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Reproductive · Clinical Topics
Pre-eclampsia
Pre-eclampsia is a multi-system pregnancy disorder defined by new-onset hypertension (≥140/90 mmHg) and significant proteinuria or organ dysfunction, developing after 20 weeks' gestation. It's a major cause of maternal and fetal morbidity, with delivery being the only definitive 'cure'.
📌 Learning Objectives
- Define pre-eclampsia and differentiate it from gestational hypertension.
- Identify key risk factors for developing pre-eclampsia.
- Explain the pathophysiology of pre-eclampsia, linking it to clinical manifestations.
- Recognise the 'red flag' symptoms and signs of severe pre-eclampsia and impending eclampsia.
- Outline the essential investigations for diagnosis, severity assessment, and monitoring of pre-eclampsia.
- Formulate a management plan for pre-eclampsia, including prevention, antihypertensive therapy, seizure prophylaxis, and timing of delivery.
📋 Overview
Pre-eclampsia is a common and critical obstetric condition affecting 2-5% of pregnancies, demanding high-yield knowledge for finals and OSCEs. It's defined as new-onset hypertension (BP ≥140/90 mmHg) after 20 weeks' gestation, accompanied by *either* significant proteinuria (PCR >30mg/mmol) *or* maternal organ dysfunction (e.g., renal impairment, hepatic involvement, neurological symptoms like headache/visual changes, or eclampsia). Crucially, proteinuria is *not* always required for diagnosis if other organ dysfunction is present. It's vital to recognise the spectrum from mild pre-eclampsia to severe forms like HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) and eclampsia (seizures). Risk factors are key for SBA questions and include previous pre-eclampsia, chronic kidney disease, autoimmune disease (high risk), and nulliparity, age >40, high BMI (moderate risk). Early aspirin prophylaxis is a key preventative strategy.
🔬 Basic Science
The core pathology is abnormal placentation. Normally, trophoblasts extensively invade maternal spiral arteries, transforming them into wide, low-resistance vessels. In pre-eclampsia, this invasion is shallow, resulting in narrow, high-resistance vessels and subsequent placental ischaemia. This ischaemia triggers the release of various factors (e.g., sFlt-1, endothelin-1) into the maternal circulation. These factors cause widespread maternal endothelial dysfunction, leading to:
- Vasoconstriction: Explains hypertension.
- Increased vascular permeability: Leads to oedema, proteinuria (renal glomerular endotheliosis), and pulmonary oedema.
- Coagulation cascade activation: Contributes to thrombocytopenia and microangiopathic haemolysis (seen in HELLP).
- Organ-specific damage: Liver (periportal necrosis, subcapsular haematoma), brain (oedema, haemorrhage, seizures).
- Vasoconstriction: Explains hypertension.
- Increased vascular permeability: Leads to oedema, proteinuria (renal glomerular endotheliosis), and pulmonary oedema.
- Coagulation cascade activation: Contributes to thrombocytopenia and microangiopathic haemolysis (seen in HELLP).
- Organ-specific damage: Liver (periportal necrosis, subcapsular haematoma), brain (oedema, haemorrhage, seizures).
🏥 Clinical Relevance
Pre-eclampsia often presents asymptomatically, detected via routine antenatal checks (BP, urine dip). When symptomatic, 'red flag' features for severe pre-eclampsia include:
- Persistent, severe frontal headache (unresponsive to simple analgesia).
- Visual disturbances (blurred vision, flashing lights, scotomata).
- Epigastric pain or right upper quadrant pain (due to liver capsule distension).
- Sudden-onset, rapid-progression oedema (face, hands, ankles).
- Hyperreflexia with clonus (OSCE finding).
- Nausea/vomiting (can be non-specific but concerning with other symptoms).
Differential diagnoses include essential hypertension, gestational hypertension, chronic kidney disease, and other causes of headache/abdominal pain in pregnancy. Complications are severe: maternal (eclampsia, stroke, pulmonary oedema, acute kidney injury, HELLP, placental abruption) and fetal (intrauterine growth restriction, prematurity, stillbirth). Recognising these symptoms and initiating prompt management is critical to prevent adverse outcomes.
- Persistent, severe frontal headache (unresponsive to simple analgesia).
- Visual disturbances (blurred vision, flashing lights, scotomata).
- Epigastric pain or right upper quadrant pain (due to liver capsule distension).
- Sudden-onset, rapid-progression oedema (face, hands, ankles).
- Hyperreflexia with clonus (OSCE finding).
- Nausea/vomiting (can be non-specific but concerning with other symptoms).
Differential diagnoses include essential hypertension, gestational hypertension, chronic kidney disease, and other causes of headache/abdominal pain in pregnancy. Complications are severe: maternal (eclampsia, stroke, pulmonary oedema, acute kidney injury, HELLP, placental abruption) and fetal (intrauterine growth restriction, prematurity, stillbirth). Recognising these symptoms and initiating prompt management is critical to prevent adverse outcomes.
🧪 Investigations
Investigations aim to diagnose, assess severity, and monitor for complications:
- **Bedside:**
- **Blood Pressure:** Crucial for diagnosis and monitoring. Repeated measurements if elevated.
- **Urinalysis:** Dipstick for protein. A 1+ or more requires further investigation.
- **Fluid balance chart:** Monitor urine output.
- **Bloods:**
- **Full Blood Count (FBC):** Look for thrombocytopenia (platelets <150 x 10^9/L) and haemolysis (low Hb, raised LDH, schistocytes on film – for HELLP).
- **Renal Function Tests (U&Es):** Raised creatinine, urea, reduced eGFR (indicates renal involvement).
- **Liver Function Tests (LFTs):** Elevated ALT/AST (hepatic involvement, especially in HELLP).
- **Uric Acid:** Often elevated in pre-eclampsia, though not diagnostic.
- **Coagulation screen:** If HELLP or DIC suspected.
- **Urine:**
- **Urine Protein:Creatinine Ratio (PCR):** >30 mg/mmol is significant proteinuria. (SBA: 24-hour urine collection for protein is less common now).
- **Fetal Monitoring:**
- **Symphysis-fundal height (SFH):** For growth restriction.
- **Ultrasound scan:** Assess fetal growth, amniotic fluid volume, umbilical artery Doppler (for fetal compromise).
- **Cardiotocography (CTG):** Assess fetal wellbeing, especially if >26 weeks or concerns.
- **Special:**
- **Placental Growth Factor (PlGF) testing:** Low levels can help rule out/predict pre-eclampsia in suspected cases, especially between 20-35 weeks (NICE guidance). Useful for triaging.
- **Bedside:**
- **Blood Pressure:** Crucial for diagnosis and monitoring. Repeated measurements if elevated.
- **Urinalysis:** Dipstick for protein. A 1+ or more requires further investigation.
- **Fluid balance chart:** Monitor urine output.
- **Bloods:**
- **Full Blood Count (FBC):** Look for thrombocytopenia (platelets <150 x 10^9/L) and haemolysis (low Hb, raised LDH, schistocytes on film – for HELLP).
- **Renal Function Tests (U&Es):** Raised creatinine, urea, reduced eGFR (indicates renal involvement).
- **Liver Function Tests (LFTs):** Elevated ALT/AST (hepatic involvement, especially in HELLP).
- **Uric Acid:** Often elevated in pre-eclampsia, though not diagnostic.
- **Coagulation screen:** If HELLP or DIC suspected.
- **Urine:**
- **Urine Protein:Creatinine Ratio (PCR):** >30 mg/mmol is significant proteinuria. (SBA: 24-hour urine collection for protein is less common now).
- **Fetal Monitoring:**
- **Symphysis-fundal height (SFH):** For growth restriction.
- **Ultrasound scan:** Assess fetal growth, amniotic fluid volume, umbilical artery Doppler (for fetal compromise).
- **Cardiotocography (CTG):** Assess fetal wellbeing, especially if >26 weeks or concerns.
- **Special:**
- **Placental Growth Factor (PlGF) testing:** Low levels can help rule out/predict pre-eclampsia in suspected cases, especially between 20-35 weeks (NICE guidance). Useful for triaging.
💊 Management
Management is stratified by severity and gestational age, but the only definitive 'cure' is delivery.
**1. Prevention:**
- **Aspirin:** 75-150mg daily from 12 weeks until birth for women with 1 high-risk factor (e.g., previous pre-eclampsia, chronic kidney disease, autoimmune disease) or ≥2 moderate-risk factors (e.g., nulliparity, age >40, BMI >35, multiple pregnancy).
**2. Monitoring (in hospital for severe cases):**
- Regular BP, urine dip, FBC, U&Es, LFTs.
- Fetal monitoring: USS growth scans, Doppler, CTG.
**3. Antihypertensive Treatment (if BP ≥140/90 mmHg):**
- **Aim:** Maintain BP <135/85 mmHg (avoiding hypotension that could compromise placental perfusion).
- **First-line:** Oral Labetalol.
- **Second-line:** Oral Nifedipine (modified release).
- **Third-line:** Oral Methyldopa.
- **Acute severe hypertension (BP ≥160/110 mmHg):** IV Labetalol or IV Hydralazine (urgent reduction to prevent stroke).
**4. Seizure Prophylaxis/Treatment (Eclampsia):**
- **Magnesium Sulphate (IV):** Indicated for severe pre-eclampsia (e.g., BP ≥160/110, persistent headache/visual changes, clonus) or actual eclamptic seizures.
- Loading dose: 4g IV over 5-10 minutes.
- Maintenance: 1g/hour IV infusion.
- Monitor for toxicity: loss of reflexes, respiratory depression, reduced urine output. Antidote: Calcium gluconate.
**5. Timing of Delivery:**
- This is the only 'cure'. Decision balances maternal and fetal risks.
- **Severe pre-eclampsia:** Delivery often indicated at 34-37 weeks, or earlier if uncontrolled BP, worsening organ dysfunction, or fetal compromise.
- **Mild pre-eclampsia:** May be managed expectantly until term (37-40 weeks).
- **Corticosteroids:** Betamethasone/Dexamethasone given before 34 weeks if delivery is anticipated, to promote fetal lung maturity.
**6. Postpartum Management:**
- Continue BP monitoring for at least 72 hours, and up to 4 weeks postpartum.
- Antihypertensives often continued and gradually weaned.
- Counsel on future pregnancy risks.
**1. Prevention:**
- **Aspirin:** 75-150mg daily from 12 weeks until birth for women with 1 high-risk factor (e.g., previous pre-eclampsia, chronic kidney disease, autoimmune disease) or ≥2 moderate-risk factors (e.g., nulliparity, age >40, BMI >35, multiple pregnancy).
**2. Monitoring (in hospital for severe cases):**
- Regular BP, urine dip, FBC, U&Es, LFTs.
- Fetal monitoring: USS growth scans, Doppler, CTG.
**3. Antihypertensive Treatment (if BP ≥140/90 mmHg):**
- **Aim:** Maintain BP <135/85 mmHg (avoiding hypotension that could compromise placental perfusion).
- **First-line:** Oral Labetalol.
- **Second-line:** Oral Nifedipine (modified release).
- **Third-line:** Oral Methyldopa.
- **Acute severe hypertension (BP ≥160/110 mmHg):** IV Labetalol or IV Hydralazine (urgent reduction to prevent stroke).
**4. Seizure Prophylaxis/Treatment (Eclampsia):**
- **Magnesium Sulphate (IV):** Indicated for severe pre-eclampsia (e.g., BP ≥160/110, persistent headache/visual changes, clonus) or actual eclamptic seizures.
- Loading dose: 4g IV over 5-10 minutes.
- Maintenance: 1g/hour IV infusion.
- Monitor for toxicity: loss of reflexes, respiratory depression, reduced urine output. Antidote: Calcium gluconate.
**5. Timing of Delivery:**
- This is the only 'cure'. Decision balances maternal and fetal risks.
- **Severe pre-eclampsia:** Delivery often indicated at 34-37 weeks, or earlier if uncontrolled BP, worsening organ dysfunction, or fetal compromise.
- **Mild pre-eclampsia:** May be managed expectantly until term (37-40 weeks).
- **Corticosteroids:** Betamethasone/Dexamethasone given before 34 weeks if delivery is anticipated, to promote fetal lung maturity.
**6. Postpartum Management:**
- Continue BP monitoring for at least 72 hours, and up to 4 weeks postpartum.
- Antihypertensives often continued and gradually weaned.
- Counsel on future pregnancy risks.
Revision Resources – expand the sections below for high-yield notes, exam pearls, key facts and further reading.
MLA High-Yield Notes & Quick Revision ⌄
- **SBA Trap:** Proteinuria is *not* always required for diagnosis if other organ dysfunction is present (e.g., new-onset hypertension + elevated LFTs). This is a common misconception.
- **OSCE/Viva:** Be prepared to discuss the definition, risk factors, red flag symptoms, and the management of severe pre-eclampsia and eclampsia (Magnesium Sulphate dosing and monitoring).
- **Key OSCE finding:** Always check for clonus (3 or more beats is abnormal and indicates severe pre-eclampsia).
- **Common misconception:** Pre-eclampsia only occurs antenatally. Remember postpartum pre-eclampsia can present up to 4 weeks post-delivery.
- **Must-know drug:** Magnesium Sulphate for eclampsia/seizure prophylaxis. Know the loading dose (4g IV) and maintenance (1g/hr IV) and signs of toxicity (loss of reflexes, respiratory depression).
- **Antihypertensive choice:** Labetalol is first-line. Nifedipine is second. Methyldopa is often reserved for those who can't tolerate others or for chronic hypertension in pregnancy.
- **PlGF:** Understand its role in triaging suspected pre-eclampsia, not as a standalone diagnostic.
- **Delivery is the only cure:** Emphasise this in any management plan.
- **OSCE/Viva:** Be prepared to discuss the definition, risk factors, red flag symptoms, and the management of severe pre-eclampsia and eclampsia (Magnesium Sulphate dosing and monitoring).
- **Key OSCE finding:** Always check for clonus (3 or more beats is abnormal and indicates severe pre-eclampsia).
- **Common misconception:** Pre-eclampsia only occurs antenatally. Remember postpartum pre-eclampsia can present up to 4 weeks post-delivery.
- **Must-know drug:** Magnesium Sulphate for eclampsia/seizure prophylaxis. Know the loading dose (4g IV) and maintenance (1g/hr IV) and signs of toxicity (loss of reflexes, respiratory depression).
- **Antihypertensive choice:** Labetalol is first-line. Nifedipine is second. Methyldopa is often reserved for those who can't tolerate others or for chronic hypertension in pregnancy.
- **PlGF:** Understand its role in triaging suspected pre-eclampsia, not as a standalone diagnostic.
- **Delivery is the only cure:** Emphasise this in any management plan.
Antenatal care and screening for pregnancy complications
Management of obstetric emergencies (e.g., eclampsia)
Differential diagnosis of hypertension in pregnancy
Pharmacology of antihypertensives and anticonvulsants in pregnancy
Fetal wellbeing assessment in high-risk pregnancies
- Pre-eclampsia: new-onset HTN (≥140/90) after 20 weeks + proteinuria OR organ dysfunction.
- Proteinuria is not always required for diagnosis.
- Pathophysiology: abnormal placentation → placental ischaemia → endothelial dysfunction.
- Risk factors: previous pre-eclampsia, CKD, autoimmune disease (high risk).
- Prevention: Aspirin 75-150mg daily from 12 weeks for at-risk women.
- Severe pre-eclampsia: BP ≥160/110 or organ dysfunction/symptoms.
Exam Pearls ⌄
⭐ High Yield
Pre-eclampsia is new-onset hypertension (BP ≥140/90 mmHg) after 20 weeks' gestation PLUS proteinuria OR organ dysfunction.
Proteinuria is NOT always required for diagnosis if other organ dysfunction (e.g., elevated LFTs, renal impairment) is present.
The only definitive 'cure' is delivery of the placenta and baby.
Magnesium Sulphate (4g IV loading, 1g/hr maintenance) is the first-line treatment for eclampsia and seizure prophylaxis in severe pre-eclampsia.
First-line oral antihypertensive for pre-eclampsia is Labetalol.
Aspirin prophylaxis (75-150mg daily from 12 weeks) is crucial for at-risk women.
Postpartum pre-eclampsia can occur up to 4 weeks post-delivery.
Abnormal placentation leading to placental ischaemia and endothelial dysfunction is the core pathophysiology.
💡 Clinical Pearl
Hypertension: Pre-eclampsia is a specific form of new-onset hypertension in pregnancy, requiring distinct management from chronic or essential hypertension.
Acute Kidney Injury: Renal involvement in pre-eclampsia can lead to AKI due to glomerular endotheliosis and vasoconstriction.
Chronic Kidney Disease: CKD is a significant high-risk factor for developing pre-eclampsia.
Pulmonary Embolism: While not directly correlated, the hypercoagulable state in pregnancy and endothelial dysfunction in pre-eclampsia can increase thrombotic risk, though PE is a distinct entity.
⚠️ Exam Tip — Common Mistakes
Assuming proteinuria is always mandatory for a diagnosis of pre-eclampsia.
Forgetting that pre-eclampsia can present postpartum.
Not knowing the correct dosing and monitoring for Magnesium Sulphate.
Delaying delivery in severe cases due to fear of prematurity, despite it being the only cure.
Confusing pre-eclampsia with gestational hypertension (no organ dysfunction/proteinuria).
Key Facts ⌄
Definition: New-onset BP ≥140/90 mmHg after 20 weeks' gestation AND proteinuria OR organ dysfunction.
Proteinuria is NOT mandatory for diagnosis if other organ dysfunction is present (SBA trap).
Pathophysiology: Incomplete spiral artery remodelling leading to placental ischaemia and endothelial dysfunction.
Prophylaxis: Aspirin 75-150mg daily from 12 weeks for at-risk women.
Severe pre-eclampsia: BP ≥160/110 mmHg or significant maternal symptoms/organ dysfunction.
First-line oral antihypertensive: Labetalol. Nifedipine (MR) is an alternative. Methyldopa is third-line.
Eclampsia (seizures) management: IV Magnesium Sulphate (loading dose 4g, then infusion).
Only definitive 'cure': Delivery of the placenta and baby.
Postpartum pre-eclampsia can occur up to 4 weeks post-delivery (OSCE/SBA point).
Related Topics ⌄
References ⌄
- NICE Guideline (NG133) - Hypertension in pregnancy
- BNF for Obstetrics
- RCOG Green-top Guidelines
Further Resources
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