📋 Key Information Summary
- Pre-eclampsia complicates 5–8% of pregnancies in Australia and remains a leading cause of maternal and perinatal morbidity and mortality
- Diagnosis requires new-onset hypertension (≥140/90 mmHg on two occasions ≥4 hours apart) plus proteinuria (≥300 mg/24 h or PCR ≥30 mg/mmol) after 20 weeks' gestation
- Renal physiological changes in normal pregnancy include a 50% rise in GFR, reduced serum creatinine (~45–70 µmol/L), and decreased uric acid due to enhanced tubular secretion
- Low-dose aspirin (100–150 mg daily from 12–36 weeks) reduces pre-eclampsia risk by ~60% in high-risk women; recommended by RANZCOG for risk-based prophylaxis
- Severe features include BP ≥160/110 mmHg, platelet count <100 × 10⁹/L, serum creatinine >90 µmol/L, LDH >600 U/L, pulmonary oedema, or new-onset cerebral/visual disturbances
- HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) is a severe variant occurring in 10–20% of pre-eclampsia cases, with significant maternal morbidity
- IV magnesium sulphate is first-line for eclampsia prevention and treatment (Sibai regimen: 4 g loading dose then 1–2 g/h infusion); available PBS General Benefit
- Labetalol (oral or IV) is the preferred antihypertensive; nifedipine slow-release oral and IV hydralazine are alternatives; target BP <140/90 mmHg
- Definitive treatment is delivery of the placenta; timing balances maternal severity against fetal maturity, guided by RANZCOG and SOMANZ guidelines
- Aboriginal and Torres Strait Islander women have higher rates of pre-eclampsia and hypertensive disorders, driven by chronic hypertension prevalence, remoteness barriers, and limited antenatal access
- Postpartum monitoring is essential as pre-eclampsia may develop or worsen up to 48–72 hours after delivery; 25% of eclampsia cases are postpartum
- Women with pre-eclampsia history have a 2–7× increased lifetime risk of cardiovascular disease; long-term cardiovascular risk reduction counselling is mandatory
Introduction & Australian Epidemiology
Pre-eclampsia is a multisystem hypertensive disorder of pregnancy affecting 5–8% of pregnancies worldwide, with similar prevalence reported in Australian population studies. It remains one of the leading causes of maternal mortality and morbidity in Australia, accounting for approximately 10–15% of direct maternal deaths as reported by the Australian Institute of Health and Welfare (AIHW) Maternal Deaths in Australia series. Pre-eclampsia is characterised by new-onset hypertension with proteinuria developing after 20 weeks' gestation, and may progress to eclampsia (seizures), HELLP syndrome, stroke, hepatic rupture, renal failure, or placental abruption.
The hypertensive disorders of pregnancy are classified by the Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) into four categories: gestational hypertension, pre-eclampsia (new-onset or superimposed on chronic hypertension), chronic hypertension, and eclampsia. Pre-eclampsia can be further stratified into early-onset (<34 weeks) and late-onset (≥34 weeks), with early-onset disease carrying higher maternal and perinatal risks and a greater association with placental insufficiency.
Renal involvement is central to the pathophysiology of pre-eclampsia. Normal pregnancy induces dramatic haemodynamic and tubular changes including a 50% increase in glomerular filtration rate (GFR), reduction in serum creatinine, and altered electrolyte handling. Understanding these physiological adaptations is essential for distinguishing normal pregnancy physiology from pathological pre-eclamptic changes and for guiding safe prescribing in pregnancy.
In Australia, the burden of pre-eclampsia disproportionately affects Aboriginal and Torres Strait Islander women, women in rural and remote communities, and those with limited access to specialist antenatal care. Improving risk stratification, prophylaxis uptake, and timely escalation remain national priorities under the National Maternity Services Capability Framework.
Renal Physiological Changes in Pregnancy
Pregnancy induces profound cardiovascular, renal, and endocrine adaptations that are essential to support fetal growth and prepare for the haemodynamic demands of labour and postpartum recovery. Clinicians must understand these changes to avoid misdiagnosing normal physiology as pathology or overlooking true renal disease.
Haemodynamic Changes
- Cardiac output increases by 30–50% by the third trimester, driven by a rise in stroke volume and heart rate (HR typically 10–20 bpm above pre-pregnancy baseline)
- Systemic vascular resistance (SVR) falls by 20–30% due to nitric oxide, progesterone-mediated vasodilation, and the low-resistance uteroplacental circulation
- Mean arterial pressure (MAP) falls by 10–15 mmHg in the second trimester, reaching a nadir at approximately 24 weeks, then gradually returns toward pre-pregnancy levels by term
- Plasma volume expands by 40–50% (peaking at 32–34 weeks), while red cell mass increases by only 20–30%, producing physiological dilutional anaemia
Renal Structural & Haemodynamic Changes
- Kidney length increases by approximately 1 cm due to increased renal blood flow and interstitial volume
- Renal plasma flow (RPF) increases by 50–80% in the first trimester (peaking by 16 weeks), then gradually declines toward non-pregnant levels by term
- GFR increases by approximately 50% (from ~90 mL/min/1.73 m² to ~140 mL/min/1.73 m²) in early pregnancy, paralleling the RPF rise
- Serum creatinine in normal pregnancy is typically 45–70 µmol/L (lower than the non-pregnant reference range of 50–90 µmol/L); a creatinine of >75 µmol/L should raise concern for renal impairment
- Serum urea falls to 2.5–4.0 mmol/L (normal non-pregnant: 2.5–7.0 mmol/L) due to increased GFR and volume expansion
Tubular & Electrolyte Changes
- Enhanced sodium and water reabsorption despite increased GFR: net positive sodium balance of ~900 mmol by term, and total body water increases by 6–8 L
- Serum sodium falls by 3–5 mmol/L (physiological hyponatraemia of pregnancy; normal range ~130–135 mmol/L)
- Serum osmolality decreases by ~10 mOsm/kg due to reset osmostat for ADH release
- Serum potassium falls slightly; aldosterone levels rise significantly, promoting distal tubular K⁺ secretion
- Serum bicarbonate falls to 18–22 mmol/L (respiratory alkalosis with compensatory renal bicarbonate excretion; pCO₂ ~30 mmHg)
- Serum uric acid decreases in early pregnancy (enhanced tubular secretion) but rises in the third trimester; elevated uric acid is an early marker of pre-eclampsia
- Glycosuria and aminoaciduria may occur due to increased filtered load exceeding tubular reabsorption capacity — this does not necessarily indicate gestational diabetes or renal pathology
Urinary Tract Changes
- Physiological hydronephrosis (more pronounced on the right) affects up to 90% of pregnant women by the third trimester; avoid overdiagnosing obstruction
- Ureteric dilation may persist for up to 12 weeks postpartum
- Bladder capacity increases but detrusor tone is reduced, contributing to urinary frequency and incomplete emptying
- Risk of asymptomatic bacteriuria is 2–10% (similar to non-pregnant women) but progression to pyelonephritis is much higher (up to 30% if untreated); screening at first antenatal visit is standard Australian practice
| Parameter | Non-Pregnant | Pregnant (3rd Trimester) | Clinical Significance |
|---|---|---|---|
| Serum Creatinine | 50–90 µmol/L | 45–70 µmol/L | >75 µmol/L suggests impairment |
| Serum Urea | 2.5–7.0 mmol/L | 2.5–4.0 mmol/L | >5.0 mmol/L is abnormal in pregnancy |
| eGFR | ~90 mL/min/1.73 m² | ~140 mL/min/1.73 m² | CKD-EPI formula unreliable; use 24-h creatinine clearance |
| Serum Uric Acid | 0.15–0.40 mmol/L | 0.18–0.32 mmol/L (varies by trimester) | Rising uric acid in 3rd trimester is a marker of pre-eclampsia |
| Serum Sodium | 135–145 mmol/L | 130–135 mmol/L | Physiological hyponatraemia; do not over-correct |
| Serum Bicarbonate | 22–28 mmol/L | 18–22 mmol/L | Compensated respiratory alkalosis is normal |
| Urine Protein | <150 mg/24 h | <300 mg/24 h | ≥300 mg/24 h or PCR ≥30 mg/mmol is pathological |
Pre-eclampsia: Pathophysiology & Diagnosis
Pathophysiology
Pre-eclampsia is a two-stage disorder. Stage 1 involves abnormal placentation: defective remodelling of the spiral arteries by extravillous trophoblast results in inadequate conversion to high-capacity, low-resistance vessels. This creates placental ischaemia and hypoperfusion, triggering release of anti-angiogenic factors (particularly soluble fms-like tyrosine kinase-1 [sFlt-1] and soluble endoglin [sEng]) into the maternal circulation.
Stage 2 represents the maternal systemic inflammatory and endothelial dysfunction response. The imbalance between pro-angiogenic (PlGF, VEGF) and anti-angiogenic factors leads to:
- Widespread endothelial dysfunction and loss of normal vasodilatory response to nitric oxide
- Increased vascular permeability → proteinuria, oedema, hypoalbuminaemia
- Activation of the coagulation cascade → microangiopathic haemolysis, thrombocytopenia
- Cerebral vasospasm and hyperperfusion → headache, visual disturbance, seizures (eclampsia)
- Hepatic sinusoidal endothelial dysfunction → right upper quadrant pain, elevated transaminases, HELLP syndrome
- Glomerular endotheliosis → reduced GFR, rising creatinine and uric acid, proteinuria
- Pulmonary endothelial leak → pulmonary oedema (a severe feature)
Risk Factors
| Risk Category | Factors |
|---|---|
| High risk (≥1 major) | Previous pre-eclampsia; chronic hypertension; pre-existing diabetes (type 1 or 2); CKD; autoimmune disease (SLE, antiphospholipid syndrome); multiple pregnancy |
| Moderate risk (≥2 moderate) | Nulliparity; BMI ≥35; maternal age ≥40; family history of pre-eclampsia; interpregnancy interval >10 years; pre-existing renal disease stage 1–2 |
| ATSI-specific | Higher baseline rates of chronic hypertension, diabetes, and obesity; lower rates of early antenatal booking; higher rates of remote residence limiting access to specialist care |
Prophylaxis with Low-Dose Aspirin
RANZCOG recommendation: Women at high risk of pre-eclampsia should receive low-dose aspirin 100–150 mg daily from 12 weeks until 36 weeks' gestation. A 2019 Cochrane review demonstrated a 60% relative risk reduction in pre-eclampsia (RR 0.40, 95% CI 0.27–0.60) when started before 16 weeks. Aspirin 100 mg is PBS General Benefit in Australia. Calcium supplementation (≥1 g/day) may be considered where dietary intake is low, per WHO recommendation.
Diagnostic Criteria (SOMANZ / ISSHP)
Pre-eclampsia is diagnosed when both of the following are present after 20 weeks' gestation:
- Hypertension: Systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg on two occasions ≥4 hours apart, measured using validated automated device with appropriate cuff size, in the seated position after 5 minutes' rest
- Significant proteinuria: ≥300 mg/24-hour urine collection, or spot urine protein:creatinine ratio (PCR) ≥30 mg/mmol, or urine dipstick ≥2+ (if quantitative testing unavailable)
Pre-eclampsia without overt proteinuria: New-onset hypertension after 20 weeks with any of the following severe features — even in the absence of proteinuria — should be managed as pre-eclampsia: platelet count <100 × 10⁹/L, serum creatinine >90 µmol/L, LDH >600 U/L, elevated ALT/AST (>2× upper limit of normal), pulmonary oedema, or new-onset cerebral/visual symptoms.
Severe Features — Criteria for Classification as "Severe Pre-eclampsia"
Mild
Non-Severe Pre-eclampsia
BP 140–159/90–109 mmHg; proteinuria ≥300 mg/24 h; no severe features; normal bloods; reassuring fetal assessment
Setting: Outpatient surveillance or day-stay assessment unit
Moderate
Worsening Pre-eclampsia
BP 160–169/110–119 mmHg; rising creatinine or uric acid; mild thrombocytopenia (100–150 × 10⁹/L); mild liver enzyme elevation; worsening proteinuria
Setting: Inpatient admission; continuous fetal monitoring; delivery planning
Severe
Severe Pre-eclampsia
BP ≥170/110 mmHg; platelets <100 × 10⁹/L; creatinine >90 µmol/L; LDH >600 U/L; ALT/AST >2× ULN; pulmonary oedema; eclampsia; visual/cerebral symptoms; HELLP
Setting: Tertiary hospital with NICU; urgent obstetric review; consider immediate delivery
HELLP Syndrome
HELLP syndrome is a severe complication of pre-eclampsia, occurring in 10–20% of cases. The acronym describes the triad of Haemolysis, Elevated Liver enzymes, and Low Platelets. It is associated with significant maternal morbidity (including hepatic rupture, DIC, placental abruption, and acute kidney injury) and perinatal mortality rates of 7–34% depending on gestational age and severity.
Diagnostic Criteria (Tennessee Classification)
| Component | Diagnostic Threshold | Notes |
|---|---|---|
| Haemolysis | LDH >600 U/L, or peripheral smear showing schistocytes, or bilirubin >20 µmol/L | Haptoglobin <0.25 g/L is the most sensitive marker |
| Elevated Liver Enzymes | AST or ALT >70 U/L (i.e., >2× ULN) | Right upper quadrant / epigastric pain in ~90% of cases |
| Low Platelets | Platelet count <100 × 10⁹/L | Severe thrombocytopenia (<50 × 10⁹/L) increases risk of haemorrhage at delivery |
Mississippi Classification (Severity Sub-classification)
- Class 1 (most severe): Platelets <50 × 10⁹/L, LDH ≥600 U/L, AST/ALT ≥70 U/L
- Class 2: Platelets 50–100 × 10⁹/L, LDH ≥600 U/L, AST/ALT ≥70 U/L
- Class 3: Platelets 100–150 × 10⁹/L, LDH ≥600 U/L, AST/ALT ≥40 U/L
Differentiating HELLP from TTP/HUS: HELLP typically occurs after 20 weeks' gestation and improves within 48–72 hours of delivery. Thrombotic thrombocytopenic purpura (TTP) and haemolytic uraemic syndrome (HUS) may present at any gestational age and do not resolve with delivery. ADAMTS13 activity measurement and haematology consultation are essential if the diagnosis is uncertain.
Complications of HELLP Syndrome
- Placental abruption (16–36%)
- Disseminated intravascular coagulation (DIC) (10–20%)
- Hepatic haematoma or rupture (rare but life-threatening)
- Acute kidney injury (7–15%)
- Pulmonary oedema (6–10%)
- Cerebral haemorrhage or infarction
- Retinal detachment
- Wound haematoma (particularly post-caesarean)
Management & Timing of Delivery
Delivery of the placenta is the only definitive treatment for pre-eclampsia and HELLP syndrome. However, the timing of delivery must be carefully balanced between the severity of maternal disease and the risks of prematurity for the fetus. Management follows a structured approach: initial stabilisation, antihypertensive therapy, seizure prophylaxis, maternal and fetal monitoring, and timely delivery.
Antihypertensive Therapy
The target BP in pre-eclampsia is <140/90 mmHg (NICE, SOMANZ). The CHIPS trial (2015) demonstrated that targeting diastolic BP of 85 mmHg (vs 100 mmHg) did not increase perinatal adverse outcomes and reduced maternal severe hypertension.
Labetalol (preferred first-line)
Labetalol® · α/β-adrenergic blocker
Oral dose
200 mg PO BD, titrate to max 800 mg BD
IV acute severe HTN
20 mg IV bolus over 2 min; repeat 40–80 mg IV every 30 min to max 300 mg; alternatively 20 mg/h IV infusion titrated to max 160 mg/h
Renal adjustment
No dose adjustment required
PBS status
✔ PBS General Benefit
Nifedipine (slow-release oral)
Adalat® · Calcium channel blocker
Dose
20 mg SR PO BD, titrate to max 60 mg SR BD
Acute use
10 mg capsule PO (bite and swallow) — not sublingual due to precipitous BP fall risk
Contraindications
Do not combine with IV magnesium sulphate within 4 hours (risk of profound hypotension and neuromuscular blockade)
PBS status
✔ PBS General Benefit
Hydralazine (IV)
Hydralazine® · Vasodilator
Dose
5 mg IV slow bolus over 5 min; repeat 5–10 mg IV every 20–30 min to max 20 mg; alternatively 0.5–10 mg/h IV infusion
Caution
May cause maternal tachycardia, headache, and precipitous fetal heart rate decelerations — continuous CTG monitoring essential
PBS status
✔ PBS General Benefit
Avoid: ACE inhibitors and ARBs are contraindicated in pregnancy (fetotoxic: renal dysgenesis, oligohydramnios, pulmonary hypoplasia, neonatal anuria). Diuretics should be avoided as plasma volume is already contracted in pre-eclampsia.
Seizure Prophylaxis — Magnesium Sulphate
Magnesium Sulphate
MgSO₄ · Anticonvulsant (obstetric)
Loading dose
4 g IV over 15–20 min (in 100 mL 0.9% NaCl or 5% glucose)
Maintenance infusion
1 g/h IV infusion for 24 hours post-delivery or 24 hours post-last seizure (whichever is later); increase to 2 g/h in severe pre-eclampsia with renal impairment
Eclampsia (active seizure)
4 g IV bolus over 5 min; repeat 2–4 g IV over 5–15 min if seizure continues; then commence maintenance
Monitoring
Check patellar reflexes hourly (loss = toxicity); urine output ≥25 mL/h; serum Mg²⁺ if renal impairment (therapeutic range 1.8–3.0 mmol/L; toxicity >3.5 mmol/L)
Antidote
Calcium gluconate 10% — 10 mL IV over 10 min for Mg²⁺ toxicity
PBS status
✔ PBS General Benefit
Antenatal Corticosteroids for Fetal Lung Maturity
- Betamethasone 11.4 mg IM × 2 doses 24 hours apart (or dexamethasone 12 mg IM × 2 doses 12 hours apart) — recommended if delivery is anticipated before 34+6 weeks
- Reduces respiratory distress syndrome by ~50% when given 24 hours to 7 days before delivery
- May transiently improve maternal platelet count and liver function in HELLP
- Monitor maternal blood glucose in diabetic women; temporary insulin dose adjustment often required
- PBS General Benefit
Timing of Delivery — RANZCOG/SOMANZ Guidance
| Gestational Age | Severe Pre-eclampsia / HELLP | Non-Severe Pre-eclampsia |
|---|---|---|
| <24 weeks | Offer delivery (perinatal mortality >90%); provide counselling re resuscitation limits | Close surveillance; consider termination if maternal condition deteriorates |
| 24+0 – 33+6 weeks | Deliver if: uncontrollable HTN, eclampsia, HELLP with deteriorating condition, placental abruption, DIC, pulmonary oedema, AKI (creatinine >150 µmol/L); otherwise stabilise then deliver at 34 weeks | Expectant management in tertiary centre with twice-weekly fetal assessment; deliver at 37 weeks |
| 34+0 – 36+6 weeks | Deliver after corticosteroid completion (if given); do not delay beyond 48 h for steroids | Deliver at 37 weeks; induction of labour appropriate if favourable cervix |
| ≥37 weeks | Deliver promptly | Deliver promptly; induction or caesarean as clinically indicated |
Absolute indications for immediate delivery regardless of gestational age: Eclampsia; uncontrollable severe hypertension (BP ≥170/110 mmHg despite ≥2 antihypertensives); pulmonary oedema; placental abruption; DIC; eclampsia not controlled by MgSO₄; intrauterine fetal death with maternal compromise.
Postpartum Management
- Continue magnesium sulphate for at least 24 hours post-delivery or 24 hours post-last eclamptic seizure
- Continue antihypertensives — BP may worsen in the first 3–6 days postpartum due to fluid redistribution and mobilisation of interstitial oedema; step-down gradually over 2–6 weeks
- Monitor FBC, LFTs, renal function, and LDH at 48–72 hours post-delivery (HELLP parameters may transiently worsen before improving)
- Labetalol, nifedipine SR, and enalapril are compatible with breastfeeding
- ACE inhibitors (enalapril, perindopril) may be used postpartum for persistent hypertension — safe in breastfeeding
- Arrange GP follow-up at 2 weeks, 6 weeks, and 6–12 months for BP review, renal function, and cardiovascular risk assessment
- Women with pre-eclampsia have a 2–7× increased lifetime risk of hypertension, ischaemic heart disease, and stroke; encourage healthy lifestyle, weight management, and regular BP screening
Investigations
The following investigations are recommended for assessment and monitoring of pre-eclampsia and HELLP syndrome. Availability of urgent pathology varies by site; metropolitan hospitals will have 24-hour turnaround, while remote and rural centres should establish clear transfer protocols with receiving tertiary centres.
Essential
Full Blood Count (FBC)
Platelet count (key severity marker); haemoglobin and haematocrit (may be elevated in haemoconcentration or low with haemolysis); blood film for schistocytes if HELLP suspected. MBS Item 65070.
Essential
Renal Function (U&E)
Serum creatinine, urea, electrolytes; remember pregnancy-adjusted ranges. Rising creatinine >90 µmol/L is a severe feature. MBS Item 66500.
Essential
Liver Function Tests (LFTs)
ALT, AST, bilirubin, albumin; ALT/AST >70 U/L (2× ULN) is diagnostic for HELLP. MBS Item 66512.
Essential
Lactate Dehydrogenase (LDH)
Marker of haemolysis in HELLP; >600 U/L is a severe feature. MBS Item 66524.
Essential
Serum Uric Acid
Elevated in pre-eclampsia (reduced tubular secretion); correlates with disease severity; useful prognostic marker in the third trimester. MBS Item 66530.
Available
Urine Protein:Creatinine Ratio (PCR)
Spot urine PCR ≥30 mg/mmol equivalent to 300 mg/24 h; faster than 24-h collection; MBS Item 65070.
Available
Coagulation Studies (INR, APTT, Fibrinogen)
Essential if DIC suspected; fibrinogen <2.0 g/L is concerning; INR prolongation may occur in severe HELLP.
Available
Haptoglobin
Most sensitive marker of haemolysis in HELLP; <0.25 g/L is highly suggestive. May require send-away in rural settings.
Available
sFlt-1 / PlGF Ratio
Research/investigational biomarker; ratio >85 suggests pre-eclampsia is likely within 4 weeks; available at some tertiary centres but not routinely MBS-funded.
Available
CTG (Cardiotocography)
Continuous electronic fetal monitoring in all cases of pre-eclampsia ≥26 weeks; assess fetal wellbeing, growth, liquor volume, and umbilical artery Doppler.
Available
Umbilical Artery Doppler Ultrasound
Increased resistance (raised S/D ratio, absent or reversed end-diastolic flow) indicates placental insufficiency; frequency of monitoring dictated by severity.
Referral
Renal Biopsy
Rarely indicated in pregnancy; may be considered postpartum if underlying renal disease is suspected (e.g., lupus nephritis, IgA nephropathy) and histology would change management.
Special Populations
Pregnancy Considerations
All antihypertensives
ACE inhibitors and ARBs are contraindicated throughout pregnancy. Methyldopa (250–500 mg PO TDS, PBS General Benefit) may be used if labetalol or nifedipine are not tolerated, though it is increasingly less preferred due to postpartum depression risk.
Magnesium sulphate
Category A in Australia; the only proven intervention to prevent eclampsia. Maintain strict input/output monitoring — risk of toxicity increased with renal impairment (eGFR <30 mL/min).
Paediatric / Neonatal
Preterm neonate
Infants born to mothers with pre-eclampsia are at increased risk of intrauterine growth restriction (IUGR), prematurity, necrotising enterocolitis, and respiratory distress syndrome. Corticosteroids for fetal lung maturity should be administered when preterm delivery is anticipated <34+6 weeks.
Long-term neonatal effects
Exposure to pre-eclampsia in utero is associated with increased risk of hypertension and metabolic syndrome in adult offspring — emphasise healthy lifestyle at childhood health checks.
Maternal Age ≥40
Risk factor
Advanced maternal age (≥40) is an independent risk factor for pre-eclampsia. Higher baseline prevalence of chronic hypertension and metabolic syndrome increases diagnostic complexity — differentiate chronic hypertension from superimposed pre-eclampsia early in pregnancy.
Pre-existing Renal Disease
CKD Stage 1–3a
Pre-eclampsia risk is 10–40× higher in women with CKD. Proteinuria at baseline makes PCR interpretation difficult — rely on clinical assessment, BP trends, and rising creatinine/uric acid. Nephrology and obstetric joint management is essential. Labetalol and nifedipine SR are first-line; hydralazine for acute severe HTN.
CKD Stage 3b–5 / Dialysis / Transplant
High-risk pregnancy requiring tertiary care from booking. Immunosuppression management (transplant) must be coordinated with maternal-fetal medicine. Delivery usually planned at 34–36 weeks. Magnesium sulphate dosing requires renal adjustment — consider monitoring serum Mg²⁺ levels.
Hepatic Considerations
HELLP with hepatic involvement
Liver capsule haematoma or rupture is a rare but life-threatening complication. Avoid hepatotoxic drugs. Platelet count must be >50 × 10⁹/L for regional anaesthesia (spinal/epidural) — general anaesthesia may be required for emergency caesarean with severe thrombocytopenia.
Immunocompromised
SLE / Antiphospholipid Syndrome
Antiphospholipid syndrome (APS) significantly increases pre-eclampsia and HELLP risk. Continue low-dose aspirin and prophylactic LMWH as per haematology/rheumatology guidance. Lupus nephritis flares may mimic pre-eclampsia — anti-dsDNA, complement (C3/C4), and haptoglobin may help differentiate.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Quick Reference — Management Summary
Acute severe hypertension (≥160/110)
Labetalol 20–80 mg IV bolus OR nifedipine 10 mg PO (bite & swallow) OR hydralazine 5 mg IV
Immediate
Target <140/90; repeat/infuse as needed; continuous CTG
Eclampsia prophylaxis / Rx
MgSO₄ 4 g IV load then 1–2 g/h infusion
24 h post-delivery / last seizure
Check reflexes, UO hourly; Ca²⁺ gluconate for toxicity
Pre-eclampsia prophylaxis
Aspirin 100–150 mg PO daily
12–36 weeks
High-risk women; 60% RRR; PBS General Benefit
Chronic HTN in pregnancy
Labetalol 200 mg PO BD (max 800 mg BD) OR nifedipine SR 20–60 mg PO BD
Ongoing
Avoid ACEi/ARBs; methyldopa 250–500 mg PO TDS if needed
Fetal lung maturity (<34+6 wk)
Betamethasone 11.4 mg IM × 2 (24 h apart)
24 h – 7 days pre-delivery
Monitor glucose in diabetic women
📚 References
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