Obstetrics & Gynaecology

Pre-eclampsia & Eclampsia

Also known as Pre-eclampsia · Eclampsia · HELLP syndrome · Hypertensive disorders of pregnancy

Pre-eclampsia is new hypertension at or after 20 weeks with proteinuria or specified maternal or uteroplacental dysfunction, interpreted using a named regional guideline. Severe hypertension and eclampsia are obstetric emergencies: stabilize, prevent or terminate seizures with protocolised magnesium sulphate, treat blood pressure urgently, assess mother and fetus, and plan birth after stabilization.

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Red flags

  • Persistent systolic BP ≥160 mmHg or diastolic BP ≥110 mmHg: confirm promptly and begin the local pregnancy severe-hypertension pathway.
  • New severe headache, visual symptoms, altered consciousness, epigastric or right-upper-quadrant pain, pulmonary oedema, falling platelets or worsening renal/liver tests: urgent senior obstetric assessment.
  • Generalised seizure in later pregnancy or postpartum: protect airway and breathing, treat possible eclampsia with magnesium while excluding neurological, metabolic and infectious causes.
  • Loss of deep-tendon reflexes, respiratory depression or oliguria during magnesium therapy: stop magnesium, support ventilation and give protocolised IV calcium gluconate for toxicity.

1. Definitions without mixing guidelines

Hypertensive disorders of pregnancy include chronic hypertension, gestational hypertension, pre-eclampsia and eclampsia. The common blood-pressure boundary is systolic ≥140 mmHg or diastolic ≥90 mmHg; either component is sufficient. Chronic hypertension predates pregnancy or is present before 20 weeks. Gestational hypertension begins at or after 20 weeks without the additional features used to diagnose pre-eclampsia. Persistent hypertension after pregnancy prompts reassessment for chronic hypertension.[1][3]

FigureClassify before treating. Pre-eclampsia adds proteinuria or specified maternal or uteroplacental dysfunction to new hypertension; eclampsia adds a seizure not better explained by another cause. Persistent systolic pressure ≥160 mmHg or diastolic pressure ≥110 mmHg is an emergency threshold, not the routine maintenance target.

International — ISSHP 2021

Pre-eclampsia is gestational hypertension accompanied by one or more of: new proteinuria, other maternal end-organ dysfunction, or uteroplacental dysfunction. Uteroplacental dysfunction includes findings such as fetal growth restriction or abnormal placental Doppler, but it must be interpreted in the full clinical context.[3]

United States — ACOG

US practice defines pre-eclampsia as new hypertension after 20 weeks plus proteinuria or specified organ dysfunction: thrombocytopenia, renal insufficiency, impaired liver function, pulmonary oedema, or cerebral or visual symptoms — proteinuria is sufficient but not necessary, and its amount does not correlate with outcome. The classic proteinuria cutoff is over 300 mg per 24 hours or a spot protein-to-creatinine ratio of at least 0.3; dipstick screening does not reliably quantify proteinuria and should not be used to diagnose it when quantitative testing is available. Severe features include systolic ≥160 mmHg or diastolic ≥110 mmHg, platelet count under 100 ×10⁹/L, liver transaminases at least twice the upper limit of normal, serum creatinine over 1.1 mg/dL or a doubling of baseline, severe persistent right-upper-quadrant pain, pulmonary oedema, or new-onset cerebral or visual disturbances.[17][18]

United Kingdom — NICE

NICE's evidence base quantifies proteinuria with spot protein-to-creatinine ratio (PCR): a threshold of PCR ≥30 mg/mmol detects significant proteinuria with high sensitivity (91%) and specificity (89%) against 24-hour collection, and higher thresholds trade sensitivity for specificity. Albumin-to-creatinine ratio data are more limited; an ACR below 2 mg/mmol helps rule out significant proteinuria. Interpret any single biochemical value alongside the complete clinical picture rather than in isolation.[19]

2. Pathophysiology

Pre-eclampsia is best understood as a placental disease with a maternal syndrome. In early pregnancy, incomplete extravillous trophoblast invasion leaves spiral arteries relatively narrow and reactive instead of transforming them into high-flow, low-resistance channels. Placental malperfusion and oxidative stress follow. The placenta releases anti-angiogenic mediators, particularly soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin. sFlt-1 binds VEGF and placental growth factor (PlGF), reducing their endothelial availability.[3][4][5]

FigureTwo-stage model: incomplete spiral-artery remodelling causes placental stress; excess sFlt-1 and soluble endoglin disrupt angiogenic signalling; maternal endothelial dysfunction produces vasoconstriction, capillary leak, platelet activation and organ injury.

Maternal endothelial injury explains the phenotype: vasoconstriction produces hypertension; glomerular endotheliosis produces proteinuria; capillary leak contributes to pulmonary oedema; platelet activation and microangiopathy contribute to thrombocytopenia and haemolysis; hepatic injury causes transaminitis and right-upper-quadrant pain; and cerebral endothelial dysfunction with failed autoregulation contributes to headache, visual symptoms, posterior reversible encephalopathy syndrome and seizures.[1][2][3]

Delivery removes the placenta and is the definitive treatment, but it is not an instantaneous cure: hypertension, neurological complications and pulmonary oedema may first appear or worsen postpartum. Continue surveillance after birth.[1][2]

3. Risk assessment and prevention

Important risk factors include previous pre-eclampsia, chronic hypertension, chronic kidney disease, pregestational diabetes, antiphospholipid syndrome or systemic lupus erythematosus, multifetal pregnancy, first pregnancy, higher BMI, older maternal age and family history. Exact aspirin eligibility differs by guideline; do not combine one region’s dose with another region’s risk list.[1][3]

United Kingdom — NICE

NICE NG133 recommends daily prophylaxis with aspirin 75–150 mg from 12 weeks of gestation until delivery for women at high risk of pre-eclampsia. NICE stratifies risk using a defined set of maternal risk factors; a systematic review found that the diagnostic accuracy of this risk-stratification algorithm varies, so apply the full NICE risk list and local protocol rather than a single factor in isolation.[20]

United States — ACOG

US guidance likewise endorses targeted prophylaxis: the US Preventive Services Task Force recommends low-dose aspirin 81 mg daily as preventive medication after 12 weeks of gestation for persons at high risk of pre-eclampsia (B recommendation), based on moderate-certainty evidence of substantial net benefit in reducing pre-eclampsia, preterm birth, small-for-gestational-age infants and perinatal mortality. Follow the complete US risk criteria rather than substituting another region's thresholds.[21]

The ASPRE randomised trial tested aspirin 150 mg per day from 11–14 weeks until 36 weeks in women selected as high risk by first-trimester screening and reduced preterm pre-eclampsia; it supports targeted prophylaxis in screened high-risk women rather than a universal 150 mg dose for every pregnancy. In populations with low dietary calcium intake, WHO recommends oral calcium supplementation of 1.5–2.0 g daily during pregnancy to reduce the risk of pre-eclampsia — a context-specific public-health recommendation, not a universal supplement for calcium-replete populations.[11][22]

4. Presentation and focused assessment

Pre-eclampsia may be asymptomatic and detected at routine antenatal review. Symptoms that demand urgent assessment are new severe or persistent headache, visual disturbance, altered mental state, epigastric or right-upper-quadrant pain, nausea or vomiting with systemic illness, dyspnoea, chest pain, reduced urine output, vaginal bleeding or reduced fetal movement. Oedema is common in normal pregnancy and is not diagnostic.[1][2]

Measure blood pressure with a validated device, correct cuff size, arm supported at heart level and the patient seated or in an appropriate lateral position. Repeat severe values promptly rather than waiting 4 hours. Assess airway and breathing, oxygen saturation, chest signs, mental state and focal neurology; palpate for hepatic tenderness and uterine tenderness; assess fetal heart activity and growth. Hyperreflexia and clonus may support neurological concern but neither replaces symptoms, blood pressure, laboratory assessment or imaging when indicated.[1][3]

A new seizure in the second half of pregnancy or postpartum should be managed as possible eclampsia while urgent differentials are considered: epilepsy, cerebral venous thrombosis, intracranial haemorrhage or ischaemic stroke, PRES, infection, hypoglycaemia, electrolyte disturbance and toxic causes. Focal deficit, prolonged coma, fever, recurrent seizures despite adequate magnesium or an atypical time course strengthens the indication for neuroimaging and specialist review.[2]

5. Investigations and surveillance

Baseline assessment includes serial correctly measured blood pressure, full blood count with platelets, creatinine and electrolytes, AST and ALT, and quantified urine protein using PCR or ACR according to the local pathway. Blood film, LDH, bilirubin, coagulation studies and group-and-screen are added when haemolysis, HELLP, DIC, abruption or delivery is a concern. Serum uric acid is neither diagnostic nor a routine severity test. NICE does not routinely recommend a 24-hour urine collection when PCR or ACR is available.[1][3]

Fetal assessment usually includes cardiotocography at diagnosis when clinically indicated and ultrasound for growth, amniotic fluid and umbilical-artery Doppler. Repeat frequency depends on gestation, severity and local protocol; continuous CTG is not required merely because magnesium is being infused.[1][3]

PlGF-based tests can assist but do not replace clinical assessment. NICE NG133 recommends a validated PlGF-based test to help rule out suspected pre-eclampsia between 20+0 and 36+6 weeks, used once per episode and alongside standard assessment. Assay cut-offs and gestational windows differ. An sFlt-1:PlGF ratio below 38 has shown high negative predictive value for approximately one week in studied populations; neither a ratio ≥38 nor PlGF below 100 pg/mL is a universal stand-alone “rule-in” threshold, and biomarkers alone must not determine early birth.[1][4]

6. Eclampsia: the first minutes

FigureEclampsia pathway: protect from injury and stabilize airway and breathing; give magnesium sulphate using the named local regimen; treat persistent systolic ≥160 or diastolic ≥110 mmHg urgently; assess mother and fetus and plan birth after stabilization. During an active generalized seizure follow the named emergency oxygen protocol; outside active convulsion, oxygen is titrated to hypoxaemia or inadequate ventilation.
  1. Call for senior obstetric, anaesthetic and neonatal help. Place the patient in the left lateral position, protect from injury, open the airway, assess breathing and circulation, obtain IV access and check bedside glucose. Do not restrain the limbs or put objects in the mouth.[2]
  2. During an active generalized eclamptic seizure, give high-flow oxygen while protecting the airway and assessing ventilation, as directed by Hypertensive Disorders in Pregnancy - SA Perinatal Practice Guidelines; suction only when needed and prepare anaesthetic airway support. After the convulsion, titrate oxygen to ventilation and saturation: a stable, normally saturated, non-seizing patient does not receive routine oxygen. Intubate for persistent depressed consciousness, respiratory failure or refractory seizures.[2]
  3. Give magnesium sulphate using the named local regimen. It is the preferred anticonvulsant for eclampsia and reduces seizure recurrence compared with diazepam or phenytoin.[6][7]
  4. Treat persistent severe hypertension urgently, monitor fluid balance, assess for pulmonary oedema and avoid unindicated fluid loading.[1][16]
  5. Assess the fetus and plan birth after maternal stabilization. Eclampsia is not itself an indication for automatic caesarean birth; route depends on obstetric factors, urgency and fetal status.[2][3]

7. Acute severe hypertension

Persistent systolic BP ≥160 mmHg or diastolic BP ≥110 mmHg is a maternal stroke emergency. ACOG describes confirmation over about 15 minutes and treatment as soon as possible, within 30–60 minutes. Use the local maternity emergency bundle; do not wait for proteinuria or laboratory results.[16]

United States — common ACOG emergency bundle examples

Randomised evidence supports three first-line options for the hypertensive emergency of severe pre-eclampsia: IV labetalol, IV hydralazine and oral nifedipine. All three significantly lowered blood pressure in a randomised comparison, but effectiveness profiles differed by dosing — nifedipine performed best after a single dose, hydralazine after three doses — so agent choice and escalation follow the local maternity emergency bundle rather than improvisation. Check asthma, bradycardia or heart block before labetalol.[23]

United Kingdom — NICE

NICE NG133 lists labetalol (oral or IV), oral nifedipine and IV hydralazine for severe hypertension. Dose and escalation follow the maternity unit protocol. For ongoing treatment, NICE offers labetalol first, nifedipine if labetalol is unsuitable, and methyldopa if both are unsuitable, aiming for 135/85 mmHg or less once treated. The emergency ceiling of 160/110 is not the maintenance target.[1]

When IV access is delayed, oral nifedipine remains an accepted emergency option alongside IV labetalol and IV hydralazine. Avoid unindicated fluid loading: monitor fluid balance, assess for pulmonary oedema, and individualise resuscitation when haemorrhage or sepsis coexist.[23]

8. Magnesium sulphate: named regimens and safety

The Magpie Trial showed that magnesium sulphate reduced eclampsia in women with pre-eclampsia; benefit was greatest in higher-risk disease. Indications are guideline-specific. ACOG recommends magnesium for gestational hypertension or pre-eclampsia with severe features and for eclampsia. NICE advises considering magnesium in severe pre-eclampsia when birth is planned within 24 hours, particularly with neurological symptoms or deteriorating laboratory features, and recommends it for eclampsia.[6][7][16]

United Kingdom — NICE IV regimen

A standard intravenous regimen in UK practice is a 4 g IV loading dose followed by a 1 g/hour maintenance infusion (the Zuspan regimen). Follow NICE NG133 and the local infusion policy for timing, total duration and any recurrent-seizure bolus.[24]

United States — ACOG IV regimen

Commonly described intravenous regimens use a 4 g IV loading dose — administered over 20 minutes in one published series — followed by maintenance of 1–2 g/hour by controlled infusion, continued according to the local protocol.[25][26]

Resource-limited protocol — Pritchard regimen

Where a trained service uses the Pritchard regimen: 4 g IV loading immediately followed by 10 g IM (5 g in each buttock), then 5 g IM every 4 hours in alternating buttocks. Continue only while reflexes, respiration and urine output are adequate and the local protocol supports ongoing monitoring. The 2023 Cochrane review found the comparative evidence for alternative regimens limited; do not claim all schedules are equivalent.[8][25]

Before and during magnesium, document respiratory rate, oxygen saturation, deep-tendon reflexes, urine output and renal function at protocol-defined intervals: careful adherence to monitoring guidelines prevents toxicity, which is rare when magnesium sulphate is carefully administered and monitored. Clinical toxicity progresses from loss of reflexes to respiratory depression and cardiac effects; exact serum thresholds vary and must not replace bedside monitoring. If toxicity is suspected: stop magnesium, call for help, support airway and ventilation, and give protocolised IV calcium gluconate as specified in the current Queensland Clinical Guideline hypertension and pregnancy flowchart. Recheck magnesium and renal function and follow the local resuscitation and medicine policy.[25]

Do not claim that early postpartum discontinuation is proved harmful. A 2024 meta-analysis found no statistically significant increase in eclampsia with early discontinuation, but confidence intervals were wide and the evidence underpowered; therefore follow the named guideline and individualize when toxicity or renal dysfunction changes the balance.[15]

9. Ongoing care and timing of birth

Birth is the definitive treatment, but timing must balance maternal safety, fetal condition and gestation. Antenatal corticosteroids are indicated when preterm birth is expected within the guideline window, but must not delay an otherwise indicated birth. European perinatal guidance allows either betamethasone 12 mg IM twice, 24 hours apart, or dexamethasone 6 mg IM in four doses 12 hours apart (or 12 mg twice, 24 hours apart); use the local preterm-birth protocol. High-dose dexamethasone solely to improve maternal HELLP outcomes is not routinely recommended.[12][27]

United States — ACOG

Without severe features, plan birth at 37+0 weeks. With severe features at 34+0 weeks or later, proceed to birth after stabilization and do not delay for corticosteroids. Before 34 weeks, expectant management is only for carefully selected stable patients in a centre with appropriate maternal and neonatal resources; uncontrolled severe hypertension, persistent neurological symptoms, pulmonary oedema, HELLP, abruption, worsening organ dysfunction or non-reassuring fetal status ends expectant management.[16]

United Kingdom — NICE

NICE NG133 generally continues surveillance before 34 weeks and from 34+0 to 36+6 weeks unless specified maternal or fetal indications require early birth. From 37 weeks, initiate birth within 24–48 hours. Record thresholds for planned early birth, involve senior obstetric and neonatal teams, and do not use PlGF alone to decide timing.[1]

Eclampsia, uncontrolled severe hypertension, pulmonary oedema, progressive renal or hepatic dysfunction, DIC, abruption and non-reassuring fetal status usually require prompt birth after stabilization. Once HELLP is identified, birth is required after maternal stabilization regardless of gestational age; individualize the immediate stabilization steps and route of birth, not whether to deliver. Antenatal corticosteroids may be given only when they do not delay the indicated birth. Vaginal birth is appropriate when feasible; caesarean birth is for obstetric or urgency indications, not the diagnosis alone.[2][3][12]

10. HELLP syndrome

HELLP means haemolysis, elevated liver enzymes and low platelets. It can occur with only mild hypertension or limited proteinuria. Suspect it with malaise, nausea, epigastric or right-upper-quadrant pain, thrombocytopenia or transaminitis. Request full blood count, blood film, LDH, bilirubin, AST/ALT, creatinine and coagulation studies as indicated; assess for abruption, DIC, acute kidney injury, pulmonary oedema and hepatic haematoma or rupture.[12]

Named research classifications support communication but must not delay care. Strict laboratory criteria define complete HELLP by all three components, and partial HELLP as only one or two of the three features — women with complete HELLP have higher rates of maternal complications, so the groups are studied and managed separately. The Mississippi classification grades severity by peripartum platelet count alongside elevated LDH with laboratory evidence of haemolysis and hepatic dysfunction: class 1 at or under 50 ×10⁹/L, class 2 over 50 to 100 ×10⁹/L, and class 3 over 100 to 150 ×10⁹/L.[28][29]

Key mimics include acute fatty liver of pregnancy—more prominent hypoglycaemia, coagulopathy and encephalopathy—TTP, atypical HUS, viral hepatitis, biliary disease and sepsis. Management combines stabilization, magnesium when indicated, severe-hypertension treatment, blood-product support guided by bleeding and laboratory findings, and birth after maternal stabilization regardless of gestation; only route and immediate stabilization are individualized. Corticosteroids for fetal lung maturation may be appropriate only when they do not delay the indicated birth; routine high-dose corticosteroids solely for maternal platelet recovery are not supported.[1][12]

11. Postpartum care and future health

Pre-eclampsia and eclampsia can first present postpartum. Continue symptom, blood-pressure, fluid and neurological surveillance; reassess immediately for headache, visual symptoms, dyspnoea, epigastric pain or seizure. Perform formal postpartum venous-thromboembolism risk assessment; pre-eclampsia contributes to risk, but LMWH dose and duration depend on the total risk profile and local protocol.[1][2]

United Kingdom — NICE

For women with pre-eclampsia who did not take antihypertensives, NICE NG133 measures BP at least 4 times daily while inpatient, at least once between day 3 and day 5, and on alternate days until normal if abnormal on day 3–5; start treatment at ≥150/100 mmHg. Stop methyldopa within 2 days after birth. Postpartum options compatible with breastfeeding include enalapril with renal-function and potassium monitoring, nifedipine or amlodipine, and combination treatment adding labetalol or atenolol when needed; avoid ARBs and diuretics where possible while breastfeeding. Review at 2 weeks if still taking treatment, review all at 6–8 weeks, check urine protein at 6–8 weeks, and arrange kidney review at 3 months if proteinuria persists.[1]

United States — ACOG

ACOG recommends blood-pressure evaluation within 72 hours after birth for severe hypertension and no later than 7–10 days for any hypertensive disorder of pregnancy, with earlier assessment for symptoms. Local services may use in-person or validated remote monitoring.[16]

Counsel that recurrence and long-term risk vary with severity and gestation. NICE frames recurrence as approximately 1 in 5 for any hypertensive disorder and about 1 in 6 for pre-eclampsia overall, with greater risk after earlier birth. Prior pre-eclampsia is associated with increased future chronic hypertension, cardiovascular disease and stroke; describe it as an important risk marker, not a universal “cardiovascular risk equivalent.” Support primary-care follow-up, healthy weight, physical activity, smoking cessation and periodic blood-pressure and cardiovascular-risk review; ISSHP recommends annual review after pre-eclampsia.[1][3]

12. Exam-ready synthesis

Recognition

classify and find danger

  • New HTN at or after 20 weeks
  • Proteinuria is not mandatory
  • Severe BP = systolic ≥160 OR diastolic ≥110
  • Protein amount and oedema do not grade severity

Eclampsia

stabilize before birth

  • Left lateral; protect airway and breathing
  • Magnesium by named protocol
  • Treat persistent severe BP urgently
  • Birth plan after maternal stabilization

Regional timing

do not mix guidance

  • ACOG: 37 weeks without severe features
  • ACOG: ≥34 weeks with severe features
  • NICE: surveillance before 37 unless triggers
  • NICE: birth within 24–48 h from 37 weeks

After birth

risk continues

  • Postpartum disease can be de novo
  • NICE and ACOG review schedules differ
  • Check breastfeeding compatibility
  • VTE and long-term CVD risk assessment
Eclampsia response — SAFE

SAFE

  • SStabilizeleft lateral, protect airway, assess breathing/circulation, bedside glucose
  • AAnticonvulsantmagnesium sulphate using the named local regimen
  • FFix severe pressurepersistent systolic ≥160 or diastolic ≥110 requires urgent protocolised treatment
  • EEvaluate and plan birthmaternal labs, fetal assessment and delivery after stabilization
[1] [2] [3] [16]
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