6.1 Preeclampsia, Eclampsia & HELLP Syndrome

Introduction to Hypertensive Disorders in Pregnancy

Hypertensive disorders are among the leading causes of maternal and perinatal morbidity and mortality worldwide. They complicate approximately 5-10% of all pregnancies. The spectrum includes chronic hypertension, gestational hypertension, preeclampsia, eclampsia, and HELLP syndrome. Early recognition and appropriate management are critical to prevent severe complications such as placental abruption, hepatic rupture, renal failure, cerebral hemorrhage, and maternal or fetal death.

Definitions and Diagnostic Criteria

• Chronic Hypertension: Blood pressure (BP) ≥140/90 mmHg present before pregnancy or diagnosed before 20 weeks of gestation. It persists beyond 12 weeks postpartum.
• Gestational Hypertension: New-onset BP ≥140/90 mmHg after 20 weeks of gestation in a previously normotensive woman, without proteinuria or end-organ dysfunction. BP normalizes within 12 weeks postpartum.
• Preeclampsia: New-onset hypertension (BP ≥140/90 mmHg on two occasions at least 4 hours apart) and proteinuria (≥300 mg/24 hours or protein/creatinine ratio ≥0.3) after 20 weeks of gestation. In the absence of proteinuria, preeclampsia is diagnosed if new-onset hypertension is accompanied by any of the following severe features: thrombocytopenia (<100,000/microL), renal insufficiency (creatinine >1.1 mg/dL or doubling of baseline), impaired liver function (elevated transaminases twice normal), pulmonary edema, or new-onset cerebral or visual disturbances.
• Eclampsia: The occurrence of generalized tonic-clonic seizures in a woman with preeclampsia, not attributable to other causes.
• HELLP Syndrome: A severe variant of preeclampsia characterized by Hemolysis (microangiopathic hemolytic anemia, schistocytes on smear, elevated bilirubin, low haptoglobin), Elevated Liver enzymes (AST/ALT twice upper limit of normal), and Low Platelets (<100,000/microL).

Pathophysiology

The exact etiology of preeclampsia remains elusive, but the central defect is believed to be abnormal placentation. In a normal pregnancy, cytotrophoblasts invade the maternal spiral arteries, converting them from narrow, high-resistance vessels to dilated, low-resistance vessels. In preeclampsia, this invasion is shallow and incomplete. The resultant placental ischemia releases anti-angiogenic factors (e.g., sFlt-1) into the maternal circulation, leading to systemic endothelial dysfunction. This widespread endothelial damage causes intense vasospasm, increased capillary permeability (leading to edema and proteinuria), and activation of the coagulation cascade.

Clinical Presentation and Evaluation

Patients may present asymptomatically or with symptoms such as a severe, persistent headache, visual changes (scotomata, blurred vision), right upper quadrant or epigastric pain (due to liver capsule distention), and rapid weight gain or nondependent edema.

Initial evaluation should include:

• Accurate BP measurement.
• Urinalysis and quantification of proteinuria.
• Complete blood count (CBC), comprehensive metabolic panel (CMP), and coagulation profile.
• Fetal assessment with a nonstress test (NST) and biophysical profile (BPP).
• Obstetric ultrasound for fetal growth and amniotic fluid volume.

Management Strategies

Antihypertensive Therapy

The goal of antihypertensive therapy is to prevent maternal cerebrovascular accidents while maintaining adequate uteroplacental perfusion. Treatment is generally initiated for severe hypertension (BP ≥160/110 mmHg).

• First-line agents:
  • Labetalol: Beta-blocker with alpha-1 blocking activity. Avoid in asthma or heart block.
  • Nifedipine: Calcium channel blocker (oral).
  • Hydralazine: Direct vasodilator (IV). May cause reflex tachycardia and maternal hypotension.
• Contraindicated agents: ACE inhibitors and ARBs (risk of fetal renal agenesis and pulmonary hypoplasia).

Seizure Prophylaxis and Treatment

Magnesium Sulfate (MgSO4) is the drug of choice for the prevention and treatment of eclamptic seizures. It is superior to phenytoin or diazepam.

• Dosing: Intravenous loading dose of 4-6 g over 15-20 minutes, followed by a maintenance infusion of 1-2 g/hour. Continue for 24 hours postpartum.
• Toxicity Monitoring: MgSO4 has a narrow therapeutic index (therapeutic range 4.8-8.4 mg/dL). Clinical signs of toxicity include loss of deep tendon reflexes (DTRs) at 9-12 mg/dL, respiratory depression at 12-14 mg/dL, and cardiac arrest at >15 mg/dL. Monitor urine output, respiratory rate, and DTRs regularly.
• Antidote: Calcium gluconate (1g IV over 3 minutes) for severe toxicity.

Timing of Delivery

Delivery is the only definitive cure for preeclampsia.

• Gestational Hypertension or Preeclampsia without severe features: Delivery is typically recommended at 37 weeks. Expectant management includes close maternal and fetal surveillance.
• Preeclampsia with severe features: Delivery is recommended at 34 weeks, or earlier if there is maternal or fetal decompensation (e.g., eclampsia, HELLP syndrome, nonreassuring fetal status, pulmonary edema). If <34 weeks and stable, administer antenatal corticosteroids (betamethasone) to accelerate fetal lung maturity and delay delivery for 48 hours if possible.
• Eclampsia/HELLP: Stabilize the mother (MgSO4, antihypertensives) and proceed with prompt delivery regardless of gestational age.

Postpartum Considerations

Preeclampsia can develop or worsen postpartum, typically within the first 48 hours, but late-onset cases can occur up to 6 weeks postpartum. Close monitoring of BP and neurological status is essential. Patients with a history of preeclampsia have an increased lifetime risk of chronic hypertension, cardiovascular disease, and stroke. Lifestyle modifications and regular screening should be emphasized.