8.2 Hypertensive Disorders of Pregnancy, Pre-eclampsia & Eclampsia

Hypertensive Disorders of Pregnancy, Pre-eclampsia & Eclampsia

Hypertensive disorders complicate up to 10% of all pregnancies worldwide and remain a primary cause of direct maternal and perinatal mortality in the United Kingdom. Prompt detection, accurate classification, early prophylactic intervention, and disciplined clinical management under NICE guideline NG133 (Hypertension in pregnancy: diagnosis and management) are essential core competencies for registered midwives.

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Classification & Definitions of Hypertensive Disorders

Hypertension in pregnancy is defined as a systolic blood pressure ≥140 mmHg and/or a diastolic blood pressure ≥90 mmHg, measured correctly and repeated to confirm; NICE NG133 defines severe hypertension as ≥160/110 mmHg. Midwives must classify hypertensive disorders based on timing of onset and multi-organ involvement:

1. Chronic Hypertension: Hypertension present preconceptionally or diagnosed before 20+0 weeks' gestation, or hypertension that persists beyond 6 weeks postpartum. It may be essential (primary) or secondary to underlying renal, endocrine, or vascular disorders.
2. Gestational Hypertension: New-onset hypertension arising at or after 20+0 weeks' gestation in the absence of significant proteinuria or maternal organ dysfunction. It resolves within 6 to 12 weeks postpartum. Approximately 15% to 25% of women with gestational hypertension subsequently develop pre-eclampsia.
3. Pre-eclampsia: New-onset gestational hypertension arising after 20+0 weeks' gestation accompanied by significant proteinuria OR new maternal organ dysfunction:
   • Proteinuria Thresholds: Spot urine protein:creatinine ratio (PCR) ≥30 mg/mmol, or albumin:creatinine ratio (ACR) ≥8 mg/mmol, or ≥300 mg protein in a 24-hour urine collection. Dipstick urinalysis of ≥1+ is a screening prompt but must always be confirmed by laboratory automated PCR or ACR.
   • Maternal Organ Dysfunction (Occurs even in the ABSENCE of Proteinuria):
     • Haematological: Thrombocytopenia (platelet count below 150 × 10^9/L), disseminated intravascular coagulation (DIC), microangiopathic haemolysis.
     • Hepatic: Elevated transaminases (ALT or AST over 40 IU/L), with or without epigastric or right upper quadrant abdominal pain.
     • Renal: Acute kidney injury (serum creatinine ≥90 µmol/L or doubling of baseline).
     • Neurological: Eclampsia, severe intractable headache, persistent visual scotomata, cortical blindness, hyperreflexia with sustained clonus (≥3 beats), or stroke.
     • Uteroplacental: Fetal growth restriction (FGR), abnormal umbilical artery Doppler velocimetry (absent or reversed end-diastolic flow), or intrauterine death.
4. Superimposed Pre-eclampsia: Development of pre-eclampsia features (new proteinuria, organ dysfunction, or severe resistant hypertension) in a woman with pre-existing chronic hypertension.

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Risk Stratification & Aspirin Prophylaxis (NICE NG133)

Pre-eclampsia is initiated by aberrant trophoblastic invasion of maternal spiral arteries during early placentation, causing defective vascular remodelling, placental ischaemia, and systemic maternal endothelial dysfunction. Low-dose aspirin inhibits platelet cyclooxygenase (COX-1), restoring the balance between pro-thrombotic thromboxane A2 and vasodilator prostacyclin.

NICE NG133 mandates risk screening at the initial booking visit. Prophylactic low-dose aspirin (75–150 mg daily; Saving Babies' Lives v3 favours 150 mg at night) is advised from 12 weeks' gestation until birth for women with:

• One High-Risk Factor OR
• Two or More Moderate-Risk Factors

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Placental Growth Factor (PlGF) Testing in Triage

Placental Growth Factor (PlGF) is a pro-angiogenic protein synthesized by the syncytiotrophoblast. In normal pregnancies, circulating PlGF rises steadily, peaking at 28–32 weeks. In pre-eclampsia, placental ischaemia stimulates excess secretion of soluble fms-like tyrosine kinase-1 (sFlt-1), an anti-angiogenic decoy receptor that binds and neutralizes free PlGF, causing maternal serum PlGF to fall precipitously.

NICE diagnostics guidance recommends using PlGF-based testing (either PlGF alone or the sFlt-1/PlGF ratio) in women presenting between 20+0 and 36+6 weeks' gestation with suspected pre-eclampsia (NICE DG49, 2022, reflected in NG133):

• Rule-Out Pre-eclampsia: A normal PlGF level (e.g., PlGF >100 pg/mL or sFlt-1/PlGF ratio <38 depending on assay) demonstrates exceptionally high negative predictive value (>98%), safely ruling out the development of pre-eclampsia requiring delivery within the subsequent 7 to 14 days. This avoids unnecessary hospital admission, enabling safe outpatient monitoring.
• Rule-In Pre-eclampsia: A severely low PlGF (<12 pg/mL) indicates severe placental dysfunction, high risk of imminent maternal-fetal compromise, and necessity for inpatient admission and delivery planning.

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Severe Pre-eclampsia & HELLP Syndrome

1. Severe Pre-eclampsia

Severe pre-eclampsia is diagnosed when hypertension is severe (BP ≥160/110 mmHg) or when pre-eclampsia is accompanied by progressive maternal organ impairment:

• Severe unremitting frontal or occipital headache resistant to analgesics.
• Visual disturbances: blurred vision, flashes, scotomata, or diplopia.
• Epigastric or right upper quadrant tenderness (due to hepatic capsular distension).
• Pulmonary oedema: sudden dyspnoea, tachypnoea, arterial oxygen desaturation (<95%), and bilateral basal crackles.
• Clonus: ≥3 rhythmic involuntary muscle contractions triggered by sudden dorsiflexion of the foot, signifying central nervous system irritability.

2. HELLP Syndrome

HELLP syndrome is a severe life-threatening variant of pre-eclampsia occurring in 10–20% of severe cases, characterized by:

• H (Haemolysis): Microangiopathic haemolytic anaemia; peripheral blood film demonstrates fragmented erythrocytes (schistocytes, helmet cells); elevated serum lactate dehydrogenase (LDH >600 IU/L); low haptoglobin and elevated indirect bilirubin.
• EL (Elevated Liver enzymes): Serum AST or ALT >70 IU/L (or twice the upper reference limit), accompanied by hepatic swelling, subcapsular haematoma risk, or spontaneous hepatic rupture.
• LP (Low Platelets): Consumptive thrombocytopenia with platelets falling <100 × 10^9/L (frequently <50 × 10^9/L in severe disease), increasing haemorrhage risks.

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Emergency Pharmacological Management of Hypertension

In women with severe hypertension (BP ≥160/110 mmHg), emergency medical therapy must be initiated within minutes to prevent maternal haemorrhagic stroke, encephalopathy, and placental abruption. The target blood pressure is <135/85 mmHg, while avoiding dropping the diastolic pressure below 80 mmHg to prevent compromising uteroplacental perfusion.

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Eclampsia: Emergency Seizure Management & Magnesium Sulfate Protocol

Eclampsia is defined as the occurrence of one or more generalized, tonic-clonic convulsions in a pregnant or postpartum woman in the presence of pre-eclampsia, not attributable to other cerebral causes. Approximately 44% of eclamptic seizures occur postnatally, 38% antepartum, and 18% intrapartum.

1. Immediate Emergency Midwifery Response

1. Call for Immediate Emergency Help: Activate the hospital obstetric emergency team (Call 2222): obstetrician, anaesthetist, senior midwife, and neonatal resuscitation team.
2. Airway, Breathing, Circulation (ABC): Turn the woman into the left lateral position to prevent aspiration and alleviate aortocaval compression. Clear the airway, apply high-flow oxygen (15 L/min via non-rebreather mask with reservoir bag), and protect the woman from physical trauma.
3. Call for the Emergency Eclampsia Box: Every maternity unit maintains a dedicated, standardized eclampsia kit containing pre-packaged magnesium sulfate ampoules, diluent, syringes, giving sets, and calcium gluconate.

2. Magnesium Sulfate Regimen (Collaborative Eclampsia Trial Regimen)

Magnesium sulfate is the definitive drug of choice for the prevention and treatment of eclamptic convulsions; standard antiepileptics (such as phenytoin or diazepam) are clinically inferior and must not be used.

• Loading Dose: 4 g Magnesium Sulfate IV administered over 5 to 15 minutes (e.g., 4 g of 50% magnesium sulfate solution diluted in 100 mL of 0.9% sodium chloride or 5% glucose).
• Maintenance Infusion: Continuous intravenous infusion of 1 g/hour for 24 hours following the last convulsion or 24 hours following delivery (whichever is later).
• Recurrent Seizures: If an eclamptic convulsion recurs while on the maintenance infusion, administer an additional 2 g IV bolus of magnesium sulfate over 5 minutes.

3. Monitoring for Magnesium Toxicity

Magnesium is eliminated almost exclusively by the maternal kidneys. In the presence of pre-eclamptic renal impairment, toxic levels can accumulate rapidly, causing neuromuscular blockade and cardiac arrest. The midwife must perform and document mandatory hourly clinical checks:

1. Deep Tendon (Patellar) Reflexes: Presence of the patellar reflex (knee jerk) confirms safe neurological conduction. Loss of patellar reflexes is the earliest clinical sign of hypermagnesaemia (serum magnesium >3.5–4.0 mmol/L). If patellar reflexes are absent, stop the infusion immediately!
2. Respiratory Rate: Must be ≥12 breaths per minute. Respiratory depression occurs at serum levels >5.0 mmol/L, progressing to respiratory arrest at >6.0–7.0 mmol/L.
3. Urine Output: Requires an indwelling Foley catheter with a precision urometer. Urine output must be ≥100 mL every 4 hours (or ≥25 mL/hour). NICE NG133 also advises limiting maintenance fluids to 80 mL/hour in severe pre-eclampsia unless there are ongoing losses such as haemorrhage. If urine output falls below the threshold, magnesium excretion is compromised, mandating urgent medical review and dose reduction.
4. Continuous Pulse Oximetry: Maintain oxygen saturation (SpO2) ≥95%.