What defines preeclampsia with severe features?

Preeclampsia is new hypertension at or after 20 weeks with proteinuria or end-organ dysfunction. Severe features include systolic at or above 160 mmHg or diastolic at or above 110 mmHg, thrombocytopenia, elevated transaminases with right upper quadrant pain, renal insufficiency, pulmonary edema, or new cerebral or visual symptoms such as headache and scotomata.

What is magnesium sulfate used for in preeclampsia and eclampsia?

Magnesium sulfate is given to prevent and treat eclamptic seizures, not to lower blood pressure. Severe hypertension is treated separately with agents such as labetalol, hydralazine, or nifedipine. Magnesium toxicity presents with loss of deep tendon reflexes, then respiratory depression, and is reversed with intravenous calcium gluconate.

What is the only definitive treatment for preeclampsia, and how does HELLP differ from acute fatty liver of pregnancy?

Delivery of the placenta is the only cure. HELLP syndrome is hemolysis, elevated liver enzymes, and low platelets, a severe variant of preeclampsia. Acute fatty liver of pregnancy instead causes hypoglycemia, marked coagulopathy, and elevated ammonia from hepatic failure, which helps separate the two.

Clinical Images

Placental spiral artery remodeling in preeclampsia

Placenta: failed spiral artery remodeling drives ischemia · tap to expand

Thrombocytopenia and petechiae in HELLP syndrome

Low platelets in HELLP · tap to expand

Home Repro Preeclampsia, Eclampsia and HELLP

Preeclampsia, Eclampsia and HELLP

Shallow spiral arteries → placental ischemia → endothelial injury → HTN, protein leak, and organ damage. Delivery is the cure. Magnesium stops the seizures.

A 28-year-old G1P0 at 34 weeks is sent from clinic with blood pressure 168/112 mmHg on repeat measurements. She reports a pounding frontal headache and blurry vision for 2 days. Urine dipstick shows 3+ protein. She has no prior hypertension. Fundoscopic exam shows arteriolar narrowing. Fetal heart tracing is reassuring.

What is the most likely diagnosis?

Gestational thrombocytopenia

Severe preeclampsia

Chronic hypertension

Gestational hypertension

The Chain

From Bad Placentation to Endothelial Injury

Chicago beats: one cause, one effect, one board move at a time.

THE CLUE

New hypertension after 20 weeks + proteinuria or end-organ dysfunction in a previously normotensive patient.

BEAT 1 → Failed spiral artery remodeling

In normal pregnancy, cytotrophoblasts invade deep into the decidua and remodel spiral arteries into wide, low-resistance channels. In preeclampsia that invasion is shallow. The arteries stay narrow and vasoreactive.

Q: What does a narrow, high-resistance placental bed do to the placenta?
A: Chronic placental ischemia and oxidative stress.

BEAT 2 → Anti-angiogenic factors flood the maternal circulation

The ischemic placenta over-releases soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin. These trap vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGF-beta).

Q: What happens when you remove VEGF signaling from maternal endothelium?
A: Endothelial dysfunction: vasospasm, increased permeability, platelet activation, and microthrombi.

BEAT 3 → The clinical syndrome

HTN: vasospasm raises systemic pressure.
Proteinuria: glomerular endotheliosis increases capillary permeability.
RUQ/epigastric pain: Glisson capsule stretch from hepatic subcapsular hemorrhage or periportal edema (think HELLP spectrum).
Headache, visual changes: cerebral edema and vasospasm (severe feature).
Thrombocytopenia, elevated liver enzymes: microangiopathic injury → HELLP.

⚡ THE PUNCH: Bad placenta → ischemia → sFlt-1 → broken endothelium → HTN + protein leak + organ damage. Fix the placenta by delivering. Everything else is temporizing.

⚠

Gestational HTN is NOT preeclampsia

Gestational hypertension: new HTN after 20 weeks without proteinuria or end-organ dysfunction. Preeclampsia: HTN plus proteinuria (≥300 mg/24 h or equivalent) or end-organ dysfunction (thrombocytopenia, creatinine rise, liver transaminase elevation, pulmonary edema, cerebral/visual symptoms). Same BP number, different diagnosis, different monitoring intensity.

Definitions

Diagnosis and Severity

clinical medicine test the thresholds and the HELLP letters.

Preeclampsia (baseline)

BP ≥140/90 after 20 weeks (or ≥160/110 once) plus proteinuria or end-organ dysfunction in a woman without chronic HTN.

Timing matters: before 20 weeks, think chronic HTN, molar pregnancy, or secondary causes.

Severe preeclampsia

Any of: BP ≥160/110, thrombocytopenia (<100k), impaired liver function, creatinine >1.1 or doubling, pulmonary edema, new cerebral/visual symptoms, or severe persistent RUQ pain.

This patient needs magnesium, antihypertensives, and a delivery plan tonight, not outpatient follow-up.

Eclampsia

Seizures in a patient with preeclampsia/eclampsia spectrum, not attributable to another cause.

Treatment = magnesium sulfate. Do not use phenytoin or diazepam as first-line.

HELLP syndrome

Severe preeclampsia variant: microangiopathic hemolysis + liver injury + thrombocytopenia. Can present with minimal HTN.

Do not wait for severe BP to act. Low platelets + hemolysis + liver enzymes = deliver.

HEMOLYSIS

Schistocytes, elevated LDH, low haptoglobin, indirect hyperbilirubinemia

ELEVATED LIVER ENZYMES

AST/ALT rise; RUQ pain from hepatic distension

LOW PLATELETS

<100k (often <50k); consumptive microangiopathy

⚠

HELLP vs acute fatty liver of pregnancy (AFLP)

Both: third trimester, RUQ pain, nausea, elevated transaminases. HELLP: thrombocytopenia + hemolysis + often HTN/proteinuria. AFLP: hypoglycemia, prolonged PT/INR, ammonia elevation, fatty infiltration on biopsy; platelets may be normal early. Both may need urgent delivery. Wrong diagnosis delays the right ICU support.

Treatment

Stabilize, Protect, Deliver

Magnesium for the brain. Antihypertensives for the vessels. Delivery for the disease.

Acute severe HTN (≥160/110)

First-line agents: IV labetalol, IV hydralazine, or oral/SL nifedipine.
Goal: lower BP to <160/110 to prevent stroke, not to normalize immediately (placental perfusion).
Never in pregnancy: ACE inhibitors, ARBs, direct renin inhibitors.

Magnesium sulfate

Indications: eclampsia treatment, severe preeclampsia seizure prophylaxis, continued 24 h postpartum if severe features.
Mechanism: CNS depressant; stabilizes neuronal membranes; peripheral vasodilation.
Toxicity signs: loss of deep tendon reflexes, respiratory depression, cardiac arrest. Antidote = calcium gluconate.
Monitoring: reflexes, respiratory rate, urine output.

Delivery: the definitive treatment

≥37 weeks with preeclampsia: deliver.
<34 weeks with severe features: stabilize mother, betamethasone for fetal lung maturity if time allows, then deliver when maternal status dictates (often cannot wait).
34 to 36+6 weeks: individualized; severe HELLP or eclampsia = deliver now.
Expect postpartum BP to improve over 48 to 72 h as placenta is gone; still monitor for late postpartum preeclampsia.

🎯 Board sequence: (1) IV access + labs + type and screen. (2) Magnesium if severe or eclamptic. (3) Antihypertensive if ≥160/110. (4) Betamethasone if preterm and stable enough. (5) Deliver. Cure = placenta out.

⚠

Do not use phenytoin for eclampsia

Eclamptic seizures recur at high rates without magnesium. Phenytoin and benzodiazepines are second-line rescue, not primary therapy. The board answer for eclamptic seizure is always magnesium sulfate loading then maintenance infusion.

Prove It

Board Walkthrough

Original vignette bank, 5 dealt per round, answer choices shuffled, never-repeat within a round. Tap a wrong answer first to see why it almost works, then read the glowing clues.

Medically reviewed by Kaitlyn Cocuzzo, MD and Fatima Ali, DO · Last reviewed June 2026

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