Pre-eclampsia Study Guide
Study Guide
📖 Core Concepts
Pre‑eclampsia: Pregnancy‑specific, multi‑system disorder beginning >20 wk gestation; defined by new‑onset hypertension ≥ 140/90 mm Hg (two readings ≥4 h apart) plus proteinuria or organ dysfunction.
Severe disease: BP ≥ 160/110 mm Hg, proteinuria > 5 g/24 h, or any major organ abnormality (thrombocytopenia, renal insufficiency, liver dysfunction, pulmonary edema, seizures, visual changes).
Eclampsia: Convulsive seizures that develop in untreated pre‑eclampsia.
HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets – a severe variant of pre‑eclampsia.
Definitive cure: Delivery of fetus + placenta; management balances fetal maturity vs maternal risk.
📌 Must Remember
Diagnostic thresholds
Hypertension: SBP ≥ 140 mm Hg or DBP ≥ 90 mm Hg (two separate measurements).
Severe hypertension: SBP ≥ 160 mm Hg or DBP ≥ 110 mm Hg.
Proteinuria: ≥ 0.3 g/24 h, protein/creatinine ratio ≥ 0.3, or dipstick ≥ 1+.
Organ‑dysfunction criteria (any one replaces proteinuria):
Platelets < 100 × 10⁹/L
Serum creatinine > 1.1 mg/dL or doubling of baseline
AST/ALT ≥ 2× upper limit of normal
Pulmonary edema, new neurologic symptoms, or visual disturbances.
Aspirin prophylaxis: 150 mg nightly started < 16 wk in high‑risk women → up to 82 % risk reduction for early‑onset disease.
First‑line antihypertensives: Labetalol, hydralazine, nifedipine (IV or PO). ACE‑I/ARBs are contraindicated in pregnancy.
Magnesium sulfate dosing (seizure prophylaxis): 4 g IV load → 1–2 g/hr maintenance (adjust for renal function).
Recurrence risk: 20 % overall; higher if prior episode was severe.
🔄 Key Processes
Abnormal placentation → shallow trophoblast invasion → high‑resistance uterine arteries.
Placental hypoxia → oxidative stress → release of anti‑angiogenic factors sFlt‑1 & sEng.
Maternal endothelial dysfunction → vasoconstriction, capillary leak → hypertension, proteinuria, edema, multi‑organ injury.
Management workflow
Confirm diagnosis → assess severity & gestational age.
Stabilize BP (target 140–160/90–105 mm Hg).
Initiate magnesium sulfate if severe.
Give corticosteroids if <34 wk and delivery anticipated.
Plan delivery: ≥ 34 wk for severe disease; otherwise balance fetal maturity.
🔍 Key Comparisons
Pre‑eclampsia vs. Gestational Hypertension
Pre‑eclampsia: hypertension + proteinuria or organ dysfunction.
Gestational HTN: hypertension only, no proteinuria/organ damage.
Early‑onset vs. Late‑onset
Early‑onset (<34 wk): placental insufficiency, fetal growth restriction, higher maternal morbidity.
Late‑onset (≥34 wk): maternal metabolic risk factors, normal/increased fetal weight, often volume‑overload phenotype.
Magnesium sulfate vs. Labetalol (purpose)
MgSO₄: prevents seizures (eclampsia).
Labetalol: lowers BP; does not prevent seizures.
⚠️ Common Misunderstandings
“Proteinuria is required for diagnosis.”
False: Severe hypertension plus any organ dysfunction meets criteria even without proteinuria.
“Bed rest cures pre‑eclampsia.”
No evidence; rest may worsen volume overload.
“All antihypertensives are safe in pregnancy.”
ACE inhibitors and ARBs are teratogenic; avoid.
🧠 Mental Models / Intuition
“Two‑hit model”: First hit = abnormal placentation → anti‑angiogenic surge. Second hit = maternal endothelial response → clinical syndrome.
“Pressure‑damage ladder”: The higher the BP, the quicker you climb to severe complications (headache → visual changes → seizures).
“Timing compass”: Early‑onset = placental compass → focus on fetal growth; Late‑onset = maternal compass → focus on volume management (diuretics).
🚩 Exceptions & Edge Cases
Post‑partum pre‑eclampsia: Can arise 48 h–6 weeks after delivery; same diagnostic criteria, but ACE‑I/ARBs become permissible if not breastfeeding.
Absence of proteinuria: Severe hypertension with thrombocytopenia or renal insufficiency still qualifies.
High‑altitude pregnancies: Increased risk independent of other factors.
📍 When to Use Which
Aspirin: Any high‑risk patient before 16 wk (history, chronic HTN, diabetes, renal disease, multiple gestation).
MgSO₄: All patients with severe pre‑eclampsia or any eclampsia suspicion.
Labetalol vs. Hydralazine vs. Nifedipine: Choose based on contraindications, rapidity needed, and provider comfort; labetalol preferred for most severe cases.
Furosemide (diuretic): Late‑onset, high‑cardiac‑output, volume‑overload phenotype; monitor electrolytes and renal function.
👀 Patterns to Recognize
Severe headache + visual changes → impending eclampsia.
Right upper‑quadrant pain + ↑ LFTs → hepatic involvement/HELLP.
Platelets < 100 × 10⁹/L + ↑ AST/ALT → think HELLP.
Sudden BP jump after 34 wk in a previously normotensive patient → consider late‑onset volume‑overload phenotype.
🗂️ Exam Traps
“A dipstick 1+ always means pre‑eclampsia.”
Dipstick is a screening tool; confirm with quantitative protein/creatinine ratio.
“All antihypertensives are safe in lactation.”
ACE‑I/ARBs are unsafe; beta‑blockers, calcium‑channel blockers, and labetalol are preferred.
“Delivery before 34 wk is always indicated.”
Not unless maternal/fetal status is unstable; steroids are given first to improve neonatal outcomes.
“Low‑dose aspirin is only for early‑onset disease.”
It reduces both early‑ and term‑pre‑eclampsia when started early.
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Study tip: Memorize the BP thresholds, proteinuria cut‑offs, and the four pillars of management (BP control, seizure prophylaxis, fetal lung maturity, delivery timing). Use the mental models above to quickly decide on treatment pathways during practice questions.
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