Lucan · Conditions

Preeclampsia

Australian guidance: RANZCOG C-Obs 61 Early Pregnancy Screening + SOMANZ Hypertension in Pregnancy

1. Definition and epidemiology

Preeclampsia is a multi-system disorder of pregnancy occurring at or after 20 weeks gestation, characterised by new-onset hypertension (systolic blood pressure at or above 140 mmHg and/or diastolic blood pressure at or above 90 mmHg on at least two occasions, four hours apart, in a previously normotensive woman) accompanied by evidence of end-organ dysfunction or proteinuria. Preeclampsia complicates approximately 3% of all pregnancies globally and is a significant contributor to maternal and perinatal morbidity and mortality, accounting for more than 76,000 maternal deaths and 500,000 infant deaths annually. In Australia, preterm preeclampsia (delivery before 37 weeks) occurs in approximately 0.7% of pregnancies, and early-onset preeclampsia (delivery before 34 weeks) in approximately 0.4%; rates are higher in Aboriginal and Torres Strait Islander women (3.4% diagnosed with hypertensive disorders of pregnancy versus 2.3% in non-Indigenous women).

2. Pathophysiology

The core lesion in preeclampsia is defective placentation driven by failure of physiological transformation of the spiral arteries. In normal pregnancy, foetal cytotrophoblasts invade the decidua and myometrium, remodelling spiral arteries into low-resistance, high-capacitance vessels. In preeclampsia, this invasion is shallow; the spiral arteries retain their musculoelastic walls and remain high-resistance conduits. The resulting uteroplacental ischaemia triggers release of soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating anti-angiogenic factor that sequesters vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). Loss of free VEGF and PlGF causes widespread maternal endothelial dysfunction, manifesting as hypertension from loss of nitric oxide-mediated vasodilatation, proteinuria from glomerular endotheliosis (loss of glomerular endothelial fenestrations), and multi-organ sequelae including hepatocellular injury, thrombocytopaenia, cerebral oedema and seizure risk. Robbins Ch 22 situates preeclampsia within the spectrum of placental implantation disorders, noting that shallow trophoblast invasion and consequent spiral artery non-transformation are the unifying upstream event across preeclampsia, foetal growth restriction and placental abruption.

3. Clinical presentation and diagnostic criteria

Preeclampsia is frequently asymptomatic in its early phase and detected on routine blood pressure monitoring. When symptomatic, the clinical picture includes severe headache (frontal, not relieved by simple analgesia), visual disturbances (blurring, scotomata), epigastric or right upper quadrant pain reflecting hepatic capsule distension, nausea and vomiting, and rapidly progressive oedema. On examination, hypertension meeting the diagnostic threshold must be confirmed on two measurements at least four hours apart; if blood pressure is 160/110 mmHg or above, a second measurement within 15 minutes is acceptable before initiating antihypertensive therapy. Diagnostic criteria per the International Society for the Study of Hypertension in Pregnancy (ISSHP 2021) require hypertension at or after 20 weeks plus one or more of the following: proteinuria (protein/creatinine ratio at or above 30 mg/mmol or urine protein at or above 300 mg/day), other maternal end-organ dysfunction (renal, hepatic, neurological, haematological), uteroplacental dysfunction, or foetal growth restriction. Severe features include blood pressure at or above 160/110 mmHg, thrombocytopaenia below 100 x 10^9/L, serum creatinine above 90 micromol/L, elevated transaminases, pulmonary oedema, or new-onset seizure (eclampsia).

4. Investigations and AU-specific cutoffs

Initial investigations are directed at confirming the diagnosis and assessing severity and end-organ involvement. Blood pressure measurement uses a validated automated device; mean arterial pressure (MAP) is the preferred screening metric. Urinalysis and spot protein/creatinine ratio (pathological at or above 30 mg/mmol) or 24-hour urine protein (pathological at or above 300 mg) are the AU standard for confirming proteinuria. Full blood examination looks for thrombocytopaenia (below 100 x 10^9/L triggers concern for HELLP syndrome). Renal function: serum creatinine above 90 micromol/L or uric acid above 0.35 mmol/L are AU-relevant thresholds. Liver function: alanine aminotransferase or aspartate aminotransferase two times the upper limit of normal indicates hepatic involvement. Lactate dehydrogenase elevation supports haemolysis in the context of HELLP. Coagulation studies are indicated if thrombocytopaenia is present or HELLP is suspected. Cardiotocography (CTG) and ultrasound for foetal growth, liquor and Doppler are mandatory to assess foetal compromise. In early pregnancy screening (11 to 14 weeks), the Fetal Medicine Foundation (FMF) algorithm combines maternal risk history, MAP, uterine artery pulsatility index (UtPI) and biochemical markers (pregnancy-associated plasma protein A [PAPP-A] and/or PlGF) to generate a preterm preeclampsia risk score; a risk cutoff of 1 in 100 is the RANZCOG-recommended threshold for offering prophylaxis.

5. Management

Management is dictated by gestational age, severity, and foetal condition. The only definitive treatment is delivery. For women with preterm preeclampsia at less than 34 weeks, conservative inpatient management is appropriate when maternal and foetal conditions permit, aiming to prolong gestation. At 34 weeks or beyond with severe features, delivery is recommended. Antihypertensive therapy targets blood pressure below 160/110 mmHg acutely; SOMANZ 2023 recommends oral labetalol, oral nifedipine immediate-release, or intravenous hydralazine as first-line agents for acute severe hypertension. Magnesium sulphate is indicated for seizure prophylaxis in women with severe preeclampsia and for treatment of eclampsia; the Australasian loading dose is 4 g intravenous over 15 to 20 minutes followed by 1 g per hour maintenance infusion. Corticosteroids (betamethasone 11.4 mg intramuscular two doses, 24 hours apart) are given for foetal lung maturity before 34 weeks. For women identified as high-risk by first-trimester FMF algorithm screening (risk at or above 1 in 100), RANZCOG recommends aspirin at least 100 mg daily commenced before 16 weeks gestation, as this most likely reduces preterm preeclampsia (OR 0.61, 95% CI 0.52 to 0.70 for birth before 37 weeks); evidence for the greatest benefit is seen for early-onset preeclampsia before 32 to 34 weeks (OR 0.38, 95% CI 0.22 to 0.64). High-dose calcium supplementation (above 1000 mg per day) may additionally be offered to women at increased risk, particularly those with low dietary calcium intake, as an adjunct to aspirin rather than a replacement.

6. Pharmacology and AU PBS notes

First-line antihypertensive for acute severe hypertension in pregnancy: oral labetalol 200 mg (titrate to 800 mg per dose), oral nifedipine immediate-release 10 to 20 mg, or intravenous hydralazine 5 mg boluses. For maintenance therapy: oral labetalol, oral methyldopa, or oral nifedipine extended-release are the standard AU choices aligned with SOMANZ 2023. Labetalol is available as Trandate (AU brand). Nifedipine extended-release is available as Adalat Oros. Methyldopa is available as Aldomet. Magnesium sulphate (Magnesium sulfate injection) is not PBS-listed for outpatient use but is standard inpatient stock. Prophylactic aspirin: plain (non-enteric-coated) aspirin 100 mg daily is the RANZCOG-recommended minimum dose, taken at bedtime to align with circadian blood pressure patterns; 150 mg may offer greater benefit but requires splitting a 300 mg tablet given no dedicated 150 mg preparation exists in Australia. Aspirin PBS listing in this indication is as a non-prescription item at pharmacy cost; there is no streamlined authority code for prophylactic preeclampsia aspirin. Calcium supplementation: calcium carbonate 600 mg tablets (widely available over the counter in Australia) taken twice daily achieve the greater than 1 g per day target.

7. Complications and monitoring

Maternal complications include eclampsia (1 to 2% of severe preeclampsia), HELLP syndrome (haemolysis, elevated liver enzymes, low platelets; occurs in approximately 10 to 20% of severe disease), acute kidney injury, pulmonary oedema, abruption, disseminated intravascular coagulation, hepatic haematoma or rupture, and stroke. Long-term, women with a history of preeclampsia carry a two to four times elevated lifetime risk of cardiovascular disease and a seven times elevated risk of hypertension. Foetal and neonatal complications include foetal growth restriction, preterm birth, neonatal intensive care unit admission, and perinatal death. Monitoring in affected pregnancies includes twice-weekly blood pressure checks initially (daily if severe features), weekly biochemistry and full blood examination, twice-weekly CTG from time of diagnosis, and ultrasound assessment for foetal growth and Doppler every two weeks from diagnosis. Delivery timing: at 37 weeks or beyond for non-severe preeclampsia; for severe features at or beyond 34 weeks, delivery should occur promptly after maternal stabilisation; aspirin may be ceased at 36 weeks gestation if delivery has not preceded this point, consistent with FMF guidance.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.