Pre-eclampsia & Eclampsia

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]

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]

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]

The ASPRE trial tested 150 mg nightly in a selected first-trimester screening programme and reduced preterm pre-eclampsia; it does not make 150 mg universal for every country or every pregnancy. WHO recommends 1.5–2.0 g elemental calcium daily during pregnancy in populations with low dietary calcium intake. This is a context-specific public-health recommendation, not a universal supplement for calcium-replete populations.[9][11]

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

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]

Use immediate-release oral nifedipine for an acute protocol when IV access is delayed; do not use sublingual nifedipine. Avoid routine crystalloid loading before hydralazine. In severe pre-eclampsia NICE limits maintenance fluids to 80 mL/hour unless there are ongoing losses; haemorrhage and sepsis require individualized resuscitation. Diuretics may be needed for pulmonary oedema, so they are not an absolute prohibition. ACE inhibitors and ARBs are avoided antenatally but selected ACE inhibitors may be used postpartum.[1][16]

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]

Before and during magnesium, document respiratory rate, oxygen saturation, deep-tendon reflexes, urine output and renal function at protocol-defined intervals. 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 and support airway and ventilation. The current Queensland Clinical Guideline eclampsia flowchart specifies 10% calcium gluconate 10 mL IV over 5 minutes—10 mL of 100 mg/mL is 1 g—for magnesium toxicity. Recheck magnesium and renal function and follow the local resuscitation and medicine policy.[16]

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. Betamethasone 12 mg IM 24 hours apart for 2 doses or dexamethasone 6 mg IM 12-hourly for 4 doses are common WHO-compatible regimens; use the local preterm-birth protocol. High-dose dexamethasone solely to improve maternal HELLP outcomes is not routinely recommended.[1][12]

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. Tennessee complete HELLP requires all three laboratory components: LDH ≥600 IU/L, AST ≥70 IU/L, and platelets <100 ×10⁹/L; partial HELLP means one or two of these components without all three, not an invented A/B class. Mississippi class 1 is platelets ≤50 ×10⁹/L, AST or ALT ≥70 IU/L, and LDH ≥600 IU/L; class 2 is platelets >50 to ≤100 ×10⁹/L with AST or ALT ≥70 IU/L and LDH ≥600 IU/L; class 3 is platelets >100 to ≤150 ×10⁹/L with AST or ALT ≥40 IU/L and LDH ≥600 IU/L.[12]

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]

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

[1] [2] [3] [16]

References

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2. [2]Fishel Bartal M, Sibai BM. Eclampsia in the 21st century American Journal of Obstetrics and Gynecology, 2022.PMID 32980358
3. [3]Magee LA, Brown MA, Hall DR, et al. The 2021 International Society for the Study of Hypertension in Pregnancy classification, diagnosis & management recommendations for international practice Pregnancy Hypertension, 2022.PMID 35066406
4. [4]Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia New England Journal of Medicine, 2004.PMID 14764923
5. [5]Levine RJ, Lam C, Qian C, et al. Soluble endoglin and other circulating antiangiogenic factors in preeclampsia New England Journal of Medicine, 2006.PMID 16957146
6. [6]Altman D, Carroli G, Duley L, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial Lancet, 2002.PMID 12057549
7. [7]Duley L, Gülmezoglu AM, Henderson-Smart DJ, et al. Magnesium sulphate and other anticonvulsants for women with pre-eclampsia Cochrane Database of Systematic Reviews, 2010.PMID 21069663
8. [8]Diaz V, Long Q, Oladapo OT. Alternative magnesium sulphate regimens for women with pre-eclampsia and eclampsia Cochrane Database of Systematic Reviews, 2023.PMID 37815037
9. [9]Roberge S, Bujold E, Nicolaides KH. Aspirin for the prevention of preterm and term preeclampsia: systematic review and metaanalysis American Journal of Obstetrics and Gynecology, 2018.PMID 29138036
10. [10]Roberge S, Bujold E, Nicolaides KH. Meta-analysis on the effect of aspirin use for prevention of preeclampsia on placental abruption and antepartum hemorrhage American Journal of Obstetrics and Gynecology, 2018.PMID 29305829
11. [11]Rolnik DL, Wright D, Poon LC, et al. Aspirin versus Placebo in Pregnancies at High Risk for Preterm Preeclampsia New England Journal of Medicine, 2017.PMID 28657417
12. [12]Jayawardena L, McNamara E. Diagnosis and management of pregnancies complicated by haemolysis, elevated liver enzymes and low platelets syndrome in the tertiary setting Internal Medicine Journal, 2020.PMID 31062430
13. [13]Abalos E, Cuesta C, Carroli G, et al. Pre-eclampsia, eclampsia and adverse maternal and perinatal outcomes: a secondary analysis of the World Health Organization Multicountry Survey on Maternal and Newborn Health BJOG, 2014.PMID 24641531
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15. [15]Quist-Nelson J, de Ruigh A, Lemoine ER, et al. Early magnesium discontinuation postpartum and eclampsia risk: A systematic review and meta-analysis Pregnancy Hypertension, 2024.PMID 39018830
16. [16]American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin, Number 222 Obstetrics & Gynecology, 2020.PMID 32443079