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Preeclampsia and Eclampsia - Complete Guide

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What Are They? (Simple Overview)

Preeclampsia = high BP + organ stress in pregnancy Eclampsia = preeclampsia + seizures

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The Core Problem - What Goes Wrong?

Step-by-Step Pathophysiology

Normal pregnancy:
Trophoblasts (placental cells) invade spiral arteries
→ Arteries widen into large, low-resistance sinusoids
→ Plenty of blood to the placenta and baby

Preeclampsia:
Trophoblast invasion FAILS
→ Spiral arteries stay narrow and coiled
→ Placenta becomes ischemic (oxygen-starved)
→ Placenta releases dangerous factors into mother's blood
→ Widespread maternal endothelial dysfunction
→ High BP + Proteinuria + Organ damage

Key Molecules Released by the Ischemic Placenta

• Creasy & Resnik's Maternal-Fetal Medicine
• Robbins & Kumar Basic Pathology, p. 702
• Guyton & Hall Textbook of Medical Physiology, p. 1041

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Risk Factors

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Diagnosis - What to Look For

Preeclampsia Diagnostic Criteria

• Systolic BP ≥ 140 mmHg OR Diastolic BP ≥ 90 mmHg
• Measured on two occasions at least 4 hours apart
• After 20 weeks of gestation

1. Proteinuria > 300 mg in 24 hours (or urine protein:creatinine ratio ≥ 0.3)
2. OR signs of end-organ damage (even without proteinuria):
   • Thrombocytopenia (platelets < 100,000)
   • Renal insufficiency (creatinine > 1.1 mg/dL)
   • Impaired liver function (elevated transaminases)
   • Pulmonary edema
   • New-onset headache unresponsive to medication
   • Visual disturbances

Preeclampsia WITH Severe Features

• BP ≥ 160/110 mmHg (on two occasions 15 minutes apart)
• Platelet count < 100,000/µL
• Serum creatinine > 1.1 mg/dL
• Doubling of liver enzymes
• Pulmonary edema
• Severe headache, visual changes, or clonus

Eclampsia

• New-onset grand mal (tonic-clonic) seizures in a woman with preeclampsia
• No other neurological cause to explain the seizure
• Can occur antepartum, intrapartum, or postpartum (up to 10 days after delivery)
• Progression from preeclampsia to eclampsia is unpredictable and can be rapid
• ROSEN's Emergency Medicine, p. 2668-2670
• Tintinalli's Emergency Medicine, p. 443

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Symptoms - What the Patient Feels

Early/Mild Preeclampsia

• High blood pressure (may be asymptomatic)
• Swelling (edema) - especially face and hands
• Rapid weight gain (fluid retention)
• Protein in urine (no symptoms, detected on testing)

Severe Preeclampsia / Warning Signs of Eclampsia

• Severe headache (frontal, persistent, not responding to paracetamol)
• Visual disturbances - blurred vision, flashing lights, scotomata (blind spots)
• Right upper quadrant / epigastric pain (liver capsule distension)
• Nausea and vomiting
• Decreased urine output
• Brisk reflexes, clonus

Eclampsia

• Seizures (tonic-clonic) - may occur without warning
• Confusion, altered consciousness post-seizure
• Can lead to coma

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Organs Affected (End-Organ Damage)

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HELLP Syndrome

H - Hemolysis (microangiopathic hemolytic anemia) EL - Elevated Liver enzymes LP - Low Platelets

• DIC (disseminated intravascular coagulation)
• Liver rupture
• Placental abruption
• Maternal/fetal death
• Robbins & Kumar Basic Pathology, p. 702

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Pathology (What You See Under the Microscope)

Placenta

• Multiple infarcts (much more numerous than normal pregnancy)
• Retroplacental hemorrhage
• Syncytial knots (aggregates of syncytial nuclei on villi - sign of ischemia)
• Acute atherosis in decidual vessels - fibrinoid necrosis + lipid-laden macrophages (resembles atherosclerosis)

Kidney

• Glomerular endotheliosis - swollen endothelial cells, obliterated capillary lumens
• Protein deposits in glomerular basement membranes
• Decreased GFR (opposite to normal pregnancy where GFR increases)
• Robbins, Cotran & Kumar Pathologic Basis of Disease

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Management

The Definitive Treatment: DELIVERY

• Maternal risk of continuing pregnancy vs.
• Fetal risk of preterm delivery

• ≥ 37 weeks + preeclampsia → deliver
• ≥ 34 weeks + severe features → deliver
• < 34 weeks without severe features → expectant management with close monitoring

1. Antihypertensive Therapy

2. Seizure Prevention and Treatment: Magnesium Sulfate

• Loading: 4 g IV over 15-20 minutes
• Maintenance: 1-2 g/hour IV infusion

• Calcium antagonism → smooth muscle relaxation
• Reduces cerebral vasospasm
• Protects blood-brain barrier → limits cerebral edema
• Central anticonvulsant activity

• Respiratory rate (respiratory depression is the major risk)
• Oxygen saturation
• Deep tendon reflexes (loss of patellar reflex is early warning)
• Urine output (magnesium is renally cleared)

• Clonus
• Severe headache
• Visual disturbances (scotomata)

3. Fluid Management

• Capillary permeability is increased
• Do NOT give aggressive IV fluids - high risk of pulmonary edema
• Restrict IV fluids to ~85 mL/hour in severe cases

4. Management of Eclamptic Seizure

• Comprehensive Clinical Nephrology, 7th Edition, p. 632
• ROSEN's Emergency Medicine, p. 2670

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Prognosis and Recovery

• After delivery: Hypertension and proteinuria usually resolve within 1-2 weeks
• Most women have no lasting sequelae after uncomplicated preeclampsia
• Preeclampsia increases lifelong cardiovascular risk (hypertension, ischemic heart disease, stroke) in the mother
• Risk of recurrence in future pregnancies: ~15-25% (higher if early onset or severe)

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Prevention

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Quick Summary Table

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Preeclampsia & Eclampsia - OB/GYN Complete Notes

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BASIC CONCEPT (Easy Understand)

These are pregnancy-specific diseases. They completely reverse after delivery. The placenta is the cause, delivery is the cure.

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PATHOPHYSIOLOGY (The "Why")

The Key Problem: Failure of Spiral Artery Remodeling

1. Trophoblast invasion of spiral arteries FAILS
        ↓
2. Spiral arteries remain narrow and coiled
        ↓
3. Placenta becomes ischemic (underperfused)
        ↓
4. Ischemic placenta releases antiangiogenic factors into maternal blood:
   - sFlt-1 (soluble fms-like tyrosine kinase-1) → blocks VEGF and PIGF
   - Soluble endoglin → blocks TGF-β
        ↓
5. Widespread MATERNAL ENDOTHELIAL DYSFUNCTION
        ↓
6. Signs and symptoms of preeclampsia:
   - ↑ Vasoconstriction (↑ TXA₂, ↓ PGI₂) → Hypertension
   - Endothelial leakage → Proteinuria, Edema
   - Platelet activation → Thrombocytopenia, DIC
   - Organ hypoperfusion → Liver, Kidney, Brain damage

• ↓ Prostacyclin (PGI₂) and ↑ Thromboxane A₂ - imbalance causes vasoconstriction
• sFlt-1 - the most studied marker; levels rise weeks before clinical disease
• Increased angiotensin II sensitivity - preeclamptic women are hypersensitive to Ang II even from early pregnancy (as early as 10-14 weeks, before clinical signs!)
• Creasy & Resnik's Maternal-Fetal Medicine

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CLASSIFICATION (OB/GYN Standard)

1. Hypertensive Disorders of Pregnancy (Classification)

2. Preeclampsia: Without vs. With Severe Features

Diagnostic Criteria for Preeclampsia:

• Systolic ≥ 140 mmHg OR Diastolic ≥ 90 mmHg

• Proteinuria ≥ 300 mg/24 hr (or protein:creatinine ratio ≥ 0.3, or dipstick 2+)
• OR without proteinuria, any of:
  • Platelets < 100,000/µL
  • Creatinine > 1.1 mg/dL (new renal insufficiency)
  • Liver enzymes > 2x upper limit of normal
  • Pulmonary edema
  • New-onset cerebral or visual disturbances

Criteria for SEVERE FEATURES:

Note (OB exam important!): Proteinuria > 5g and fetal growth restriction are NO LONGER criteria for severe features (per current ACOG).

• Creasy & Resnik's Maternal-Fetal Medicine, p. 1055

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RISK FACTORS

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CLINICAL FEATURES

A. Symptoms (by system)

Most women with early preeclampsia are asymptomatic - this is why frequent antenatal visits matter!

B. Signs

• Hypertension (hallmark)
• Edema - especially facial and hand edema (note: edema alone is NOT diagnostic; it occurs in normal pregnancy too)
• Proteinuria on urine dipstick or 24-hr collection
• Brisk deep tendon reflexes and clonus (warning sign of eclampsia)
• Papilledema (severe cases)

Eclampsia - Clinical Picture

• Seizures are grand mal (tonic-clonic) type
• Preceded by prodrome in 80%: headache, visual changes
• 30% of eclampsia occurs postpartum (90% within 7 days of delivery)
• Can occur without warning in 20% of cases
• Progression from preeclampsia to eclampsia is unpredictable
• Creasy & Resnik's Maternal-Fetal Medicine, p. 1058

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PATHOLOGY - ORGAN CHANGES

1. Kidney - "Glomerular Endotheliosis" (Pathognomonic Lesion)

• Swollen endothelial cells occlude capillary lumen
• Protrusion of glomerular tuft into proximal tubule
• Decreased GFR (opposite of normal pregnancy where GFR increases by 40-50%)
• Protein deposits in glomerular basement membrane
• Result: Proteinuria, oliguria, rising creatinine

2. Liver

• 60% of eclamptic women have gross hepatic lesions
• Early: Periportal hemorrhage - vasodilation → hepatocyte displacement
• Late: Hepatic infarction from intense vasospasm
• Hemorrhagic changes in 66%, necrotic changes in 40% of eclamptic women
• Severe: Subcapsular hemorrhage → risk of hepatic rupture (rare but fatal)

3. Brain

• Cerebral vasospasm + loss of autoregulation → cerebral edema
• PRES (Posterior Reversible Encephalopathy Syndrome) - vasogenic parietooccipital edema, typically reversible
• Petechial hemorrhages, white matter necrosis in severe/fatal cases
• Autopsy: white-matter predominant injury, ranging from mild edema to extensive necrosis

4. Placenta

• Multiple infarcts (from chronic hypoperfusion)
• Retroplacental hemorrhage → risk of abruption
• Syncytial knots (ischemic villi)
• Acute atherosis of decidual vessels (fibrinoid necrosis + lipid macrophages)
• Leads to: IUGR, oligohydramnios, fetal distress

5. Coagulation

• DIC in 10% of severe preeclampsia/eclampsia
• Platelet consumption → thrombocytopenia
• Elevated fibrin degradation products
• Microthrombi in liver, kidney
• Overt DIC → spontaneous hemorrhage

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HELLP SYNDROME

H = Hemolysis (microangiopathic hemolytic anemia - schistocytes on smear) EL = Elevated Liver enzymes (AST, ALT > 2x normal) LP = Low Platelets (< 100,000/µL, often < 50,000)

• May present WITHOUT classic hypertension or proteinuria
• RUQ/epigastric pain + malaise + nausea + vomiting
• Often confused with cholecystitis, hepatitis, or gastritis
• Can present in emergency department

• DIC
• Acute renal failure
• Pulmonary edema
• Placental abruption
• Hepatic rupture (rare, surgical emergency)
• Maternal and perinatal mortality

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INVESTIGATIONS

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MANAGEMENT

The Definitive Treatment = DELIVERY (delivery of the placenta)

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A. Antihypertensive Therapy

• Goal: SBP < 160 mmHg, DBP < 110 mmHg
• Do NOT lower BP too fast - risk of uteroplacental insufficiency

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B. Seizure Prophylaxis & Treatment: Magnesium Sulfate

• Calcium antagonism → smooth muscle relaxation → peripheral and cerebral vasodilation
• Protects blood-brain barrier → limits cerebral edema
• Increases prostacyclin release from endothelium
• Decreases plasma renin activity
• Central anticonvulsant activity
• Note: Has only modest antihypertensive effect - additional drugs still needed for BP

• Preeclampsia WITH severe features (especially clonus, severe headache, visual scotomata)
• Does NOT need to be given for preeclampsia without severe features (seizure risk is extremely low and drug toxicity occurs in up to 25%)

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C. Management of an Eclamptic Seizure

1. AIRWAY - Position left lateral, suction airway, give O₂
2. SECURE IV ACCESS
3. MgSO₄ 4g IV bolus (if not already on it)
   → If already on MgSO₄: give extra 2g IV
   → If seizure persists: diazepam 5-10 mg IV
4. BLOOD PRESSURE CONTROL - if ≥ 160/110 mmHg
5. FETAL MONITORING - continuous CTG after stabilization
6. DO NOT rush to deliver during the seizure
7. PLAN DELIVERY after maternal stabilization
8. AIRWAY PROTECTION - intubation if needed

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D. Fluid Management

• Capillary permeability is increased - IV fluids leak into interstitium
• Do NOT give aggressive IV fluids - risk of pulmonary edema
• Restrict IVF to ~85 mL/hour in severe cases
• Central venous pressure monitoring is NOT routinely indicated

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E. Delivery Timing (OB Exam Favourite!)

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F. HELLP Syndrome Management

1. Urgent delivery (regardless of gestational age)
2. Correct coagulopathy (FFP, platelets if < 20,000-30,000)
3. Platelet transfusion for platelets < 20,000-30,000/µL (for delivery)
4. MgSO₄ for seizure prophylaxis
5. Antihypertensives for severe BP
6. No evidence for corticosteroids or plasma exchange improving outcomes
7. Refer to tertiary center if local facilities inadequate

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PREVENTION

• Any 1 HIGH-risk factor: previous preeclampsia, multifetal gestation, CKD, autoimmune disease (APS, SLE), diabetes, chronic HTN
• Any 2+ MODERATE-risk factors: nulliparity, obesity, family history, Black race, low socioeconomic status, age ≥ 35, IVF

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MATERNAL COMPLICATIONS SUMMARY

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FETAL COMPLICATIONS

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PROGNOSIS & LONG-TERM EFFECTS

• HTN and proteinuria resolve within 1-2 weeks postpartum in most cases
• No lasting sequelae in uncomplicated cases
• Preeclampsia is a marker for future cardiovascular disease in the mother:
  • 2x lifetime risk of hypertension
  • 2x risk of ischemic heart disease
  • 2x risk of stroke
• Recurrence risk: ~15-25% in future pregnancies; higher if early-onset or severe

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QUICK EXAM SUMMARY BOX

PREECLAMPSIA = BP ≥ 140/90 after 20 wks + Proteinuria OR end-organ damage

SEVERE FEATURES = BP ≥ 160/110 OR platelets <100K OR creatinine >1.1
                  OR liver enzymes >2x OR pulmonary edema OR neuro symptoms

ECLAMPSIA = Preeclampsia + Grand mal seizures

HELLP = Hemolysis + Elevated Liver enzymes + Low Platelets (10% of severe PE)

TREATMENT:
- Definitive = DELIVERY
- Seizure = MgSO₄ (4g IV load → 1-2g/hr)
- BP ≥ 160/110 = Labetalol / Hydralazine / Nifedipine
- Antidote for Mg toxicity = Calcium gluconate 1g IV

DELIVER AT:
- ≥37 wks = any preeclampsia
- ≥34 wks = severe features
- Any gestation = eclampsia, HELLP

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