Preeclampsia & Eclampsia

Detailed Overview

It is a placenta-driven disease. The fundamental defect is abnormal placentation leading to placental ischemia. The stressed placenta releases anti-angiogenic factors into the maternal circulation, causing massive, systemic maternal endothelial dysfunction. This widespread blood vessel damage leads to hypertension, leaky capillaries (edema, proteinuria), vasoconstriction, and microthrombi formation, threatening every major maternal organ (brain, liver, kidneys) and restricting fetal growth. Delivery of the fetus and placenta is the only definitive cure.

Epidemiology & Demographics

Complicates 3-5% of pregnancies worldwide. It is a leading cause of maternal and perinatal morbidity and mortality, responsible for approximately 50,000 maternal deaths annually globally. Highest risk is in nulliparous (first-time) mothers.

Etiological Mechanism

The exact initiating event is unknown, but it begins at the time of placental implantation in the first trimester. A failure of maternal immune tolerance to paternal antigens on the trophoblast is highly suspected as the root cause of the poor placental invasion.

Primary Causes

Failure of the extravillous trophoblasts to properly invade and remodel the maternal spiral arteries. The arteries remain narrow and rigid, leading to placental hypoperfusion and hypoxia as fetal demand grows.

• Nulliparity: First pregnancy carries the highest risk; risk resets with a new partner.
• Prior Preeclampsia: Increases risk in subsequent pregnancies by up to 7-fold.
• Medical Comorbidities: Pre-existing chronic hypertension, pregestational diabetes, obesity (BMI >30), and autoimmune diseases (Lupus, Antiphospholipid syndrome).
• Multiple Gestation: Twins or triplets vastly increase placental mass and demand.

Normally, trophoblasts invade maternal spiral arteries, replacing their muscular walls to create large, low-resistance vessels. In preeclampsia, this remodeling fails. As pregnancy progresses, the hypoxic placenta releases anti-angiogenic proteins, notably sFlt-1 (soluble fms-like tyrosine kinase-1) and soluble endoglin. sFlt-1 binds and neutralizes VEGF and PlGF in the maternal blood. The profound lack of VEGF causes severe maternal endothelial dysfunction. Endothelial damage leads to: 1) vasoconstriction (hypertension), 2) increased vascular permeability (proteinuria, pulmonary edema, cerebral edema causing seizures), 3) activation of the coagulation cascade (thrombocytopenia, DIC), and 4) hepatic ischemia (elevated transaminases).

Characteristic Clinical Presentation

• Severe Headache: Frontal or occipital, unyielding to acetaminophen (sign of cerebral edema/vasospasm).
• Visual Disturbances: Scotomata (blind spots), photophobia, or blurred vision.
• Right Upper Quadrant Pain: Epigastric or RUQ pain due to liver swelling stretching Glisson's capsule.
• Rapid Swelling: Sudden, severe edema, especially of the face and hands (not just the feet).

Physical Examination Signs

• Hypertension (BP ≥140/90 mmHg, or ≥160/110 mmHg in severe features)
• Hyperreflexia and Clonus (signs of profound CNS irritability impending seizure)
• Fetal Growth Restriction (SGA infant) or oligohydramnios on ultrasound

• HELLP Syndrome: Life-threatening microangiopathic hemolytic anemia and liver dysfunction.
• Placental Abruption: Premature separation of the placenta leading to massive hemorrhage.
• Maternal Stroke/Hemorrhage: Leading cause of maternal death in preeclampsia.
• Fetal Death: Due to profound hypoxia from abruption or extreme placental insufficiency.

Diagnostic Criteria & Guidelines

ACOG Criteria: Systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg on two occasions at least 4 hours apart after 20 weeks gestation in a previously normotensive patient. PLUS Proteinuria (≥300 mg per 24-hour collection, or Protein/Creatinine ratio ≥0.3). If proteinuria is absent, diagnosis can be made if new-onset hypertension is accompanied by ANY severe feature: Thrombocytopenia (<100,000), Renal insufficiency (Creatinine >1.1), Impaired liver function (AST/ALT twice normal), Pulmonary edema, or New-onset cerebral/visual symptoms.

Differential Diagnosis

• Chronic/Gestational Hypertension (no proteinuria or end-organ damage)
• Chronic Kidney Disease or Lupus Nephritis (causes baseline proteinuria)
• Thrombotic Thrombocytopenic Purpura (TTP) or Hemolytic Uremic Syndrome (HUS)
• Epilepsy (if seizures occur)

Laboratory Tests & Biomarkers

• Urine Protein/Creatinine Ratio: Elevated (≥0.3 mg/mg).
• Platelet Count: Decreased (<100,000/μL indicates severe feature and HELLP risk).
• AST / ALT: Elevated (≥2 times the upper limit of normal indicates severe feature).
• Serum Creatinine: Elevated (>1.1 mg/dL or a doubling of baseline).

Imaging Modalities & Findings

• Obstetric Ultrasound & Doppler:

• Preeclampsia without severe features
  BP ≥140/90 and proteinuria, but asymptomatic with normal labs.
• Preeclampsia with severe features
  BP ≥160/110, or end-organ damage (impaired liver function, renal insufficiency, thrombocytopenia, pulmonary edema, cerebral/visual symptoms).
• Eclampsia
  Occurrence of grand mal seizures.
• HELLP Syndrome
  A severe variant: Hemolysis, Elevated Liver enzymes, Low Platelets.

Second-Line & Adjunctive Therapy

For preterm pregnancies (<34 weeks) without severe features, expectant management with strict bed rest, daily monitoring, and twice-weekly labs until 37 weeks. If delivery is planned <34 weeks, administer IM Betamethasone (12 mg q24h x 2 doses) to accelerate fetal lung maturity before delivery.

Surgical & Procedural Management

Cesarean section is frequently required if the mother is unstable, the cervix is unfavorable for rapid induction, or there is fetal distress. However, vaginal delivery is generally preferred if safe to avoid surgical stress in a coagulopathic patient.

Recommended Lifestyle Changes

Patient Counseling & Advice

Educate the mother on the warning signs (headache, visual changes, belly pain) and instruct her to present to L&D immediately if they occur. Explain that Magnesium Sulfate will make her feel flushed, hot, and lethargic, but it is vital to prevent brain damage/seizures. Advise her that having preeclampsia permanently doubles her lifetime risk for cardiovascular disease and stroke, necessitating lifelong primary care follow-up.

Follow-Up & Monitoring Schedule

Maternal BP can remain dangerous postpartum. Monitor BP closely for 72 hours post-delivery, and again 7-10 days postpartum. Magnesium should be continued for 24 hours post-delivery. Postpartum eclampsia can occur up to 4-6 weeks after delivery.

Preventive Strategies

Prophylactic low-dose aspirin (81 mg daily) initiated between 12 and 16 weeks of gestation in women with high-risk factors (e.g., prior preeclampsia, chronic HTN, diabetes, multiple gestation).

Usually resolves completely within days to weeks postpartum. However, HELLP syndrome and eclampsia carry a significant risk of maternal mortality. Babies born prematurely face risks of RDS, IVH, and necrotizing enterocolitis.