Identify placental and multisystem disease promptly, distinguish severe hypertension from other severe features, and stabilise eclampsia before coordinating definitive obstetric management.
Pre-eclampsia is a syndrome of maternal endothelial dysfunction arising in association with placental disease. Its bedside diagnosis combines new hypertension after 20 weeks with an additional maternal or placental abnormality. NICE recognises renal insufficiency, liver involvement, neurological features, haematological complications and uteroplacental dysfunction as alternatives to proteinuria. In chronic hypertension or established kidney disease, diagnosis of superimposed pre-eclampsia needs particular attention to new organ injury and the trajectory from baseline.
The useful distinction is between a currently stable presentation and one with evidence of imminent deterioration. Severe hypertension is one danger, but progressive thrombocytopenia, rising creatinine, persistent epigastric pain, worsening oxygenation or neurological symptoms may be equally decisive. Heavy proteinuria alone is a poor substitute for assessing these features. Measure pressure repeatedly, examine the chest and nervous system, assess urine output and compare blood results with earlier values.
Abnormal placental development interacts with maternal vascular susceptibility, with higher risk after previous pre-eclampsia and in chronic hypertension, renal disease, diabetes or autoimmune disease.
Multiple pregnancy, first pregnancy and combinations of maternal age, BMI and family history increase risk, although serious disease can occur without recognised risk factors.
Incomplete remodelling of maternal spiral arteries can produce high-resistance placental circulation and cellular stress, contributing to impaired exchange and fetal growth.
Placental signals promote widespread maternal endothelial dysfunction, disturbing vascular tone and permeability and affecting renal, cerebral, hepatic and pulmonary circulation.
Platelet consumption, haemolysis and organ hypoperfusion may develop together, explaining why disease severity cannot be assessed from blood pressure or proteinuria alone.
Severe persistent headache, scotomata, clonus or altered awareness may precede a seizure and should prompt urgent senior review.
Right upper quadrant pain with transaminitis, haemolysis or a falling platelet count suggests serious systemic involvement, including HELLP.
New oxygen requirement or crackles may represent pulmonary oedema, which is worsened by excessive intravenous fluid administration.
Reduced fetal movements, restricted growth or abnormal umbilical artery flow may reveal fetal impact even before striking maternal symptoms.
Active urinary sediment, systemic lupus symptoms and immunological trends may favour a renal flare, but nephritis and superimposed pre-eclampsia can coexist.
TTP and atypical haemolytic uraemic syndrome can resemble HELLP; disproportionate neurological or renal injury and failure to improve require urgent haematological or renal input.
Epilepsy, cerebral venous thrombosis, intracranial haemorrhage and metabolic disturbance remain important when the presentation is atypical or neurological abnormalities persist after stabilisation.
Eclampsia, posterior reversible encephalopathy and intracranial haemorrhage can cause lasting disability or death, requiring rapid recognition and treatment of neurological warning signs.
Pulmonary oedema, acute kidney injury, hepatic haematoma and disseminated intravascular coagulation may develop, often requiring coordinated obstetric and intensive-care management.
Abruption, growth restriction, stillbirth and indicated preterm delivery threaten fetal or neonatal health and shape the balance between surveillance and delivery.
New hypertension with convincing organ or placental dysfunction can meet pre-eclampsia criteria despite a negative urine protein result.
Magnesium reduces seizure risk while antihypertensives reduce pressure-related injury, so administering either one does not complete acute treatment.
Circulating mediators and postpartum fluid shifts can sustain illness after birth, making the early puerperium a continuing period of risk.
A rapidly falling platelet count or rising creatinine may require escalation even before a laboratory value crosses a dramatic threshold.
Waiting for a 24-hour urine collection before treating a clinically unstable patient with suspected pre-eclampsia.
Using diazepam or phenytoin instead of magnesium as routine eclampsia treatment without a specific exceptional reason.
Giving repeated unreviewed fluid boluses for oliguria in severe pre-eclampsia and precipitating pulmonary oedema.
Assuming seizure recovery proves the cause is uncomplicated epilepsy in a previously hypertensive pregnancy.
Delaying indicated birth solely to finish corticosteroids while maternal condition continues to deteriorate.
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A woman at 35 weeks has a generalised seizure with blood pressure 172/114 mmHg and persistent headache. Airway support and obstetric resuscitation are underway. Which magnesium regimen follows NICE guidance?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Eclampsia is a seizure attributable to pre-eclampsia. Protect the patient from injury, assess airway and breathing, obtain intravenous access and check glucose while giving magnesium sulfate. Do not restrain the patient or place objects in the mouth. Fetal bradycardia can follow the maternal seizure; maternal oxygenation, circulation and seizure control take priority. Persistent focal signs, unusually prolonged unconsciousness or recurrent events despite treatment also demand evaluation for intracranial haemorrhage, venous thrombosis, epilepsy and metabolic causes.
Magnesium prevents and treats seizures; antihypertensives protect against pressure-related injury. Neither replaces the other. Give magnesium for eclampsia and consider it in severe pre-eclampsia, particularly when birth is planned within 24 hours or neurological, abdominal or laboratory features are concerning. Monitor respiration, reflexes, renal function and hourly urine output. Reduced renal clearance increases toxicity risk and should prompt senior dose review and serum measurement when indicated.
Delivery removes the placenta but must follow organised maternal stabilisation unless an immediate obstetric catastrophe dictates otherwise. The senior team weighs gestation, response to pressure treatment, maternal laboratory trends and fetal findings, involving neonatology for preterm birth. Antenatal corticosteroids and fetal neuroprotection are considered when indicated; a course should not delay birth for deteriorating maternal or fetal condition. A caesarean section is not automatically required solely because eclampsia occurred.
Postnatal care includes repeated blood pressure, symptom checks and laboratory follow-up until improvement is established. Transfer to community care requires acceptable pressure, improving or stable tests and no persisting symptoms of pre-eclampsia. Arrange review of antihypertensive treatment, renal abnormalities and psychological effects. Explain future recurrence and cardiovascular risk in a way that supports subsequent pregnancy planning and long-term prevention.
Monitor breathing, tendon reflexes and urine output; renal dysfunction increases accumulation. Stop for suspected toxicity, support ventilation and ensure injectable calcium gluconate is immediately available.
Use an infusion pump and close blood-pressure and pulse monitoring; asthma, bradycardia, heart block and decompensated failure alter the choice.
Stop magnesium and support respiration simultaneously; cardiac monitoring and product-specific dilution are required rather than guessing millilitres from a different calcium salt.