less-tight control (diastolic 85) increases maternal complications, target 130-150/80-100
- Antihypertensives: Labetalol 20mg IV boluses, hydralazine 5-10mg IV, nifedipine 10-20mg PO - all equally effective
- HELLP syndrome: Haemolysis, Elevated Liver enzymes, Low Platelets - ICU admission, delivery within 24-48h
- ICU admission: Eclampsia, pulmonary oedema, severe hypertension requiring infusion, HELLP, AKI, altered consciousness
- Fluid management: Restrictive - patients are intravascularly depleted but interstitially overloaded, pulmonary oedema risk
- PRES: Posterior Reversible Encephalopathy Syndrome - typical MRI finding in eclampsia, usually reversible
- Postpartum risk: Can occur up to 6 weeks postpartum - 63% have no antepartum history
Epidemiology
| Metric | Value | Source |
|---|---|---|
| Global incidence | 2-8% of pregnancies | [1] |
| Australian incidence | 5-10% of pregnancies | [3] |
| Eclampsia incidence | 0.5-1 per 1000 deliveries (developed countries) | [4] |
| Maternal mortality | 10-15% of all maternal deaths | [1] |
| ICU admission rate | 5-10% of severe pre-eclampsia | [5] |
| Recurrence risk | 14-18% in subsequent pregnancies | [6] |
| ICU mortality (severe pre-eclampsia) | 0.5-2% | [7] |
| ICU mortality (HELLP) | 1-3% | [8] |
| ICU mortality (eclampsia) | 1-5% | [9] |
Australian/NZ Specific
Indigenous Health Disparities:
- Aboriginal and Torres Strait Islander maternal mortality ratio: 17.5 per 100,000 vs 5.5 per 100,000 for non-Indigenous women (2012-2021) [2]
- Māori women: 2× higher maternal mortality than NZ Europeans [10]
- Higher rates of ICU admission for severe pre-eclampsia (OR 1.8) [11]
- Earlier onset pre-eclampsia, more severe at presentation
- Higher prevalence of chronic hypertension, renal disease, diabetes
- Delayed antenatal care access contributes to later diagnosis and ICU presentation
Rural/Remote Variations:
- Late presentation more common due to distance from tertiary centres
- Higher severity at ICU admission (more HELLP, AKI, pulmonary oedema)
- RFDS retrieval for pre-term deliveries and maternal stabilisation common [12]
- Limited access to early antenatal screening and preventive care
- Higher rates of postpartum eclampsia requiring readmission
ICU Utilisation Patterns:
- Larger ICUs (greater than 20 beds) have better maternal outcomes (case-mix adjusted mortality OR 0.67) [13]
- Tertiary obstetric ICUs have lower mortality than regional ICUs for HELLP
- Multidisciplinary obstetric ICU models improve outcomes
Pathophysiology
Two-Stage Model
Stage 1: Abnormal Placentation (First Trimester)
- Failed remodelling of maternal spiral arteries by extravillous trophoblasts
- Spiral arteries retain high-resistance, muscular structure
- Results in placental hypoxia and oxidative stress [14]
Stage 2: Maternal Syndrome (Second/Third Trimester)
- Hypoxic placenta releases anti-angiogenic factors
- Systemic endothelial dysfunction develops
- Multi-organ involvement ensues
Angiogenic Factor Imbalance
Placental Hypoxia
↓
↑ sFlt-1 (soluble fms-like tyrosine kinase-1)
↑ Soluble Endoglin (sEng)
↓
Sequestration of VEGF and PlGF
↓
Endothelial Dysfunction
↓
Hypertension + Proteinuria + End-Organ Damage
Key Molecules:
- sFlt-1: Decoy receptor binding VEGF/PlGF (elevated in pre-eclampsia) [15]
- PlGF: Placental growth factor (reduced in pre-eclampsia) [16]
- sEng: Inhibits TGF-β signalling, contributes to endothelial dysfunction [17]
- sFlt-1/PlGF ratio greater than 38: Highly predictive of pre-eclampsia development (PROGNOSIS study) [18]
Why It Matters Clinically
Endothelial damage explains:
- Proteinuria: Glomerular endotheliosis (endothelial cell swelling, capillary lumen occlusion)
- Hypertension: Vasoconstriction, increased vascular resistance
- Oedema: Capillary leak (interstitial) but intravascular depletion
- HELLP: Hepatic periportal necrosis, fibrin deposition
- Pulmonary oedema: Cardiac diastolic dysfunction, increased capillary permeability
- Cerebral involvement: Autoregulation failure, PRES, eclampsia
- Renal impairment: Afferent arteriolar vasoconstriction, AKI
- Fetal growth restriction: Placental insufficiency, reduced uteroplacental flow
ICU-Relevant Pathophysiological Considerations
Haemodynamics:
- Reduced plasma volume (15-20% decrease vs normal pregnancy)
- Increased SVR (systemic vascular resistance)
- Left ventricular diastolic dysfunction in severe disease
- Increased cardiac output requirement but impaired filling
Fluid Balance Paradox:
- Intravascular depletion: Due to endothelial leak, proteinuria, reduced oncotic pressure
- Interstitial overload: Capillary leak causes oedema
- Clinical implication: High risk of pulmonary oedema with seemingly "appropriate" fluid resuscitation
Coagulation:
- Thrombocytopenia (platelet consumption)
- Low-grade DIC in 5-10% of severe cases
- Increased fibrinolysis in HELLP
Renal:
- Afferent arteriolar vasoconstriction
- Reduced GFR despite normal filtration fraction
- Sodium and water retention despite intravascular depletion
Cerebral:
- Loss of cerebral autoregulation at lower BP than non-pregnant state
- Posterior circulation most vulnerable (PRES pattern)
- Blood-brain barrier disruption contributes to seizures
Definitions and Diagnostic Criteria
Classification (SOMANZ/ISSHP)
| Type | Definition |
|---|---|
| Gestational Hypertension | New-onset BP ≥140/90 after 20 weeks, no proteinuria, no end-organ dysfunction |
| Pre-eclampsia | New-onset BP ≥140/90 after 20 weeks + proteinuria OR end-organ dysfunction |
| Severe Pre-eclampsia | Pre-eclampsia + severe features (see below) |
| Eclampsia | Seizures in context of pre-eclampsia |
| HELLP Syndrome | Haemolysis, Elevated Liver enzymes, Low Platelets |
| Chronic Hypertension | BP ≥140/90 before 20 weeks or pre-existing |
| Superimposed Pre-eclampsia | Pre-eclampsia features developing in chronic hypertension |
Diagnostic Criteria for Pre-eclampsia (SOMANZ 2023) [3]
Hypertension: BP ≥140/90 mmHg on two occasions ≥4 hours apart after 20 weeks gestation
PLUS one or more of:
| Criterion | Threshold |
|---|---|
| Proteinuria | ≥300 mg/24h, or PCR ≥30 mg/mmol, or ≥2+ dipstick |
| Renal insufficiency | Creatinine ≥90 μmol/L (or doubling from baseline) |
| Liver dysfunction | ALT/AST greater than 2x upper limit of normal |
| Haematological | Platelets below 100 × 10⁹/L, haemolysis, DIC |
| Neurological | Severe headache, persistent visual disturbances, hyperreflexia with clonus |
| Pulmonary | Pulmonary oedema |
| Fetal | Fetal growth restriction, abnormal Dopplers, stillbirth |
Severe Features (Warrants Immediate ICU Consideration) [19]
Any ONE of the following = Severe Pre-eclampsia:
- BP ≥160/110 mmHg (confirmed within 15-30 minutes)
- Thrombocytopenia (below 100 × 10⁹/L)
- Liver transaminases ≥2x ULN
- Serum creatinine greater than 97 μmol/L (or doubling from baseline)
- Pulmonary oedema
- New-onset persistent headache
- Visual disturbances (scotomata, photopsia, blurred vision)
- Epigastric or RUQ pain
- Eclamptic seizure
- HELLP syndrome
- Altered consciousness or confusion
HELLP Syndrome
Diagnostic Criteria (Tennessee Classification) [20]
| Parameter | Criterion |
|---|---|
| Haemolysis | Abnormal peripheral smear (schistocytes), LDH greater than 600 U/L, bilirubin ≥20 μmol/L |
| Elevated Liver Enzymes | AST ≥70 U/L (or ≥2x ULN) |
| Low Platelets | below 100 × 10⁹/L |
Mississippi Classification (Severity)
| Class | Platelet Count | LDH | AST | Prognosis |
|---|---|---|---|---|
| Class 1 | below 50 × 10⁹/L | greater than 600 U/L | greater than 70 U/L | Severe |
| Class 2 | 50-100 × 10⁹/L | greater than 600 U/L | greater than 70 U/L | Moderate |
| Class 3 | 100-150 × 10⁹/L | greater than 600 U/L | greater than 70 U/L | Mild |
HELLP Complications
| Complication | Incidence | ICU Relevance |
|---|---|---|
| Placental abruption | 7-20% | Emergency delivery, massive transfusion |
| Acute renal failure | 3-8% | May require CRRT |
| DIC | 10-15% | Coagulopathy management, blood products |
| Subcapsular liver haematoma | 1-2% | Catastrophic if ruptures, surgical emergency |
| Hepatic rupture | below 1% | Mortality 50-80%, surgical + massive transfusion |
| Pulmonary oedema | 5-10% | Ventilation, diuretics, CRRT |
| Maternal death | 1-3% | Multidisciplinary critical care |
ICU Management of HELLP
Important Note: HELLP Syndrome ICU Management Principles:
- Urgent delivery planning - definitive treatment, usually within 24-48h
- Platelet threshold for regional anaesthesia - platelets ≥80 × 10⁹/L (relative), ≥50 × 10⁹/L (absolute if epidural bleeding risk acceptable)
- Blood product preparedness - crossmatch 4-6 units PRBCs, FFP, platelets on standby
- Corticosteroids - betamethasone 12mg IM q24h ×2 for fetal lung maturity; dexamethasone 10mg IV q12h may improve maternal lab parameters (evidence mixed)
- Monitor for complications - DIC, hepatic haematoma, abruption, pulmonary oedema
- Postpartum ICU observation - HELLP may worsen or develop postpartum (first 24-48h critical)
- Avoid excessive fluids - capillary leak, pulmonary oedema risk
Clinical Approach
Recognition
High-Risk Patients for ICU Admission:
- Primigravida
- Age extremes (below 20 or greater than 40 years)
- Multiple gestation
- Pre-existing hypertension, renal disease, diabetes
- Previous pre-eclampsia (especially severe/early-onset)
- Antiphospholipid syndrome, SLE
- BMI greater than 35
- IVF pregnancy
- Indigenous women (Aboriginal, Torres Strait Islander, Māori)
- Chronic hypertension with superimposed pre-eclampsia
Initial Assessment
Primary Survey
- A: Patent airway (eclamptic seizure may compromise), cervical spine if seizure with trauma
- B: SpO2 (pulmonary oedema), RR, work of breathing, ABG if concerning
- C: BP (manual sphygmomanometer - automated may underestimate), HR, ECG, IV access ×2, bloods
- D: GCS, pupils, hyperreflexia, clonus (greater than 3 beats = pathological), focal signs
- E: Epigastric tenderness (liver capsule), oedema assessment, fundal height, uterine tenderness
Secondary Survey - ICU Focus
| System | ICU Assessment | Significance |
|---|---|---|
| Cardiovascular | MAP, CVP (if line), ECG, bedside echo | LV function, volume status, arrhythmias |
| Respiratory | SpO2, ABG, CXR, lung ultrasound (B-lines) | Pulmonary oedema, ARDS, pneumonia |
| Renal | Hourly urine output, creatinine, electrolytes | AKI severity, fluid balance |
| Neurological | GCS, pupils, reflexes, CT/MRI if indicated | PRES, ICH, cerebral oedema |
| Coagulation | Platelets, INR, APTT, fibrinogen, D-dimer | DIC, bleeding risk, transfusion |
| Fetal | CTG, ultrasound | Fetal wellbeing, delivery urgency |
History
Key Questions for ICU Admission
| Question | ICU Significance |
|---|---|
| Gestational age? | Guides delivery timing, steroid administration, neonatal ICU involvement |
| Time of symptom onset? | Disease progression, severity assessment |
| BP readings at home? | Baseline, rate of rise |
| Fetal movements? | Fetal compromise, placental insufficiency |
| Headache characteristics? | Cerebral involvement, PRES risk |
| Visual symptoms? | Posterior circulation involvement |
| Epigastric/RUQ pain? | Hepatic involvement (HELLP, subcapsular haematoma) |
| Seizure history? | Eclampsia, status epilepticus risk |
| Previous pregnancies? | Recurrence risk, prior pre-eclampsia severity |
| Medical comorbidities? | Chronic hypertension, renal disease, diabetes |
| Medications? | Antihypertensives, NSAIDs (avoid in ICU) |
| Allergies? | Drug selection, magnesium toxicity precautions |
Red Flag Symptoms
Immediate ICU referral/admission:
- Severe persistent headache (not relieved by paracetamol)
- Visual disturbances (scotomata, flashing lights, transient blindness)
- Epigastric or RUQ pain radiating to back
- Sudden severe oedema (especially facial)
- Nausea/vomiting in late pregnancy
- Reduced or absent fetal movements
- Altered consciousness or confusion
- Seizure activity
- Dyspnoea or orthopnoea (pulmonary oedema)
- Oliguria (below 500 mL/24h or below 30 mL/h)
Investigations
Immediate (Resus Bay - Pre-ICU Transfer)
| Test | Purpose | Critical Finding |
|---|---|---|
| BP (manual) | Confirm severity | ≥160/110 = severe |
| SpO2 | Pulmonary oedema | below 94% = oxygen, consider CXR, intubation |
| ABG | Respiratory status, acid-base | Hypoxaemia, metabolic acidosis |
| Urinalysis | Proteinuria | ≥2+ = significant |
| FBC | Platelets, haemolysis | below 100 = HELLP, check film |
| LFT | Liver involvement | AST/ALT ≥2x ULN = HELLP |
| UEC | Renal function | Cr ≥90 = significant, rising |
| Coagulation | DIC screen | Fibrinogen below 2 g/L, ↑D-dimer, prolonged PT/APTT |
| Blood film | Microangiopathy | Schistocytes, fragmented RBCs (HELLP/TTP) |
| G&H | Blood availability | Crossmatch if bleeding risk |
| CTG | Fetal wellbeing | Late decels, reduced variability = fetal compromise |
| ECG | Ischaemia, arrhythmia | LV strain, QT changes |
Standard ICU Admission Workup
| Test | Indication | ICU Interpretation |
|---|---|---|
| LDH | HELLP screen, haemolysis | greater than 600 U/L = haemolysis |
| Bilirubin | Haemolysis, liver dysfunction | Elevated unconjugated = haemolysis |
| Uric acid | Severity marker | greater than 350 μmol/L associated with worse outcomes |
| PCR (urine) | Quantify proteinuria | ≥30 mg/mmol = significant |
| Troponin | Cardiac involvement, demand ischaemia | Elevated in severe disease |
| BNP/NT-proBNP | Cardiac dysfunction, pulmonary oedema | Elevated indicates cardiac strain |
| Magnesium level | Toxicity monitoring | Therapeutic 2-3.5 mmol/L, greater than 5 = respiratory depression |
| Calcium | Magnesium antidote preparedness | Ionised Ca checked if toxicity suspected |
| Phosphate | Refeeding risk, renal function | Monitor if severe AKI |
Advanced/Specialist
| Test | Indication | Availability |
|---|---|---|
| sFlt-1/PlGF ratio | Diagnostic uncertainty | Major centres (greater than 38 = high risk) [18] |
| ADAMTS13 activity | Differentiate TTP vs HELLP | below 10% = TTP (urgent plasma exchange) |
| Complement studies | Atypical HUS | C3, C4, factor H/I antibodies |
| MRI brain | Eclampsia, PRES | Tertiary - shows posterior cerebral oedema |
| CT head | Exclude haemorrhage | If focal signs, GCS reduction, post-seizure deficit |
| CT angiogram | CVST, RCVS | Headache, focal neurology |
| Liver ultrasound/CT | RUQ pain, suspected haematoma | Urgent if HELLP, epigastric pain |
| Echocardiography | Cardiac dysfunction, pulmonary oedema | Bedside TTE for LV function, filling pressures |
| Lower limb dopplers | DVT screen | Immobility, hypercoagulable state |
Point-of-Care Ultrasound (ICU Applications)
Lung:
- B-lines for pulmonary oedema
- Pleural effusions
- Diaphragm excursion
Cardiac (TTE):
- LV systolic and diastolic function
- RV strain
- Valvular disease
- Volume status (IVC collapsibility, stroke volume variation)
Abdominal:
- Free fluid (haemoperitoneum, liver haematoma)
- Liver capsule integrity
- Gallbladder (cholecystitis mimics epigastric pain)
Neurological:
- Optic nerve sheath diameter (ICP surrogate) - limited evidence
Obstetric (if trained):
- Fetal heart rate
- Presentation
- Amniotic fluid index
ICU Management
Immediate Management (First 10 Minutes)
1. CALL FOR HELP - ICU team, obstetrics, anaesthetics, paediatrics
2. LARGE BORE IV ACCESS x2 (14G/16G)
3. BLOODS: FBC, LFT, UEC, coag, G&H, magnesium level, ABG
4. BP CONTROL if ≥160/110 (treat within 30-60 min)
5. MAGNESIUM SULFATE if severe/eclampsia
6. CONTINUOUS CTG MONITORING
7. STRICT FLUID BALANCE (avoid overload)
8. URINARY CATHETER with hourly urine output
9. O2 if SpO2 below 94%
10. PREPARE FOR POSSIBLE INTUBATION
ICU Admission Criteria
Important Note: Admit to ICU for:
- Eclampsia (especially with recurrent seizures, status epilepticus)
- Severe hypertension requiring IV infusion (despite oral/IV bolus therapy)
- Pulmonary oedema requiring CPAP/NIV or intubation
- HELLP syndrome (especially Class 1, hepatic complications, DIC)
- AKI requiring renal replacement therapy
- Altered consciousness or PRES
- Postpartum deterioration requiring level 2-3 care
- Postoperative ICU care post-delivery (caesarean under general anaesthesia)
- Multidisciplinary coordination requirement
- Remote/rural transfer stabilisation
Eclamptic Seizure Management in ICU
During Seizure:
- Call for help - note time, duration
- Position: Left lateral (prevents aspiration, optimises uterine blood flow)
- Airway: Do NOT insert tongue blade, clear secretions, give O2 15 L/min
- Protect from injury (side rails, soft surroundings, bed rails up)
- Most seizures self-terminate within 60-90 seconds
- Prepare medications: magnesium, benzodiazepines
Post-Seizure/Stabilisation:
- Assess ABCDE: Airway protection (consider intubation if GCS below 8, recurrent seizures)
- Magnesium sulfate (if not already given) - see below
- If recurrent seizure: Additional MgSO4 2g IV bolus
- If refractory (greater than 2 seizures despite Mg): IV diazepam 5-10mg or IV midazolam 2-5mg
- Do NOT give phenytoin (inferior to MgSO4, teratogenic risk) [21]
- CT head - exclude ICH, PRES (especially if postictal GCS below 13, focal deficit)
- ICU monitoring: EEG if status epilepticus suspected
Status Epilepticus in Eclampsia:
- Follow standard status epilepticus protocol
- First-line: Benzodiazepines (lorazepam 0.1 mg/kg IV)
- Second-line: Phenytoin 15-20 mg/kg IV (if magnesium failed) OR Levetiracetam
- Consider rapid sequence intubation if prolonged, airway compromise
- Continue magnesium throughout
Magnesium Sulfate Protocol
MAGPIE Trial Evidence [22]
- 58% reduction in eclampsia (RR 0.42, 95% CI 0.29-0.60)
- NNT = 63 for moderate pre-eclampsia
- NNT = 109 for mild pre-eclampsia
- Maternal mortality reduced (RR 0.55, 95% CI 0.26-1.18)
- Number needed to treat to prevent one maternal death = 100 (trend)
Dosing Regimen (SOMANZ 2023) [3]
| Phase | Dose | Administration | ICU Monitoring |
|---|---|---|---|
| Loading | 4g MgSO4 | IV over 20 minutes | BP, RR, reflexes immediately |
| Maintenance | 1g/hour | IV continuous infusion | BP q15min until stable, then q1h |
| Duration | 24 hours | After last seizure or after delivery | Throughout |
| Recurrent seizure | 2g MgSO4 | IV over 5 minutes | Repeat if needed |
Alternative IM Regimen (IV Access Unavailable)
- Loading: 4g IV + 5g IM each buttock (10g IM total)
- Maintenance: 5g IM every 4 hours in alternating buttocks
Magnesium in Renal Failure/AKI
| Creatinine (μmol/L) | Mg Dose Adjustment |
|---|---|
| below 90 | Standard 1g/hour |
| 90-150 | 0.5-1g/hour |
| greater than 150 | 0.5g/hour |
| greater than 250 with oliguria | 0.5g/hour + check Mg level q12h |
| Dialysis | 0.5g/hour or consider alternative (dialysis removes Mg) |
Magnesium Pharmacokinetics
| Parameter | Value | ICU Relevance |
|---|---|---|
| Mechanism | NMDA receptor antagonist, calcium channel blocker, vasodilation | Seizure prophylaxis, neuroprotection |
| Onset | 5-10 minutes IV | Rapid therapeutic effect |
| Therapeutic level | 2.0-3.5 mmol/L | Target for seizure prevention |
| Half-life | 4-5 hours (normal renal) | Accumulation risk in renal failure |
| Elimination | Renal (90%) | Dose reduce in AKI |
| Dialysis clearance | 70-80% removed | Redose post-dialysis if needed |
| Pregnancy category | A (safe) | Can use throughout pregnancy |
Monitoring for Magnesium Toxicity
| Parameter | Normal (Continue Mg) | Action Required (Stop Mg) |
|---|---|---|
| Respiratory rate | ≥12/min | below 12/min - stop, consider Ca²⁺ |
| Patellar reflexes | Present | Absent - stop immediately |
| Urine output | ≥25-30 mL/hr | below 25 mL/hr - consider dose reduction |
| Serum Mg level | 2-3.5 mmol/L | greater than 5 mmol/L - stop, treat toxicity |
| Level of consciousness | Alert/good | Drowsy/confused - assess toxicity |
Magnesium Toxicity Progression
Therapeutic: 2-3.5 mmol/L → Seizure prevention
Loss of reflexes: 3.5-5 mmol/L → STOP infusion
Respiratory depression: 5-6.5 mmol/L → Support ventilation
Cardiac arrest: greater than 6.5 mmol/L → CPR + calcium
Magnesium Toxicity Treatment
- STOP magnesium infusion immediately
- Calcium gluconate 1g (10 mL of 10%) IV over 10 minutes
- Repeat if no improvement in 5-10 minutes (max 3g)
- Supportive care:
- Airway protection
- Bag-mask ventilation if apnoeic
- Intubation and mechanical ventilation if needed
- Check serum magnesium level
- ECG monitoring (may show prolonged PR, widened QRS, bradyarrhythmias)
- Do NOT give diuretics (will further reduce Mg clearance)
CRITICAL: Magnesium toxicity mimics worsening pre-eclampsia
- Respiratory depression may be mistaken for pulmonary oedema
- Drowsiness may be mistaken for PRES or encephalopathy
- Always check magnesium level and reflexes before attributing to pre-eclampsia progression
Antihypertensive Therapy
Blood Pressure Targets (CHIPS Trial Evidence)
CHIPS Trial (Control of Hypertension In Pregnancy Study) [23]:
- Design: RCT comparing less-tight (diastolic 85 mmHg) vs tight (diastolic 100 mmHg) control
- N: 983 women with chronic hypertension or gestational hypertension
- Primary outcome: Composite of perinatal loss or high-level neonatal care
- Results: Perinatal outcomes similar between groups (RR 0.97, 95% CI 0.80-1.17)
- Maternal outcomes: Less-tight control had higher maternal complications (RR 1.34, 95% CI 1.02-1.77)
- Conclusion: Target diastolic BP 85 mmHg (less-tight) did not improve perinatal outcomes but increased maternal complications
Important Note: BP Targets for ICU Management:
- Acute severe hypertension (≥160/110): Treat within 30-60 min
- Initial target: below 160/110 mmHg
- Maintenance target: 130-150 / 80-100 mmHg (SOMANZ 2023)
- Avoid precipitous drops: Risk of placental hypoperfusion, fetal distress
- Permissive hypertension: 150-160 systolic acceptable if asymptomatic
First-Line Options (All Equally Effective) [24]
| Drug | Dose | Route | Onset | ICU Considerations |
|---|---|---|---|---|
| Labetalol | 20mg initially, then 20-80mg q10-15min (max 300mg) | IV bolus | 5 min | α/β-blocker, avoid asthma, HF |
| Labetalol infusion | 1-2 mg/min, titrate to BP | IV infusion | 5-10 min | Use for refractory hypertension |
| Hydralazine | 5-10mg q20min (max 20mg) | IV bolus | 10-20 min | Reflex tachycardia, headache |
| Nifedipine | 10-20mg q20-30min (max 50mg) | PO (immediate release) | 10-20 min | No IV access needed, avoid sublingual |
Labetalol Escalating Regimen (Standard)
- 20mg IV bolus
- If no response in 10 min: 40mg IV
- If no response: 80mg IV
- If no response: 80mg IV (max cumulative 300mg)
- Then commence infusion 1-2 mg/min if needed
Labetalol Infusion Protocol
Starting dose: 1 mg/min (60 mg/hour)
Titration: Increase by 0.5 mg/min q15min until BP target
Maximum: 4 mg/min (240 mg/hour)
Monitoring: BP q5-15min initially, HR, ECG
Stop if: HR below 60, systolic BP below 130
Hydralazine Protocol
Starting dose: 5mg IV bolus
If no response in 20 min: 10mg IV
If no response: 10mg IV (max 20mg)
Duration: 2-6 hours per dose
Monitoring: BP q10-20min, HR (tachycardia expected)
Nifedipine Protocol
Starting dose: 10mg PO (immediate release)
If no response in 20 min: 20mg PO
If no response: 20mg PO (max 50mg)
Duration: 4-8 hours per dose
Monitoring: BP q10-30min
Avoid: Sublingual (unpredictable, precipitous hypotension)
Interaction: May potentiate MgSO4 effect (monitor closely)
Second-Line/Refractory Hypertension
| Drug | Dose | ICU Indication |
|---|---|---|
| Nicardipine infusion | 5 mg/hour, titrate 2.5 mg/hour q5-15min | Refractory hypertension, labetalol failure |
| Sodium nitroprusside | 0.25-10 mcg/kg/min | Life-threatening hypertension, last resort (cyanide/thiocyanate toxicity risk) |
| Nitroglycerin infusion | 5-200 mcg/min | Pulmonary oedema + hypertension |
IMPORTANT CONSIDERATIONS:
- Avoid sublingual nifedipine: Unpredictable absorption, precipitous hypotension, fetal distress
- Do NOT use ACE inhibitors/ARBs: Teratogenic, fetal renal failure
- Avoid atenolol: Fetal growth restriction
- Avoid diuretics unless pulmonary oedema: Worsen intravascular depletion
- Sodium nitroprusside: Last resort only - cyanide/thiocyanate toxicity risk, fetal cyanide exposure
- Hydralazine headache: May mimic worsening pre-eclampsia - consider in assessment
Fluid Management
Important Note: CRITICAL: Avoid fluid overload in pre-eclampsia
- Pre-eclamptic patients have intravascular depletion but interstitial overload
- Capillary leak due to endothelial dysfunction
- Pulmonary oedema is a leading cause of maternal death
- Restrict total IV fluid to 80-100 mL/hour (including drug infusions)
- Target urine output ≥25 mL/hour (≥0.5 mL/kg/hr)
- Avoid colloids (increases capillary leak)
- Use Hartmann's or N/Saline
- Consider diuretics for pulmonary oedema despite low CVP (interstitial overload)
Fluid Protocol
| Situation | Fluid Strategy | Target |
|---|---|---|
| Resuscitation | Bolus 250-500 mL crystalloid, reassess | MAP greater than 65, urine output greater than 0.5 mL/kg/hr |
| Maintenance | 80-100 mL/hour total fluids | Maintain euvolaemia |
| Pulmonary oedema | Restrict fluids, diuretics (furosemide 20-40mg IV) | Negative balance, dry lungs |
| Oliguria with AKI | Consider CRRT, avoid fluid overload | Maintain K+, avoid volume overload |
| Pre-delivery | Minimal fluids, blood products for losses | Maintain MAP, avoid pulmonary oedema |
| Postpartum | Mobilise fluid, diuretics if overloaded | Gradual negative balance |
Fluid Balance Monitoring
- Hourly urine output (catheter)
- Strict intake/output chart
- Daily weights (if not too unstable)
- CVP (if line in situ) - interpret with caution (poor predictor of volume status)
- Bedside echo (IVC collapsibility, LV filling)
- Lung ultrasound (B-lines for pulmonary oedema)
Mechanical Ventilation Considerations
Indications for Intubation
- GCS below 8 (protect airway)
- Refractory seizures/status epilepticus
- Severe respiratory failure (SpO2 below 90% on NIV, PaO2/FiO2 below 150)
- Pulmonary oedema requiring intubation (CPAP/NIV failure)
- Airway protection for procedures (caesarean)
- Coma/PRES with impaired airway reflexes
Ventilation Strategy
| Parameter | Target | Rationale |
|---|---|---|
| FiO2 | 0.3-0.6 | Maintain SpO2 92-96% |
| PEEP | 5-10 cmH2O | Avoid excessive PEEP (reduces venous return, fetal perfusion) |
| Tidal volume | 6-8 mL/kg IBW | Lung protective, avoid barotrauma |
| Respiratory rate | 12-16 | Normocapnia (PaCO2 35-45) |
| Plateau pressure | below 30 cmH2O | Lung protective |
| PaCO2 | 35-45 mmHg | Avoid hypocapnia (uterine vasoconstriction) |
| PaO2 | 80-100 mmHg | Adequate oxygenation |
Considerations in Pregnancy
- Supine position - avoid aortocaval compression (left lateral tilt 15°)
- Higher minute ventilation - maintain normocapnia
- Lower PaCO2 normal - 30-32 mmHg in normal pregnancy
- Avoid excessive PEEP - reduces uterine blood flow
- Sedation - propofol, midazolam, fentanyl safe; avoid ketamine (↑BP)
- Paralysis - rocuronium, vecuronium safe
Renal Replacement Therapy (RRT)
Indications in Pre-eclampsia
Important Note: RRT Indications:
- Refractory hyperkalaemia (K+ greater than 6.5 despite medical management)
- Severe metabolic acidosis (pH below 7.15 or HCO3 below 10)
- Volume overload/pulmonary oedema refractory to diuretics
- Uremic complications (pericarditis, encephalopathy)
- Oliguria/anuria with rising creatinine
- Toxic metabolite removal (if indicated)
- Severe AKI with expected duration greater than 5 days
RRT Modality Selection
| Modality | Advantages in Pre-eclampsia | Disadvantages |
|---|---|---|
| CRRT (CVVHDF) | Gradual solute/fluid removal, haemodynamically stable, continuous Mg removal | Requires anticoagulation (citrate or heparin), expensive |
| SLED | Intermittent, allows off-dialysis for procedures | Less haemodynamically stable than CRRT |
| IHD | Rapid removal of Mg if toxicity | Haemodynamic instability risk |
CRRT Prescription
Effluent dose: 20-25 mL/kg/hour
Blood flow: 150-200 mL/min
Dialysate flow: 500 mL/min (CVVHD) or 1000 mL/hour (CVVHDF)
Replacement fluid: Pre-dilution or mixed (CVVH)
Anticoagulation: Regional citrate preferred (reduce bleeding risk)
Duration: Until renal recovery or patient transferred to nephrology
RRT and Magnesium
- CRRT removes magnesium (70-80% clearance)
- Adjust magnesium dose during CRRT: 0.5g/hour or monitor levels q6-12h
- Check magnesium level after 4-6 hours of CRRT initiation
- Consider extra magnesium bolus if levels drop below 2 mmol/L
Coagulation and Blood Product Management
Coagulation Abnormalities
| Abnormality | Threshold | Management |
|---|---|---|
| Thrombocytopenia | Platelets below 50 × 10⁹/L | Platelet transfusion before invasive procedures, delivery |
| Thrombocytopenia | Platelets below 20 × 10⁹/L | Platelet transfusion (bleeding risk) |
| DIC | Fibrinogen below 2 g/L | Cryoprecipitate or fibrinogen concentrate |
| DIC | PT/APTT prolonged greater than 1.5× | FFP transfusion |
| Fibrinogen low | below 2 g/L | Fibrinogen concentrate 2-4g or cryoprecipitate 10U |
| Bleeding | Active haemorrhage | Massive transfusion protocol |
Blood Product Preparation (HELLP)
Crossmatch: 4-6 units PRBCs (O negative if emergency)
FFP: 2-4 units available
Platelets: 1 pool (5 units) available
Cryoprecipitate: 10U available (if fibrinogen low)
Massive Transfusion Protocol
- Activate if: greater than 4 units PRBCs in 4 hours, greater than 1 unit/hour ongoing
- Ratio: 1:1:1 (PRBC:FFP:Platelets)
- Check fibrinogen q30min
- Use point-of-care testing (TEG/ROTEM) if available
- Give tranexamic acid 1g IV (if not contraindicated)
Regional Anaesthesia and Coagulation
| Platelet Count | Epidural | Spinal |
|---|---|---|
| greater than 100 | Safe | Safe |
| 80-100 | Consider relative risk | Safe |
| 50-80 | Generally avoid | Avoid |
| below 50 | Contraindicated | Contraindicated |
Fetal Considerations
Antenatal Corticosteroids
Administer if delivery anticipated below 34+6 weeks:
Betamethasone (Preferred):
- 11.4mg IM (Celestone Chronodose)
- Two doses, 24 hours apart
- Fetal lung maturation, reduces IVH, RDS, necrotising enterocolitis
Dexamethasone:
- 6mg IM
- Four doses, 12 hours apart
Late Preterm (34+0 to 36+6 weeks):
- Consider single course if delivery likely within 7 days and no prior course (ALPS trial) [25]
- Betamethasone 12mg IM ×2 doses, 24 hours apart
Rescue Course:
- If greater than 14 days since first course and still below 34 weeks
- Repeat betamethasone course
Fetal Monitoring
- Continuous CTG if admitted
- Abnormalities: Late decelerations, reduced variability, sinusoidal pattern
- Ultrasound: Growth, AFI, Doppler (umbilical artery, MCA)
- Biophysical profile if reduced fetal movements or growth restriction
Delivery Timing
| Scenario | Timing | Rationale |
|---|---|---|
| Pre-eclampsia without severe features | 37+0 weeks [26] | HYPITAT trial - induction reduces maternal complications |
| Severe pre-eclampsia ≥34 weeks | After maternal stabilisation (within 24-48h) | Benefit of delivery outweighs prematurity |
| Severe pre-eclampsia below 34 weeks (stable) | Expectant management at tertiary centre until 34 weeks OR deterioration | BALANCE-ITT trial ongoing |
| Eclampsia | After maternal stabilisation (seizures controlled, BP managed) | Usually within 12-24h |
| HELLP syndrome | Urgent (within 24-48h) | Deterioration common, especially hepatic |
| Pulmonary oedema | After stabilisation (intubation, diuresis) | Often emergency caesarean |
Immediate Delivery Indications (Regardless of Gestation)
DELIVER IMMEDIATELY:
- Uncontrolled severe hypertension despite maximal therapy (≥3 antihypertensives)
- Eclampsia with recurrent seizures or status epilepticus
- Placental abruption (vaginal bleeding + fetal distress)
- DIC with bleeding
- Non-reassuring fetal status (bradycardia, sinusoidal pattern)
- Pulmonary oedema not responsive to intubation/diuresis
- Hepatic capsule haematoma or rupture
- Maternal cardiac arrest
- Maternal compromise (severe PRES, ICH)
- Stillbirth with deteriorating maternal condition
Postpartum Management
Postpartum ICU Considerations
- Fluid mobilisation: Third-spacing fluid mobilises day 2-4
- Pulmonary oedema risk: High in first 24-48 hours postpartum
- BP worsening: May worsen in first week postpartum
- HELLP progression: May develop or worsen postpartum (first 48h critical)
- Magnesium: Continue for 24 hours post-delivery
Postpartum Pre-eclampsia
Incidence and Risk:
- Occurs up to 6 weeks postpartum
- 63% of delayed postpartum pre-eclampsia have no antepartum hypertensive disease [27]
- Present with headache, visual changes, hypertension
- Highest risk: 3-6 days postpartum
Management:
- Same as antepartum (labetalol, hydralazine, nifedipine)
- Magnesium sulfate for severe features or seizures
- Avoid NSAIDs (worsen hypertension, fluid retention)
- Avoid ergometrine (causes vasoconstriction)
- Outpatient BP monitoring if mild
- Clear return advice
Long-Term Cardiovascular Risk
Pre-eclampsia as a Cardiovascular Risk Marker:
- 2× increased lifetime risk of cardiovascular disease
- 4× risk of chronic hypertension
- 3.7× risk of ischaemic heart disease
- 4.2× risk of heart failure
- 1.8× risk of stroke
Counselling at Discharge:
- Lifestyle modification (weight, exercise, diet)
- Annual BP monitoring
- Cardiovascular risk factor screening (lipids, glucose)
- Consider aspirin prophylaxis in future pregnancies
- Preconception counselling for future pregnancies [28]
Special Populations
Atypical Presentations
- Pre-eclampsia without proteinuria: End-organ dysfunction alone sufficient for diagnosis
- HELLP without hypertension: 15-20% of HELLP cases present with normal BP [20]
- Eclampsia as first presentation: 20% have no preceding symptoms
- Postpartum presentation: Up to 6 weeks, de novo in 63%
- Chronic hypertension with superimposed pre-eclampsia: Earlier, more severe
Pre-existing Chronic Hypertension
Diagnostic Challenge:
- Elevated BP before 20 weeks
- Distinguish from gestational hypertension
- Superimposed pre-eclampsia: Sudden BP rise, proteinuria, end-organ dysfunction
Management:
- Continue chronic antihypertensives if safe
- Avoid ACE inhibitors/ARBs throughout pregnancy
- Labetalol, nifedipine, methyldopa preferred
- Earlier delivery consideration (often 37-38 weeks)
Multiple Gestation
Higher Risk:
- 2-3× increased risk of pre-eclampsia
- Earlier onset, more severe
- Higher rate of HELLP
Management:
- Low threshold for admission
- Earlier delivery consideration
- More aggressive BP control
Obesity (BMI greater than 35)
Management Challenges:
- Difficult BP measurement (larger cuff)
- Difficult IV access
- Higher risk of pulmonary oedema
- Technical challenges for caesarean
ICU Considerations:
- Larger tidal volumes required
- Higher PEEP often needed for oxygenation
- Higher risk of aspiration
Pre-existing Renal Disease
Diagnostic Challenge:
- Elevated creatinine baseline
- Proteinuria baseline
- Differentiate superimposed pre-eclampsia
Management:
- Earlier nephrology input
- Lower threshold for RRT
- Adjust drug dosing (magnesium, antihypertensives)
Indigenous Health
Important Note: Aboriginal, Torres Strait Islander, and Māori Considerations:
Health Disparities:
- Aboriginal/Torres Strait Islander maternal mortality: 17.5/100,000 vs 5.5/100,000 non-Indigenous [2]
- Māori maternal mortality: 2× higher than NZ Europeans [10]
- Higher rates of ICU admission for severe pre-eclampsia (OR 1.8) [11]
- Higher rates of chronic hypertension, diabetes, renal disease
- Earlier onset and more severe pre-eclampsia
- Later presentation to antenatal care
- Higher severity at ICU admission
Barriers to Care:
- Geographic isolation (remote communities, 4-6+ hours to tertiary centre)
- Transport challenges to tertiary maternity services
- Cultural safety concerns may delay presentation
- Language barriers (English as second language)
- Mistrust of health system due to historical trauma
- Family responsibilities (caring for other children)
- Financial constraints (travel costs)
Cultural Safety Approaches:
- Involve Aboriginal Health Workers/Aboriginal Liaison Officers immediately
- Māori Health Workers/Kaiāwhina for NZ patients
- Family-centred care (whānau involvement in decision-making)
- Respect for cultural practices around birth (Birthing on Country)
- Clear, jargon-free communication
- Consider cultural protocols around bad news
- Involve Elders if appropriate and requested
- Plan for "Birthing on Country" support where possible
- Ensure interpreter services if required
- Acknowledge connection to Country/whenua
- Allow time for family decision-making (collective vs individual)
Clinical Implications:
- Lower threshold for ICU admission and tertiary transfer
- Early involvement of multidisciplinary team
- Proactive transfer planning for remote patients (RFDS)
- Consider social supports for relocation of family
- Ensure culturally safe discharge planning
- Longer ICU observation period if concerns
Remote/Rural Considerations
Pre-Hospital/Remote Area Management
- Early activation of retrieval services (RFDS, state-based retrieval)
- Remote Area Nurses (RANs) and Rural GPs: Initial stabilisation
- Telemedicine consultation with tertiary obstetric/ICU service
- Have magnesium sulfate and antihypertensives available
- Urinary catheter for output monitoring
- Manual BP monitoring (automated may be inaccurate in pre-eclampsia)
Resource-Limited Setting Management
| Situation | Resource-Limited Strategy | Rationale |
|---|---|---|
| No IV access | Oral nifedipine 10-20mg PO q30min | Equally effective to IV labetalol [29] |
| No IV infusion pump | IM magnesium protocol | Loading: 4g IV + 10g IM, maintenance 5g IM q4h |
| No CTG | Handheld Doppler or intermittent auscultation | Assess fetal heart rate |
| No blood bank | Early transfer, type-specific O negative available | Massive haemorrhage risk |
| No ICU bed | Early referral, stabilise for transfer | Deterioration can be rapid |
RFDS/Retrieval Medicine
Pre-eclampsia/eclampsia retrieval considerations:
- Common indication for maternal retrieval [12]
- Risk of "in-flight birth"
- ensure obstetric kit available
- Neonatal resuscitation capability required
- Consider flight physiology (mild hypoxia at altitude)
- Secure IV access and magnesium infusion before flight
- Continue CTG monitoring if possible
In-flight considerations:
- Physiological stress: Hypoxia, vibration, noise
- Fluid shifts: Microgravity effect
- Reduced barometric pressure: Mild hypoxaemia
- Limited access: Cannot stop for emergencies
Retrieval Criteria:
- Severe pre-eclampsia below 34 weeks
- Any eclampsia
- HELLP syndrome
- Need for delivery without local surgical/anaesthetic capability
- Preterm labour in context of pre-eclampsia
- Postpartum deterioration
- Pulmonary oedema
- Severe hypertension refractory to oral therapy
Telemedicine
- Real-time consultation with tertiary MFM specialists
- Photo of blood film (schistocytes for HELLP)
- Shared CTG review
- Decision support for expectant management vs transfer
- Video conferencing for family discussions
- Remote monitoring of vitals if available
Differential Diagnosis
Conditions Mimicking Pre-eclampsia
| Condition | Key Differentiating Features |
|---|---|
| Chronic hypertension | HTN before 20 weeks, no proteinuria, stable BP |
| Gestational hypertension | No proteinuria, no end-organ dysfunction |
| Thrombotic microangiopathy (TTP/HUS) | ADAMTS13 below 10% (TTP), severe renal failure, fever, neurological features |
| Acute fatty liver of pregnancy (AFLP) | Hypoglycaemia, coagulopathy, encephalopathy, normal platelets initially |
| Lupus nephritis flare | Active SLE markers, low C3/C4, anti-dsDNA positive |
| Antiphospholipid syndrome | Thrombosis, recurrent pregnancy loss, aPL positive |
| Primary seizure disorder | History of epilepsy, normal BP, no proteinuria |
| Migraine | History of migraine, normal BP, no proteinuria, no end-organ dysfunction |
| Cerebral venous sinus thrombosis (CVST) | Headache, focal neurology, thrombosis on imaging |
HELLP Mimics
| Condition | Distinguishing Features |
|---|---|
| Thrombotic thrombocytopenic purpura (TTP) | ADAMTS13 below 10%, pentad (thrombocytopenia, MAHA, neurological, renal, fever), normal LFT |
| Haemolytic uraemic syndrome (HUS) | Severe AKI predominant, diarrhoeal prodrome (typical), complement abnormalities (atypical) |
| Acute fatty liver of pregnancy (AFLP) | Hypoglycaemia, elevated ammonia, low fibrinogen, nausea/vomiting predominant, normal platelets initially |
| Viral hepatitis | Hepatitis serology positive, higher transaminases |
| Cholestasis of pregnancy | Pruritus predominant, elevated bile acids, mildly elevated LFT |
| Disseminated intravascular coagulation (DIC) | Global coagulopathy, bleeding, fibrinogen low |
When to Consider Alternative Diagnoses
- Onset before 20 weeks gestation
- ADAMTS13 below 10% (TTP - urgent plasma exchange)
- Hypoglycaemia or encephalopathy (AFLP)
- Severe AKI out of proportion to other features (HUS)
- Thrombosis or recurrent pregnancy loss history (APS)
- Active SLE with complement consumption
- Fever, severe neurological symptoms, renal failure out of proportion (TTP)
- Diarrhoea prodrome (typical HUS)
Complications
Maternal Complications
| Complication | Incidence | ICU Management |
|---|---|---|
| Eclampsia | 1-2% of severe pre-eclampsia | MgSO4, airway protection, ICU admission |
| HELLP syndrome | 10-20% of severe cases | ICU, blood products, delivery planning |
| Placental abruption | 1-4% | Emergency delivery, massive transfusion protocol |
| Acute kidney injury | 1-5% (severe), up to 50% in HELLP | Fluid restriction, CRRT if indicated |
| Pulmonary oedema | 2-5% (up to 10% in HELLP) | Diuretics, NIV/intubation, fluid restriction |
| Cerebrovascular accident (ICH/SAH) | 0.5-1% | Neurosurgery, BP control, neuroprotective ICU care |
| Hepatic rupture | below 1% | Surgical emergency, massive transfusion, ICU |
| DIC | 5-10% of HELLP | Blood products, FFP, platelets, cryoprecipitate |
| PRES | Up to 80% of eclampsia on MRI | BP control, neuroprotective care |
| Cardiac failure | below 1% | Inotropes, diuretics, mechanical support if needed |
| Maternal death | 0.2-0.5% (overall), 1-3% in HELLP | Multidisciplinary critical care |
Posterior Reversible Encephalopathy Syndrome (PRES)
Pathophysiology:
- Failure of cerebral autoregulation
- Hyperperfusion → capillary leak → vasogenic oedema
- Posterior circulation most vulnerable (less sympathetic innervation)
Clinical Features:
- Headache (severe)
- Visual disturbances (cortical blindness, scotomata)
- Altered consciousness
- Seizures
- Focal neurological deficits
MRI Findings:
- Bilateral posterior white matter hyperintensities (T2/FLAIR)
- Parieto-occipital lobes typical
- Restricted diffusion if cytotoxic oedema (infarction)
Management:
- BP control (target 140-150 systolic)
- Magnesium sulfate
- Seizure prophylaxis/treatment
- ICU monitoring
- Usually reversible with BP control
ICU Considerations:
- Continuous EEG if seizures suspected
- Neuroprotective care (avoid hypoxia, hyperglycaemia)
- Neurological assessment q1-2h
- Consider ICP monitoring if severe oedema
Fetal/Neonatal Complications
| Complication | Incidence | ICU/Neonatal Considerations |
|---|---|---|
| Fetal growth restriction | 25-30% | Serial growth scans, Doppler surveillance |
| Preterm birth | 15-65% | Antenatal steroids, NICU involvement |
| Intrauterine fetal death | 1-2% | May precipitate DIC, maternal counselling |
| Neonatal complications | Variable | Related to prematurity (RDS, IVH, NEC) |
| Placental insufficiency | Up to 50% in severe | Doppler abnormalities, CTG monitoring |
Long-Term Maternal Sequelae
Pre-eclampsia is associated with significant long-term cardiovascular risk:
| Outcome | Relative Risk | Time to Event |
|---|---|---|
| Chronic hypertension | 3.7× | Years |
| Ischaemic heart disease | 2.2× | 10-20 years |
| Heart failure | 4.2× | 10-30 years |
| Stroke | 1.8× | 10-20 years |
| Venous thromboembolism | 1.8× | Years |
| End-stage renal disease | 4.7× | 10-30 years |
| Diabetes mellitus | 1.8× | Years |
| Cardiovascular mortality | 2-3× | 10-30 years |
Counselling Points:
- Lifestyle modification (weight, exercise, diet)
- Annual BP monitoring
- Cardiovascular risk factor screening (lipids, glucose, BMI)
- Consider aspirin prophylaxis in future pregnancies
- Preconception counselling for future pregnancies
- Primary prevention interventions (statins, antihypertensives) if indicated
Prognosis
Maternal Outcomes
| Severity | Maternal Mortality | ICU Morbidity |
|---|---|---|
| Mild pre-eclampsia | below 0.1% | 2-5% (pulmonary oedema, ICU admission) |
| Severe pre-eclampsia | 0.2-0.5% | 5-10% (pulmonary oedema, AKI, ICU admission) |
| Eclampsia | 1-2% | 15-25% (PRES, ICH, prolonged ICU stay) |
| HELLP syndrome | 1-3% | 20-40% (pulmonary oedema, AKI, DIC, hepatic complications) |
Factors Associated with Poor Maternal Outcome:
- Late presentation (greater than 34 weeks) with severe features
- Delayed treatment of severe hypertension
- HELLP with hepatic complications
- Eclampsia (especially remote from medical care)
- Aboriginal, Torres Strait Islander, or Māori ethnicity (due to systemic barriers)
- Remote geographic location
- Pulmonary oedema
- Cerebral haemorrhage
- DIC with bleeding
ICU Prognostic Factors:
- APACHE II score on admission
- SOFA score trend
- Platelet count trajectory
- Serum creatinine
- Lactate level
- Need for mechanical ventilation
- Need for RRT
Fetal/Neonatal Outcomes
| Gestational Age at Delivery | Neonatal Survival | Major Morbidity |
|---|---|---|
| below 24 weeks | below 20% | greater than 80% |
| 24-28 weeks | 60-80% | 40-60% |
| 28-32 weeks | 85-95% | 20-30% |
| 32-34 weeks | 95-98% | 10-15% |
| 34-37 weeks | 98-99% | 5-10% |
| greater than 37 weeks | greater than 99% | below 5% |
Recurrence Risk
| Previous History | Recurrence Risk |
|---|---|
| Term pre-eclampsia (≥37 weeks) | 14-18% |
| Preterm pre-eclampsia (below 34 weeks) | 25-35% |
| Early preterm (below 28 weeks) | 40-65% |
| HELLP syndrome | 5-19% |
| Eclampsia | 2-16% |
| Multiple previous pre-eclampsia | Higher with each episode |
| Superimposed on chronic HTN | 30-50% |
Pharmacology Details
Magnesium Sulfate Pharmacology
| Parameter | Value |
|---|---|
| Mechanism | NMDA receptor antagonist, calcium channel blocker, vasodilation |
| Neuroprotective effect | Reduces excitotoxicity, stabilises membranes |
| Onset | 5-10 minutes IV |
| Therapeutic level | 2.0-3.5 mmol/L |
| Half-life | 4-5 hours (normal renal function) |
| Volume of distribution | 0.5 L/kg (extracellular fluid) |
| Elimination | Renal (90%) - excreted unchanged |
| Toxicity sequence | Loss of reflexes (3.5-5) → Respiratory depression (5-6.5) → Cardiac arrest (greater than 6.5 mmol/L) |
| Pregnancy category | A (safe in pregnancy) |
| Breastfeeding | Safe |
| Antidote | Calcium gluconate 1g IV (10 mL of 10%) |
| Dialysis removal | 70-80% removed during CRRT |
| CNS penetration | Crosses BBB (therapeutic for seizures) |
Clinical Pearls:
- Does NOT lower blood pressure (separate antihypertensive needed)
- Continue for 24 hours after delivery OR last seizure
- Monitor closely if oliguria (accumulation risk)
- Fetal effects: transient hypotonia, decreased variability on CTG (rare)
- Reduces cerebral vasogenic oedema (mechanism of PRES reversal)
Antihypertensive Pharmacology
Labetalol
| Parameter | Value |
|---|---|
| Mechanism | Non-selective β-blocker + α1-blocker (β:α ratio 7:1) |
| Onset | 2-5 minutes IV |
| Peak | 5-15 minutes IV |
| Duration | 2-4 hours (bolus), 30-60 min (infusion) |
| Half-life | 5-8 hours |
| Metabolism | Hepatic (glucuronidation) |
| Excretion | Renal (metabolites) |
| Contraindications | Asthma, heart block, severe bradycardia, decompensated heart failure, cardiogenic shock |
| Caution | Diabetes (masks hypoglycaemia), liver failure |
| Pregnancy category | C (safe, commonly used) |
| Breastfeeding | Safe |
| Fetal effects | Transient bradycardia, hypoglycaemia (monitor neonate) |
| Dosing | 20mg IV, then 40mg, 80mg, 80mg q10min (max 300mg) |
ICU Considerations:
- Can cause bronchospasm in asthmatics
- May mask hypoglycaemia symptoms
- Useful in patients with tachycardia from other antihypertensives
- Avoid in severe heart failure (negative inotrope)
Hydralazine
| Parameter | Value |
|---|---|
| Mechanism | Direct arteriolar vasodilation (smooth muscle relaxation) |
| Onset | 10-20 minutes IV |
| Peak | 20-30 minutes IV |
| Duration | 2-6 hours |
| Half-life | 2-4 hours |
| Metabolism | Hepatic (acetylation) |
| Excretion | Renal (metabolites) |
| Side effects | Reflex tachycardia, headache, flushing, nausea, lupus-like syndrome (rare, chronic use) |
| Pregnancy category | C (safe, commonly used) |
| Breastfeeding | Safe |
| Fetal effects | May cause fetal distress with precipitous maternal hypotension |
| Dosing | 5-10mg IV q20min (max 20mg) |
ICU Considerations:
- Headache may mimic worsening pre-eclampsia
- Reflex tachycardia expected
- Avoid in tachyarrhythmias
- May worsen myocardial ischaemia in CAD
Nifedipine
| Parameter | Value |
|---|---|
| Mechanism | Dihydropyridine calcium channel blocker (vascular > cardiac) |
| Onset | 10-20 minutes PO (immediate release) |
| Peak | 30-60 minutes PO |
| Duration | 4-8 hours |
| Half-life | 2-5 hours |
| Metabolism | Hepatic (CYP3A4) |
| Excretion | Renal (metabolites) |
| Advantages | Oral route, no IV access needed, equally effective |
| Caution | Avoid sublingual (unpredictable absorption, precipitous hypotension) |
| Interaction | May potentiate MgSO4 effect (monitor closely) |
| Pregnancy category | C (safe, commonly used) |
| Breastfeeding | Safe |
| Fetal effects | Minimal direct effects |
| Dosing | 10-20mg PO q20-30min (max 50mg) |
ICU Considerations:
- Useful when IV access unavailable
- Interaction with magnesium: both cause vasodilation, monitor for hypotension
- Avoid in severe aortic stenosis
- CYP3A4 inhibitors increase levels (clarithromycin, azole antifungals)
Calcium Gluconate (Magnesium Antidote)
| Parameter | Value |
|---|---|
| Mechanism | Competitive antagonist to magnesium at NMJ and cardiac myocytes |
| Onset | Immediate (1-2 minutes) |
| Duration | 30-60 minutes |
| Dose | 1g (10 mL of 10%) IV over 10 minutes |
| Repeat | May repeat up to 3g total if no response |
| Indications | Magnesium toxicity (respiratory depression, cardiac arrest) |
| Side effects | Bradycardia, hypotension (if given too rapidly) |
| Pregnancy category | C (safe as antidote) |
| Breastfeeding | Safe |
ICU Considerations:
- Have drawn up and readily available when starting magnesium
- Check magnesium level after administration
- May need repeated doses in severe toxicity
- Supportive care (ventilation) still required if respiratory depression
- Does NOT remove magnesium (just antagonises effects)
Quality Assurance Checklist
Pre-eclampsia ICU Management Bundle
On Arrival:
- Manual BP confirmed ≥140/90
- IV access established (×2 large bore)
- Bloods sent: FBC, LFT, UEC, coagulation, G&H, magnesium, ABG
- Urinalysis performed (or PCR sent)
- Fetal heart rate assessed (CTG if greater than 24 weeks)
- Rapid bedside assessment (ABCDE)
Severe Features (BP ≥160/110 or symptoms):
- Antihypertensive given within 30-60 minutes
- MgSO4 loading dose given (4g IV over 20 min)
- MgSO4 infusion commenced (1g/hour)
- ICU team notified
- Obstetric team notified
- Anaesthetic team alerted
- Paediatric team alerted (if preterm)
- CTG monitoring initiated
- Steroids given if below 34+6 weeks
ICU Admission:
- Monitor BP q15min until stable, then q1h
- Hourly urine output
- Patellar reflexes q4h
- Respiratory rate monitored continuously
- Magnesium level checked (if indicated)
- Repeat bloods 6-12 hourly
- Fluid balance chart (restrictive)
- Daily weight (if stable)
- Daily bedside echo (if indicated)
Documentation:
- Time of antihypertensive administration
- Time of MgSO4 loading and infusion start
- Delivery plan discussed with patient
- Risks and benefits explained
- Red flag advice given (patient and family)
Pitfalls & Pearls
Clinical Pearls:
- Automated BP cuffs may underestimate BP in pre-eclampsia - use manual
- Proteinuria NOT required for diagnosis if end-organ dysfunction present
- Postpartum pre-eclampsia occurs without antepartum disease in 63% of cases
- Headache in late pregnancy/postpartum is pre-eclampsia until proven otherwise
- MgSO4 is for seizure prevention/treatment, NOT BP control
- sFlt-1/PlGF ratio below 38 rules out pre-eclampsia within 1 week
- Long-term cardiovascular risk counselling is essential at follow-up
- PRES on MRI is characteristic finding in eclampsia (posterior white matter)
- CHIPS trial: Less-tight control (diastolic 85) increases maternal complications
- MAGPIE trial: MgSO4 reduces eclampsia by 58% (NNT 63)
- HELLP can occur without hypertension - check LFT and platelets
- Patients are intravascularly depleted but interstitially overloaded - avoid fluids
- Pulmonary oedema risk highest postpartum (day 2-4) when third-spacing mobilises
- Consider atypical diagnoses if presentation atypical (TTP, AFLP, HUS)
- ADAMTS13 below 10% = TTP (urgent plasma exchange, NOT delivery)
- Magnesium toxicity mimics worsening pre-eclampsia - check reflexes and level
Pitfalls to Avoid:
- Delaying antihypertensive treatment when BP ≥160/110 (stroke risk)
- Using sublingual nifedipine (precipitous hypotension, fetal distress)
- Giving excessive IV fluids (pulmonary oedema risk, patients are intravascularly depleted)
- Not checking platelets before epidural/spinal (HELLP risk)
- Missing postpartum pre-eclampsia (attributing headache to "normal")
- Stopping magnesium too early (below 24 hours post-seizure or delivery)
- Using phenytoin instead of magnesium (inferior efficacy)
- Discharging without clear red flag advice
- Failing to consider Indigenous health disparities and cultural safety
- Not involving multidisciplinary team early (obstetrics, anaesthetics, ICU)
- Missing atypical presentations (HELLP without hypertension, AFLP)
- Not considering TTP/HUS (check ADAMTS13 if severe MAHA + neurological features)
- Over-resuscitating with fluids (restrictive strategy is safer)
- Assuming BP will normalize after delivery immediately (may worsen postpartum)
- Forgetting long-term cardiovascular risk counselling
- Using sodium nitroprusside prematurely (cyanide/thiocyanate toxicity)
- Not adjusting magnesium dose in renal failure (toxicity risk)
CICM SAQ Practice
SAQ 1 (15 marks)
Stem: A 32-year-old primigravida at 28 weeks gestation is admitted to ICU with severe pre-eclampsia. Her BP is 174/116 mmHg, she has a severe headache, and visual disturbances. Initial investigations show platelets 58 × 10⁹/L, ALT 345 U/L, creatinine 112 μmol/L.
Question: Outline your immediate management priorities and justify your approach with relevant evidence.
Model Answer:
This patient has severe pre-eclampsia with HELLP syndrome (Class 1 - platelets below 50, elevated LFT, renal impairment). My management priorities are:
1. Immediate stabilisation (2 marks)
- ABC assessment: Airway protection if altered GCS, oxygen if SpO2 below 94%
- Large bore IV access ×2
- Manual BP confirmation (automated may underestimate)
- ICU monitoring: ECG, SpO2, continuous BP
2. Seizure prophylaxis (3 marks)
- Magnesium sulfate 4g IV loading over 20 minutes
- Then 1g/hour maintenance infusion
- Justification: MAGPIE trial showed 58% reduction in eclampsia (RR 0.42), NNT 63 for moderate pre-eclampsia [22]
- Continue for 24 hours after delivery or last seizure
- Monitor: patellar reflexes, respiratory rate, urine output, magnesium level (if oliguria)
3. Blood pressure control (3 marks)
- Indication: BP ≥160/110 - treat within 30-60 min to prevent stroke
- Target: Initial below 160/110, then 130-150/80-100 mmHg
- First-line: IV labetalol 20mg bolus, repeat 40mg, 80mg, 80mg q10min (max 300mg)
- OR oral nifedipine 10-20mg (if IV access issues)
- Justification: CHIPS trial showed less-tight control (diastolic 85) did not improve perinatal outcomes but increased maternal complications (RR 1.34) [23]
- Avoid precipitous drops (risk of placental hypoperfusion)
4. HELLP syndrome management (2 marks)
- Notify obstetrics, anaesthetics, paediatrics
- Blood products prepared: crossmatch 4-6 units PRBCs, FFP, platelets on standby
- Consider corticosteroids: Dexamethasone 10mg IV q12h (may improve maternal lab parameters, evidence mixed)
- Plan delivery within 24-48 hours (definitive treatment)
5. Fetal considerations (1 mark)
- Continuous CTG monitoring
- Betamethasone 11.4mg IM ×2 doses, 24 hours apart (fetal lung maturity)
- Ultrasound: growth, AFI, Doppler
6. ICU supportive care (2 marks)
- Strict fluid restriction: 80-100 mL/hour total (avoid pulmonary oedema)
- Urinary catheter: hourly urine output (greater than 25 mL/hour)
- Monitor for complications: pulmonary oedema, AKI, PRES, DIC
- Daily bloods: FBC, LFT, UEC, coagulation
7. Multidisciplinary coordination (2 marks)
- Early obstetric review (delivery timing)
- Anaesthetic review (regional vs general anaesthesia for caesarean)
- Neonatal team (preterm delivery at 28 weeks)
- Consider tertiary transfer if local NICU unavailable
Examiner Notes:
- Accept: Alternative antihypertensives (hydralazine 5-10mg IV)
- Accept: Detailed magnesium toxicity monitoring
- Accept: Discussion of regional anaesthesia contraindication with platelets below 50
- Do not accept: Sublingual nifedipine, ACE inhibitors, excessive fluids
- Must mention: MAGPIE and CHIPS trials for justification
SAQ 2 (15 marks)
Stem: A 26-year-old woman at 35 weeks gestation has a generalised tonic-clonic seizure in ICU while being observed for pre-eclampsia. She becomes apnoeic and GCS drops to 3/15. Her BP is 188/118 mmHg.
Question: a) Describe your immediate management during the seizure (5 marks) b) Outline your ICU management post-seizure (10 marks)
Model Answer:
a) Immediate management during seizure (5 marks):
-
Call for help (1 mark) - ICU team, obstetrics, anaesthetics, airway equipment
-
Positioning (1 mark):
- Left lateral position (prevents aspiration, optimises uterine blood flow)
- Protect from injury (side rails, remove objects)
- Do NOT insert tongue blade or objects into mouth
-
Airway management (1 mark):
- Clear secretions (suction)
- Administer oxygen 15 L/min via face mask
- Assess airway patency
-
Monitoring (1 mark):
- Note time and duration of seizure
- Continuous ECG, SpO2, BP monitoring
- Prepare for intubation if prolonged
-
Most seizures self-terminate (1 mark):
- If greater than 3 minutes: Prepare for airway intervention
- If greater than 5 minutes: Consider benzodiazepines (lorazepam 0.1 mg/kg IV)
b) ICU management post-seizure (10 marks):
1. Airway and ventilation (2 marks):
- Assess GCS: If GCS below 8 or inadequate airway protection: Intubate
- RSI: Preoxygenation, cricoid pressure, rapid sequence agents (ketamine avoided - ↑BP, use propofol/rocuronium)
- Ventilation strategy: Normocapnia (PaCO2 35-45), avoid hypocapnia (uterine vasoconstriction)
- Maintain left lateral tilt 15°
2. Seizure control (2 marks):
- Magnesium sulfate 4g IV loading over 20 minutes (if not already infusing)
- Then 1g/hour maintenance infusion
- If recurrent seizure: Additional MgSO4 2g IV bolus
- If refractory (greater than 2 seizures despite Mg): IV diazepam 5-10mg or midazolam 2-5mg
- Do NOT use phenytoin (inferior to MgSO4) [21]
3. Blood pressure control (2 marks):
- Indication: BP ≥160/110 with eclampsia - urgent treatment
- Target: 130-150/80-100 mmHg (avoid precipitous drops)
- IV labetalol 20mg bolus, repeat q10min (max 300mg)
- Consider labetalol infusion 1-2 mg/min if refractory
- Monitor BP q5-10min initially
4. Diagnostic investigations (1 mark):
- CT head - exclude intracranial haemorrhage, PRES
- MRI brain if CT negative (shows characteristic PRES - posterior white matter oedema)
- EEG if status epilepticus suspected or prolonged encephalopathy
- Bloods: FBC, LFT, UEC, coagulation, magnesium level, ABG
5. ICU supportive care (2 marks):
- Strict fluid restriction: 80-100 mL/hour (avoid pulmonary oedema)
- Urinary catheter: hourly urine output (greater than 25 mL/hour)
- Monitor magnesium toxicity: Reflexes, RR, level
- Consider EEG monitoring for subclinical seizures
- Prepare for delivery (definitive treatment)
6. Delivery planning (1 mark):
- Definitive treatment is delivery
- After stabilisation (seizures controlled, BP managed)
- Usually within 12-24 hours
- Caesarean if vaginal delivery not imminent or fetal distress
Examiner Notes:
- Accept: Alternative antihypertensives (hydralazine, nifedipine)
- Accept: Mention of PRES on MRI as typical finding
- Accept: Discussion of EEG monitoring
- Do not accept: Delaying treatment, inadequate BP control, phenytoin as first-line
- Must emphasise: Magnesium as first-line for seizures, left lateral positioning, avoiding tongue blades
CICM Viva Practice
Viva Scenario 1: Severe Pre-eclampsia in ICU
Stem: A 30-year-old primigravida at 31 weeks gestation is admitted to ICU with severe pre-eclampsia. Her BP is 170/112 mmHg, she has severe frontal headache, visual "flashes", and epigastric pain. Bloods show platelets 62 × 10⁹/L, ALT 289 U/L, creatinine 98 μmol/L.
Opening Question: What are your immediate priorities and why?
Model Answer:
This patient has severe pre-eclampsia with HELLP syndrome (Class 2 - platelets 50-100). My immediate priorities are:
-
Simultaneous assessment and resuscitation
- ABC assessment: Airway protection, oxygen if needed
- Large bore IV access ×2
- Bloods: FBC, LFT, UEC, coagulation, G&H, magnesium level
- Manual BP confirmation
-
Blood pressure control (treat within 30-60 minutes)
- IV labetalol 20mg bolus, repeat q10-15min (max 300mg)
- Target: 130-150/80-100 mmHg
- Justification: CHIPS trial - less-tight control increases maternal complications [23]
-
Seizure prophylaxis
- Magnesium sulfate 4g IV loading over 20 minutes
- Then 1g/hour maintenance infusion
- Justification: MAGPIE trial - 58% reduction in eclampsia, NNT 63 [22]
-
Fetal assessment
- Continuous CTG
- Ultrasound: growth, AFI, Doppler
-
Consider steroids for fetal lung maturity (betamethasone 11.4mg IM)
-
Multidisciplinary coordination
- Obstetrics, anaesthetics, neonatology
- Plan delivery within 24-48 hours
Follow-up Questions:
-
She has a generalised tonic-clonic seizure lasting 90 seconds. How do you manage this?
- Model answer: Position left lateral, protect from injury, do NOT insert tongue blade, give O2, note time. Most seizures self-terminate. Ensure magnesium infusing (loading 4g IV if not given). If recurrent seizure, give additional MgSO4 2g IV bolus. If refractory (greater than 2 seizures despite Mg), consider diazepam 5-10mg IV. Do NOT give phenytoin. Urgent delivery planning after stabilisation. Consider CT head if postictal GCS below 13 or focal deficit.
-
She becomes oliguric (urine output 20mL/hour) and drowsy with absent patellar reflexes. What do you suspect and how do you manage this?
- Model answer: Magnesium toxicity due to reduced renal excretion (oliguria). Immediate management: STOP magnesium infusion. Check respiratory rate (if below 12 or respiratory depression), give calcium gluconate 1g (10mL of 10%) IV over 10 minutes. Check serum magnesium level (expect greater than 5 mmol/L). Supportive care - consider intubation if apnoeic. Calcium is antidote and first-line treatment. If severe toxicity persists, may need dialysis for magnesium removal. Do not restart magnesium unless renal function improves and still indicated.
-
Her BP remains 178/120 despite labetalol 300mg total. What are your options?
- Model answer: Options include: (1) Labetalol infusion 1-2 mg/min, (2) Hydralazine 5-10mg IV q20min (watch for reflex tachycardia and headache), (3) Nicardipine infusion 5 mg/hour titrated, (4) Sodium nitroprusside infusion (last resort - cyanide/thiocyanate toxicity risk, fetal cyanide exposure). I would start labetalol infusion 1 mg/min and titrate to BP. Avoid sublingual nifedipine. Avoid ACE inhibitors/ARBs.
-
What are the delivery timing considerations at 31 weeks?
- Model answer: At 31 weeks with severe pre-eclampsia + HELLP, options include: (1) Immediate delivery if maternal deterioration, (2) Expectant management with corticosteroids and close monitoring at tertiary centre until 34 weeks, (3) Delivery at 32-34 weeks if maternal condition stabilises. This requires multidisciplinary discussion with obstetrics, neonatology, and patient. Given severe features and HELLP, I would trend towards earlier delivery after corticosteroids and maternal stabilisation.
Discussion Points:
- CHIPS trial evidence and BP targets
- MAGPIE trial evidence and magnesium dosing
- HELLP classification and management
- Delivery timing considerations for preterm severe pre-eclampsia
- Magnesium toxicity recognition and treatment
- Antihypertensive options for refractory hypertension
Viva Scenario 2: Postpartum Eclampsia
Stem: A 34-year-old woman is readmitted to ICU 6 days postpartum after an uncomplicated vaginal delivery. She had a witnessed generalised tonic-clonic seizure at home. On arrival she is post-ictal with BP 188/118 mmHg, GCS 12, and complaining of severe headache.
Opening Question: What is your differential diagnosis and immediate management?
Model Answer:
My primary differential is postpartum eclampsia - this is the most likely cause of seizure in the early postpartum period with severe hypertension. However, I must also consider:
Differential Diagnosis:
- Postpartum eclampsia (most likely)
- Intracranial haemorrhage (ICH)
- Cerebral venous sinus thrombosis (CVST)
- Posterior reversible encephalopathy syndrome (PRES)
- Postpartum preeclampsia (pre-seizure)
- Primary seizure disorder (new or known)
- Other causes: Hypoglycaemia, electrolyte disturbance, drug-related, infection
Immediate Management:
-
ABC stabilisation
- Airway: Protect if GCS below 8, position left lateral
- Breathing: O2 15 L/min, SpO2 monitoring, ABG
- Circulation: IV access ×2, ECG, manual BP
-
Bloods: FBC, LFT, UEC, coagulation, glucose, magnesium level, G&H, toxicology
-
BP control
- IV labetalol 20mg, repeat q10min (max 300mg)
- Target: 130-150/80-100 mmHg
-
Magnesium sulfate 4g IV loading + 1g/hour infusion (even if no further seizures)
-
CT head - to exclude ICH, CVST (may show PRES features)
-
Continuous monitoring: BP, SpO2, GCS, neurological checks q1h
Follow-up Questions:
-
She has no antepartum history of hypertension. Is this still likely eclampsia?
- Model answer: Yes. 63% of delayed postpartum pre-eclampsia/eclampsia occurs without antepartum hypertensive disease. Postpartum eclampsia can occur up to 6 weeks post-delivery, with peak risk at days 3-6. The diagnosis is new-onset hypertension with proteinuria or end-organ dysfunction (seizure in this case) in the postpartum period. Key is maintaining high index of suspicion.
-
CT head shows bilateral posterior white matter changes. What is this and how do you manage it?
- Model answer: Posterior Reversible Encephalopathy Syndrome (PRES). This is the typical imaging finding in eclampsia - vasogenic oedema predominantly affecting posterior cerebral regions due to endothelial dysfunction and failure of autoregulation. Management includes: BP control (target 140-150 systolic), continue magnesium, neuroprotective care, ICU monitoring. Usually reversible with BP control over days to weeks. Rarely may progress to cytotoxic oedema/infarction if severe or untreated.
-
Her GCS drops to 6 and she requires intubation. What is your RSI approach?
- Model answer: Preoxygenation with head-up 30°, left lateral tilt 15°. RSI agents: Propofol 2mg/kg (reduces BP, which is beneficial) OR etomidate 0.3mg/kg (haemodynamically neutral). Rocuronium 1.2mg/kg (avoid succinylcholine if hyperkalaemia from AKI). Cricoid pressure (modified by left lateral tilt). Avoid ketamine (increases BP). Ventilation: Normocapnia (PaCO2 35-45), avoid hypocapnia (uterine vasoconstriction, postpartum still relevant for involution). Maintain left lateral tilt 15°.
-
How long do you continue magnesium?
- Model answer: Continue for 24 hours after the last seizure OR 24 hours postpartum (whichever is later). In this case, seizure was day 6 postpartum, so continue magnesium for 24 hours after the seizure, then reassess. Monitor: reflexes, respiratory rate, urine output, magnesium level. If renal impairment, reduce dose (0.5g/hour) or check levels.
Discussion Points:
- Postpartum eclampsia epidemiology (63% no antepartum disease)
- PRES pathophysiology and management
- RSI considerations in postpartum period
- Magnesium duration in postpartum eclampsia
- Differential diagnosis of postpartum seizures
Viva Scenario 3: HELLP Syndrome with Complications
Stem: A 28-year-old primigravida at 33 weeks gestation is admitted to ICU with HELLP syndrome. Platelets 42 × 10⁹/L, ALT 487 U/L, LDH 890 U/L, fibrinogen 1.2 g/L. She develops RUQ pain radiating to back and BP drops to 85/45.
Opening Question: What are you concerned about and what is your management?
Model Answer:
I am concerned about subcapsular liver haematoma or impending hepatic rupture - this is a catastrophic complication of HELLP syndrome with high mortality (up to 80% if ruptures).
Immediate Management:
-
Call for help - urgent obstetrics, surgery, anaesthesia, blood bank
-
Massive transfusion protocol
- Activate immediately
- O negative blood until crossmatched
- Target ratio 1:1:1 (PRBC:FFP:Platelets)
- Cryoprecipitate 10U for fibrinogen below 2 g/L
- Fibrinogen concentrate 2-4g if available
-
Haemodynamic stabilisation
- IV fluids: Crystalloid bolus 500-1000mL (cautious - capillary leak)
- Vasopressors: Norepinephrine infusion if hypotensive despite fluids
- Invasive arterial line and CVC for monitoring
-
Bloods stat: FBC, coagulation, fibrinogen, crossmatch 8-10 units PRBCs, ABG, lactate
-
Imaging
- Urgent liver ultrasound (look for subcapsular haematoma)
- CT abdomen if ultrasound equivocal and patient stable enough
-
Prepare for delivery - definitive treatment for HELLP
- Emergency caesarean section
- General anaesthesia likely (platelets below 50, contraindicates epidural)
- Blood products in theatre
-
Surgical consultation
- Prepare for possible laparotomy
- Liver packing or resection if rupture
Follow-up Questions:
-
Ultrasound shows large subcapsular liver haematoma but no rupture. What are the options?
- Model answer: Options include: (1) Continue medical management and deliver by caesarean (if maternal stabilises), (2) Caesarean + surgical drainage of haematoma, (3) Expectant management (not recommended given clinical deterioration). Given hypotension and expanding haematoma, I would favour urgent delivery by caesarean under general anaesthesia with blood product support, and intraoperative assessment of liver with surgical standby for possible drainage if haematoma enlarges or ruptures.
-
During caesarean, the liver ruptures with massive haemorrhage. What is your management?
- Model answer: Continue massive transfusion, activate all personnel, maintain perfusion pressure (MAP greater than 65). Surgical options: Packing of liver, segmental resection if localised, hepatic artery ligation if uncontrolled, liver transplantation in extreme cases (unlikely in acute setting). Resuscitation focus: Blood products, factor VIIa if available, tranexamic acid 1g IV, normothermia, calcium repletion, correct acidosis. Involve hepatobiliary surgeon if available. Mortality high (50-80%).
-
Post-operatively, she develops acute kidney injury with creatinine 250 μmol/L and oliguria. Do you start CRRT?
- Model answer: Indications for CRRT in this setting: (1) Refractory hyperkalaemia, (2) Severe metabolic acidosis, (3) Volume overload/pulmonary oedema unresponsive to diuretics, (4) Uremic complications, (5) Oliguria/anuria with rising creatinine. Given oliguria and AKI in context of multi-organ failure (liver, haemorrhage), I would initiate CRRT earlier rather than later. Use CRRT (CVVHDF) with regional citrate anticoagulation (reduce bleeding risk). Adjust magnesium dose to 0.5g/hour (CRRT removes magnesium).
-
What are the long-term outcomes for patients with HELLP requiring ICU?
- Model answer: Maternal mortality 1-3% (higher with complications like hepatic rupture). Recurrence risk in future pregnancies 5-19% (HELLP specific). Long-term cardiovascular risk increased (2-3×). Long-term liver function usually recovers fully unless resection/transplantation. Renal function may recover but some develop CKD. Counselling about cardiovascular risk, future pregnancy planning, and close follow-up is essential.
Discussion Points:
- HELLP complications (haematoma, rupture, DIC, AKI, pulmonary oedema)
- Massive transfusion protocol in obstetric haemorrhage
- CRRT indications and prescription in obstetric AKI
- Long-term outcomes and counselling
- Hepatic surgery in pregnancy
Australian Guidelines
SOMANZ (Society of Obstetric Medicine of Australia and New Zealand) [3]
SOMANZ 2023 Guidelines - Key Points:
- Hypertension definition: ≥140/90 mmHg
- Pre-eclampsia diagnosis: HTN + proteinuria OR end-organ dysfunction after 20 weeks
- Target BP in treatment: 130-150/80-100 mmHg
- Aspirin 150mg nocte for high-risk women (start below 16 weeks)
- Calcium 1.5-2g/day for women with low dietary calcium
- MgSO4 for eclampsia and severe pre-eclampsia
- Delivery at 37+0 weeks for mild pre-eclampsia
- Urgent delivery for severe pre-eclampsia ≥34 weeks
RANZCOG
C-Obs 06: Hypertension in Pregnancy:
- Endorses SOMANZ guidelines
- Emphasises multidisciplinary care
- Recommends tertiary referral for severe preterm disease
- Regional anaesthesia platelet threshold: ≥80 × 10⁹/L (relative), ≥50 × 10⁹/L (absolute)
ANZICS
ANZICS Statement on Critical Care in Pregnancy (2020):
- Recognises pregnancy as a cause for ICU admission (2-4% of ICU admissions)
- Recommends multidisciplinary team approach
- Emphasises maternal stabilisation as priority
- Fetal monitoring secondary but important
- Transfer to obstetric ICU if specialised care needed
State-Specific Guidelines
NSW Health Clinical Guidelines:
- PD2019_038: Maternity - Hypertensive Disorders of Pregnancy
- Specific protocols for escalation and transfer
- Rural and regional transfer pathways
Queensland Health:
- Statewide Maternity and Neonatal Clinical Guideline: Hypertension in pregnancy
- Emergency management algorithms
- Retrieval medicine protocols
Victorian Department of Health:
- Victorian Hypertensive Disorders of Pregnancy Guidelines
- Perinatal Service Network protocols
WA Health:
- WA Clinical Guidelines: Hypertensive Disorders of Pregnancy
- Remote area management protocols
References
Epidemiology
- Mol BWJ, et al. Pre-eclampsia. Lancet. 2016;387:999-1011. PMID: 26342729
- Australian Institute of Health and Welfare. Maternal deaths in Australia 2012-2021. AIHW. 2023.
- Lowe SA, et al. SOMANZ guidelines for the management of hypertensive disorders of pregnancy 2023. ANZJOG. 2023;63:529-555. PMID: 37705353
- Knight M. Eclampsia in the United Kingdom 2005-2014. BJOG. 2007;114:1072-8. PMID: 17617191
- Creanga AA, et al. Maternal morbidity for obstetric intensive care admissions in the United States. Am J Obstet Gynecol. 2014;210:298.e1-8. PMID: 24480620
- Barton JR, Sibai BM. Prediction and prevention of recurrent preeclampsia. Obstet Gynecol. 2008;112:359-372. PMID: 18669736
- Polin RA, et al. Intensive care and the obstetric patient. J Intensive Care Med. 2016;31:234-245.
- Martin JN Jr, et al. HELLP syndrome: The state of the art. Am J Obstet Gynecol. 2006;195:40-7. PMID: 16813742
- Altman D, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial. Lancet. 2002;359:1877-1890. PMID: 12057549
Indigenous Health
- Perinatal and Maternal Mortality Review Committee. 14th Annual Report of the PMMRC. Wellington: Health Quality & Safety Commission. 2020.
- Chamberlain M, et al. Indigenous status and outcomes for women admitted to intensive care with hypertensive disorders of pregnancy. Aust Crit Care. 2022;35:123-129.
- Margolis SA, et al. Aeromedical retrieval for obstetric emergencies. Aust J Rural Health. 2011;19:77-83.
Pathophysiology
- Phipps EA, et al. Pre-eclampsia: pathogenesis, novel diagnostics and therapies. Nat Rev Nephrol. 2019;15:275-289. PMID: 31273318
- Roberts JM, et al. Preeclampsia: an endothelial cell disorder. Am J Obstet Gynecol. 1989;161:1200-1204.
- Maynard SE, et al. Excess placental sFlt1 may contribute to preeclampsia pathogenesis. J Clin Invest. 2003;111:649-658. PMID: 12618519
- Levine RJ, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. 2004;350:672-683. PMID: 14764923
- Venkatesha S, et al. Soluble endoglin contributes to preeclampsia pathogenesis. Nat Med. 2006;12:642-649. PMID: 16751773
- Zeisler H, et al. Predictive value of the sFlt-1:PlGF ratio in women with suspected preeclampsia. N Engl J Med. 2016;374:13-22. PMID: 26735993
HELLP Syndrome
- ACOG Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia. Obstet Gynecol. 2020;135:e237-e260. PMID: 32443079
- Sibai BM. Diagnosis, controversies, and management of HELLP syndrome. Obstet Gynecol. 2004;103:981-991. PMID: 15121574
Seizure Management
- The Eclampsia Trial Collaborative Group. Which anticonvulsant for women with eclampsia? Lancet. 1995;345:1455-1463. PMID: 7769899
- Altman D, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial. Lancet. 2002;359:1877-1890. PMID: 12057549
Antihypertensives and CHIPS
- Magee LA, et al. Less-tight versus tight control of hypertension in pregnancy. N Engl J Med. 2015;372:407-417. PMID: 25629739
- Duley L, et al. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev. 2013;7:CD001449. PMID: 23897483
Delivery Timing
- Gyamfi-Bannerman C, et al. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374:1311-1320. PMID: 26842679
- Koopmans CM, et al. Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks' gestation (HYPITAT). Lancet. 2009;374:979-988. PMID: 19632407
Postpartum Pre-eclampsia
- Al-Safi Z, et al. Delayed postpartum preeclampsia and eclampsia: demographics, clinical course, and complications. Obstet Gynecol. 2011;118:1102-1107. PMID: 22015879
- Bellamy L, et al. Pre-eclampsia and risk of cardiovascular disease and cancer in later life. BMJ. 2007;335:974. PMID: 17975258
Remote/Rural
- Shekhar S, et al. Oral nifedipine versus intravenous labetalol for severe hypertension in pregnancy: a randomised controlled trial. BJOG. 2013;120:1747-1752. PMID: 23906215
Additional Evidence
- Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol. 1998;92:883-889. PMID: 9794695
- Sibai BM. Magnesium sulfate prophylaxis in preeclampsia: lessons learned from recent trials. Am J Obstet Gynecol. 2004;190:1520-1526. PMID: 15284724
- Duley L, et al. Magnesium sulphate and other anticonvulsants for women with pre-eclampsia. Cochrane Database Syst Rev. 2010;11:CD000025. PMID: 21069663
- Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005;105:402-410. PMID: 15684172
- American College of Obstetricians and Gynecologists. Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Obstet Gynecol. 2013;122:1122-1131. PMID: 24150343
- ACOG Practice Bulletin No. 203. Chronic Hypertension in Pregnancy. Obstet Gynecol. 2019;133:e26-e50. PMID: 30575676
- Lowe SA, et al. SOMANZ guidelines for the management of hypertensive disorders of pregnancy 2014. ANZJOG. 2015;55:11-16. PMID: 25312330
- Steegers EA, et al. Pre-eclampsia. Lancet. 2010;376:631-644. PMID: 20598363
- Magee LA, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. Pregnancy Hypertens. 2014;4:105-145. PMID: 26104418
- Brown MA, et al. Hypertensive Disorders of Pregnancy: ISSHP Classification. Hypertension. 2018;72:24-43. PMID: 29899139
- Abalos E, et al. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev. 2018;10:CD002252. PMID: 30277556
- Roberts D, et al. Antenatal corticosteroids for accelerating fetal lung maturation. Cochrane Database Syst Rev. 2017;3:CD004454. PMID: 28321847
- Shear RM, et al. Postpartum hypertension and preeclampsia: incidence and associated complications. Obstet Gynecol Clin North Am. 2015;42:37-47.
- Chames MC, et al. Late postpartum eclampsia: a preventable disease? Am J Obstet Gynecol. 2002;186:1174-1177. PMID: 12066094
- Euser AG, et al. Acute kidney injury in pregnancy: a systematic review. Clin J Am Soc Nephrol. 2017;12:2162-2172.
- Gutiérrez G, et al. Acute fatty liver of pregnancy: a systematic review. Ann Hepatol. 2015;14:289-297.
- Scully M, et al. Management of thrombotic thrombocytopenic purpura. Blood. 2019;133:1554-1564.
- Huisman EL, et al. Posterior reversible encephalopathy syndrome: clinical and radiological characteristics. J Clin Neurol. 2012;8:134-140.
- Fugate JE, et al. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outcome. J Neurol Neurosurg Psychiatry. 2015;86:380-386.
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Frequently asked questions
Quick clarifications for common clinical and exam-facing questions.
What is the definition of pre-eclampsia?
New-onset hypertension (≥140/90 mmHg) with proteinuria or end-organ dysfunction after 20 weeks gestation.
When should I give magnesium sulfate in ICU?
For eclampsia treatment, severe pre-eclampsia with neurological symptoms, and prophylaxis in severe disease. Give 4g IV loading over 20 min, then 1g/hour maintenance.
What is the definitive treatment for pre-eclampsia?
Delivery of the fetus and placenta - timing depends on gestational age, severity, and maternal stability.
What are ICU admission criteria for pre-eclampsia?
Eclampsia, severe hypertension requiring IV infusion, pulmonary oedema, HELLP syndrome, AKI requiring RRT, altered consciousness, postoperative ICU care post-delivery.
What does the CHIPS trial show?
Less-tight BP control (target diastolic 85 vs 100) did not improve perinatal outcomes but increased maternal complications. Target BP 130-150/80-100 mmHg.
Learning map
Use these linked topics to study the concept in sequence and compare related presentations.
Prerequisites
Start here if you need the foundation before this topic.
- Obstetric Critical Care Overview
- Advanced Haemodynamic Monitoring
Differentials
Competing diagnoses and look-alikes to compare.
- Hypertensive Emergency in ICU
- Seizure Management in ICU
- Acute Liver Failure
- Thrombotic Microangiopathy (TTP/HUS)
Consequences
Complications and downstream problems to keep in mind.
- HELLP Syndrome ICU Management
- Haemorrhagic Stroke
- Posterior Reversible Encephalopathy Syndrome