Female ReproductiveMay 21, 20266 min readUpdated August 24, 2026

Everything You Need to Know About Preeclampsia/eclampsia for Step 1

New HTN after 20 weeks points to preeclampsia, especially with proteinuria or organ injury. Lock in severe features, HELLP, pathophysiology, and treatment.

Preeclampsia/eclampsia is one of those OB topics that shows up everywhere on Step 1 and Step 2: vignettes, pharm questions, ethics “what’s the next step?”, and postpartum complications. If you can connect abnormal placentation → endothelial dysfunction → vasospasm + leaky capillaries + end-organ injury, most questions become predictable.


The Core Definitions (Know These Cold)

Preeclampsia

New-onset hypertension after 20 weeks gestation plus either:

  • Proteinuria or
  • End-organ dysfunction (even without proteinuria)

Hypertension criteria

  • ≥140/90\ge 140/90 on 2 readings at least 4 hours apart, after 20 weeks, in a previously normotensive patient
  • Severe-range: ≥160/110\ge 160/110

Proteinuria criteria (any one)

  • ≥300\ge 300 mg/24 hours
  • Protein/creatinine ratio ≥0.3\ge 0.3
  • Dipstick ≥2+\ge 2+ (less preferred)

Eclampsia

Preeclampsia + seizures (generalized tonic-clonic) not attributable to another cause.

HELLP Syndrome (a severe variant)

  • Hemolysis (often microangiopathic hemolytic anemia)
  • Elevated Liver enzymes
  • Low Platelets
💡

First Aid tie-in: Preeclampsia/eclampsia and HELLP appear in the pregnancy HTN disorders section (OB/GYN + pathology + pharm overlaps). This is a classic “vascular/endothelial injury” concept.


Pathophysiology: The Story You Should Tell Yourself

Step 1-level mechanism: abnormal placentation

In normal pregnancy, trophoblasts remodel maternal spiral arteries into high-capacitance, low-resistance vessels.

In preeclampsia, trophoblastic invasion is shallow/incomplete → spiral arteries stay narrow, high-resistance → placental ischemia.

What does the ischemic placenta do?

It releases anti-angiogenic and inflammatory factors (classically tested concept):

  • ↑ sFlt-1 (soluble Fms-like tyrosine kinase-1) binds and reduces free VEGF and PlGF
  • ↓ angiogenesis → endothelial dysfunction

The consequences of endothelial dysfunction

Think: vasospasm + increased vascular permeability + activation of coagulation

  • Hypertension (vasoconstriction)
  • Proteinuria (glomerular endothelial injury)
  • Edema (capillary leak; can be pulmonary)
  • End-organ ischemia (brain, liver, kidney, placenta)

Kidney pathology you should recognize

Glomerular endotheliosis = swelling of glomerular endothelial cells with narrowed capillary lumens → ↓ GFR and proteinuria.


Risk Factors (High-Yield Associations)

Preeclampsia is more likely when there’s more placental tissue or less maternal immune tolerance to placental antigens:

Classic risk factors

  • Nulliparity (first pregnancy)
  • History of preeclampsia (strong risk for recurrence)
  • Multifetal gestation (more placenta)
  • Molar pregnancy (abnormal trophoblast, lots of placental tissue)
  • Chronic hypertension
  • Diabetes mellitus
  • CKD
  • Autoimmune disease (esp. antiphospholipid syndrome, SLE)
  • Obesity, advanced maternal age

Step-friendly memory hook: “First placenta exposure, more placenta, or maternal vascular disease”.


Clinical Presentation: How It Shows Up in Vignettes

Common findings

  • HTN after 20 weeks
  • Proteinuria
  • Edema (not required for diagnosis, but commonly present)

Severe features (these convert “preeclampsia” → “preeclampsia with severe features”)

Any of the following can qualify, even without massive proteinuria:

  • Severe BP: ≥160/110\ge 160/110
  • Thrombocytopenia: platelets < 100,000
  • Renal insufficiency: creatinine > 1.1 mg/dL or doubling baseline
  • Impaired liver function: elevated AST/ALT, RUQ/epigastric pain
  • Pulmonary edema
  • New-onset cerebral/visual symptoms: headache, scotomata, hyperreflexia, altered mental status

Eclampsia clues

  • Severe headache, visual changes, hyperreflexia/clonus → then seizure
  • Can occur antepartum, intrapartum, or postpartum (postpartum eclampsia is a classic trap)

Diagnosis: What the Question Actually Wants

Step-style diagnostic checklist

  1. Confirm timing: after 20 weeks
  2. Confirm BP
  3. Look for proteinuria OR end-organ dysfunction
  4. Decide if severe features are present

Key labs to order/interpret

ConcernWhat you’ll seeWhy it matters
Hemolysis↑ LDH, ↑ indirect bilirubin, schistocytesHELLP / microangiopathic hemolysis
Platelets↓ plateletsSeverity; DIC risk
Liver↑ AST/ALT, RUQ painHELLP; hepatic ischemia, subcapsular hematoma
Kidney↑ creatinine, proteinuriaRenal endotheliosis
CoagMay show DIC in severe disease/abruptionBleeding risk
FetusGrowth restriction, oligohydramniosPlacental insufficiency
💡

High-yield vignette: “Pregnant at 32 weeks with HTN, RUQ pain, elevated AST/ALT, low platelets” → HELLP.


Management: The Boards-First Approach

The only definitive treatment

Delivery of the placenta (i.e., delivery of the fetus and placenta).

But the timing depends on gestational age and severity.


Treatment Algorithms (What to Do and When)

Preeclampsia without severe features

  • If ≥ 37 weeks → deliver
  • If < 37 weeks → expectant management + close monitoring (maternal labs, BP, fetal status)

Preeclampsia with severe features

  • If ≥ 34 weeks → deliver
  • If < 34 weeks → stabilize mom, consider corticosteroids for fetal lung maturity if time allows, then proceed based on maternal/fetal status (many will still require delivery)

Eclampsia (seizure = emergency)

  1. Magnesium sulfate for seizure treatment and prophylaxis (first-line)
  2. Stabilize (ABCs)
  3. Control severe BP
  4. Delivery once stabilized (do not delay for prolonged “expectant management”)

Medications You Must Know (Step 1 Pharm + Step 2 OB)

Magnesium sulfate

Use: seizure prophylaxis/treatment in severe preeclampsia and eclampsia

Toxicity signs (classic Step question)

  • Loss of deep tendon reflexes
  • Respiratory depression
  • Cardiac arrhythmias

Antidote: Calcium gluconate

Antihypertensives used in pregnancy (acute severe HTN)

Common board answers:

  • IV labetalol
  • IV hydralazine
  • Oral nifedipine

Drugs to avoid in pregnancy HTN

  • ACE inhibitors/ARBs (fetal renal dysgenesis, oligohydramnios, skull hypoplasia)
  • Aliskiren (similar pathway concerns)
💡

First Aid cross-reference idea: This topic integrates with FA’s antihypertensive pharm section (pregnancy contraindications) and reproductive pathology.


Complications (Maternal + Fetal)

Maternal complications

  • Eclampsia (seizures)
  • Stroke/intracranial hemorrhage (from severe HTN)
  • Pulmonary edema
  • Acute kidney injury
  • HELLP
  • DIC
  • Placental abruption (painful bleeding + uterine tenderness)

Fetal complications

  • IUGR (uteroplacental insufficiency)
  • Oligohydramnios
  • Preterm delivery
  • Fetal hypoxia/distress
  • Stillbirth (severe cases)

HELLP Syndrome: Extra High-Yield Mini-Section

How it presents

  • RUQ/epigastric pain, nausea/vomiting, malaise
  • HTN/proteinuria may be present but not always dramatic
  • Labs: hemolysis + elevated LFTs + low platelets

Management (boards)

  • Stabilize + deliver (especially if maternal instability)
  • Magnesium sulfate (seizure prophylaxis)
  • Blood products as needed (platelets if significant thrombocytopenia with bleeding/procedures)

Differentials You’ll Be Asked to Separate

Preeclampsia vs gestational hypertension

  • Gestational HTN: HTN after 20 weeks without proteinuria or end-organ findings
  • Preeclampsia: HTN after 20 weeks with proteinuria or end-organ dysfunction

Preeclampsia vs chronic HTN

  • Chronic HTN: HTN before pregnancy or before 20 weeks
  • Superimposed preeclampsia: chronic HTN + new proteinuria or end-organ dysfunction after 20 weeks

Eclampsia vs epilepsy

  • Eclampsia often preceded by headache/visual symptoms/hyperreflexia, occurs around pregnancy/postpartum in a preeclampsia context.
  • If vignette includes severe HTN + proteinuria + seizure → assume eclampsia unless proven otherwise.

High-Yield “Exam Triggers” (Quick Hits)

  • After 20 weeks + HTN + proteinuria → preeclampsia until proven otherwise.
  • Seizure in a pregnant/postpartum patient → treat as eclampsia and give MgSO₄.
  • Mg toxicity → loss of reflexes is an early warning; antidote calcium gluconate.
  • RUQ pain + low platelets + high AST/ALT → HELLP, think urgent management.
  • Molar pregnancy/multifetal gestation → increased risk (more trophoblastic tissue).
  • Definitive treatment is delivery—everything else is stabilization/bridging.

Rapid Review Table (Great for Last-Minute Passes)

DisorderKey criteriaHallmark dangerTreatment cornerstone
Gestational HTNHTN after 20 wks, no proteinuria/end-organ signsCan progressMonitor; deliver at term
PreeclampsiaHTN after 20 wks + proteinuria or end-organ dysfunctionEnd-organ damage, abruptionDeliver (timing by severity/GA)
Preeclampsia w/ severe featuresSevere BP or severe symptoms/labsStroke, HELLP, pulmonary edemaMgSO₄ + BP control + deliver
EclampsiaPreeclampsia + seizuresMaternal/fetal mortalityMgSO₄ + stabilize + deliver
HELLPHemolysis, ↑ LFTs, ↓ plateletsDIC, liver hematoma/ruptureStabilize + deliver

Visual explanations from the StepGenie QBank

Infographics StepGenie drew to explain questions in its own QBank, matched to this article's topic. Each caption is the takeaway of the question it explains.

Disorders of pregnancy, childbirth, and puerperium — StepGenie USMLE Step 2 explanation infographic
Disorders of pregnancy, childbirth, and puerperium

Preeclampsia (new-onset HTN, proteinuria, edema after 20 weeks) increases risk of placental abruption due to abnormal placental vasculature.

USMLE Step 2
Disorders of pregnancy, childbirth, and puerperium — StepGenie USMLE Step 2 explanation infographic
Disorders of pregnancy, childbirth, and puerperium

Pulmonary edema from preeclampsia/gestational hypertension causes acute dyspnea, crackles, and severe hypertension in late pregnancy.

USMLE Step 2
See more obstetrics & gynecology explanation images

Frequently Asked Questions

What actually causes preeclampsia on Step 1?

Preeclampsia is caused by abnormal placentation that leads to endothelial dysfunction. In normal pregnancy, trophoblasts remodel spiral arteries into high-capacitance, low-resistance vessels. In preeclampsia, trophoblastic invasion is shallow, so the arteries stay narrow and high-resistance, causing placental ischemia. The ischemic placenta releases anti-angiogenic and inflammatory factors such as increased sFlt-1, which lowers free VEGF and PlGF and drives vasospasm, capillary leak, and end-organ injury.

How do you diagnose preeclampsia if there is no proteinuria?

You can still diagnose preeclampsia without proteinuria if there is new-onset hypertension after 20 weeks plus end-organ dysfunction. The diagnosis requires blood pressure of at least 140/90 on two readings at least four hours apart in a previously normotensive patient, and then either proteinuria or findings like renal insufficiency, thrombocytopenia, impaired liver function, pulmonary edema, or new cerebral or visual symptoms.

How do you tell preeclampsia from eclampsia and HELLP syndrome?

Preeclampsia is new-onset hypertension after 20 weeks with proteinuria or end-organ dysfunction, while eclampsia is preeclampsia plus generalized tonic-clonic seizures not explained by another cause. HELLP is a severe variant marked by hemolysis, elevated liver enzymes, and low platelets. A vignette with hypertension, right upper quadrant pain, elevated AST or ALT, and thrombocytopenia strongly points to HELLP.

What are the severe features of preeclampsia that change management?

Severe features are findings that upgrade the diagnosis to preeclampsia with severe features and make management more urgent. These include blood pressure at least 160/110, platelets below 100,000, creatinine above 1.1 mg/dL or doubled from baseline, elevated AST or ALT with right upper quadrant or epigastric pain, pulmonary edema, and new-onset neurologic or visual symptoms such as headache, scotomata, hyperreflexia, or altered mental status.

What is the first-line treatment for eclampsia, and what is the definitive treatment for preeclampsia?

Magnesium sulfate is the first-line treatment for eclampsia, and delivery is the definitive treatment for preeclampsia. In eclampsia, the immediate steps are magnesium sulfate for seizure treatment and prophylaxis, stabilization of ABCs, control of severe blood pressure, and then delivery once the patient is stabilized. More broadly, the only definitive treatment for preeclampsia is delivery of the fetus and placenta.

Try free Obstetrics & Gynecology questions

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