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Obstetrics and Gynecology›Condition·Updated Jul 11, 2026·v1

Preeclampsia

Preeclampsia is a multisystem pregnancy disorder defined by new-onset hypertension after 20 weeks with proteinuria or end-organ dysfunction. It complicates 2-8% of pregnancies and is a leading cause of maternal and perinatal morbidity. Pathophysiology involves defective placentation leading to angiogenic imbalance (elevated sFlt-1/PlGF ratio). Evaluation requires blood pressure measurement, urine protein quantification, and assessment for end-organ involvement. Management of severe disease includes urgent antihypertensive therapy (labetalol, hydralazine, or nifedipine) and magnesium sulfate for seizure prophylaxis. Delivery is the definitive cure, with timing based on gestational age and severity. Low-dose aspirin before 16 weeks reduces preterm preeclampsia risk. Long-term cardiovascular risk is elevated, necessitating postpartum follow-up.

High Evidence549 references·3,232 words·13 min read·v1
preeclampsiahypertension in pregnancyobstetricseclampsiaHELLP syndromematernal-fetal medicinegestational hypertensionplacental dysfunction

Quick Reference

RxDrug of choiceMagnesium sulfate for seizure prophylaxis in severe preeclampsia (4-6 g IV loading, then 1-2 g/h for 24 h); labetalol (IV 20-80 mg) or nifedipine (oral immediate-release 10-20 mg) for acute severe hypertension.
AltAlternativesHydralazine IV 5-10 mg for acute hypertension; methyldopa (oral 250-500 mg BID-QID) for non-severe hypertension in pregnancy.
⊘AvoidACE inhibitors, ARBs, and direct renin inhibitors during pregnancy (fetal nephrotoxicity); ergometrine (severe vasoconstriction); NSAIDs if hypertension or renal impairment present.
DxTest of choicesFlt-1/PlGF ratio (cutoff ≤38 rules out preeclampsia within 1 week, NPV 99.3% at 24-34 weeks); 24-hour urine protein (≥300 mg) or protein/creatinine ratio (≥0.3) for diagnosis.
ScKey scorefullPIERS model: predicts adverse maternal outcome within 48 hours using gestational age, chest pain/dyspnea, oxygen saturation, platelet count, creatinine, AST. Score ≥30 → risk >20% → prompt delivery.
→When to referMaternal-fetal medicine consultation for early-onset (<34 wk), severe features, HELLP syndrome, eclampsia, superimposed preeclampsia, or failure to control BP. Also for first-trimester screening and aspirin prophylaxis counseling.
Preeclampsia is a multisystem disorder of pregnancy defined by new-onset hypertension after 20 weeks with proteinuria or end-organ dysfunction; delivery is the only cure. Acute management focuses on blood pressure control (target <160/105 mmHg) and seizure prophylaxis with magnesium sulfate. Low-dose aspirin started before 16 weeks reduces preterm preeclampsia by 62% in high-risk women.
Preeclampsia is a multisystem disorder unique to pregnancy, defined by new-onset hypertension after 20 weeks with proteinuria or end-organ dysfunction. It complicates 2-8% of pregnancies globally and remains a leading cause of maternal and perinatal morbidity. This concise reference summarizes key clinical facts, diagnostic criteria, management algorithms, and evidence-based interventions, including aspirin prophylaxis, antihypertensive therapy, magnesium sulfate, and delivery timing.

Overview and Recommendations

Background

  • •Preeclampsia is a multisystem progressive disorder unique to pregnancy, defined by new-onset hypertension (systolic ≥140 mmHg or diastolic ≥90 mmHg) after 20 weeks' gestation, with proteinuria (≥300 mg/24 h or protein/creatinine ratio ≥0.3) or, in its absence, evidence of maternal end-organ dysfunction. It complicates 2-8% of pregnancies globally and accounts for approximately 10% of maternal deaths in low- and middle-income countries, as well as a substantial proportion of iatrogenic preterm births.
  • •The disorder is not a single disease but a syndrome with multiple etiologies converging on a common pathway of placental dysfunction and systemic endothelial injury. The mechanistic chain begins with defective trophoblast invasion of spiral arteries in the first trimester, leading to high-resistance uteroplacental circulation, placental ischemia, and oxidative stress.
  • •The ischemic placenta releases excessive antiangiogenic factors, notably soluble fms-like tyrosine kinase 1 (sFlt-1), which neutralizes vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), while placental PlGF production falls. The resulting rise in the sFlt-1/PlGF ratio typically precedes clinical disease by weeks and is a hallmark of evolving preeclampsia. A second antiangiogenic factor, soluble endoglin (sEng), amplifies endothelial injury.
  • •Two major clinical subtypes exist: early-onset preeclampsia (diagnosed before 34 weeks), driven predominantly by placental dysfunction and severe angiogenic imbalance, and late-onset preeclampsia (≥34 weeks), linked more to maternal cardiovascular maladaptation with subtler placental changes. Approximately 20-30% of cases are early-onset, carrying higher maternal and fetal morbidity.
  • •The syndrome manifests through systemic endothelial dysfunction: vasospasm causes hypertension, glomerular endotheliosis leads to proteinuria, cerebral edema can trigger eclampsia, and hepatic inflammation may produce HELLP syndrome (hemolysis, elevated liver enzymes, low platelets). Magnesium sulfate reduces eclamptic seizures by more than half through cerebral vasospasm reduction.
  • •Low-dose aspirin (≥100 mg daily) started before 16 weeks of gestation reduces the risk of preterm preeclampsia by 62% (RR 0.38, 95% CI 0.20-0.74), as demonstrated in the ASPRE trial. The USPSTF recommends screening for preeclampsia with blood pressure measurements throughout pregnancy, and first-trimester combined screening using maternal factors, mean arterial pressure, uterine artery Doppler, and PlGF can detect 76% of preterm cases at a 10% false-positive rate.

Evaluation

  • •Suspect preeclampsia in any pregnant woman after 20 weeks' gestation presenting with new-onset hypertension (systolic ≥140 mmHg or diastolic ≥90 mmHg) on two occasions at least 4 hours apart, or with symptoms such as headache, visual disturbances (scotomata, photophobia, blurred vision), epigastric or right upper quadrant pain, or dyspnea.
  • •Ask about the classic triad of symptoms: headache (often frontal or occipital, not relieved by acetaminophen), visual changes (flashing lights, floaters, blurring), and epigastric or right upper quadrant pain. Additionally, screen for 10 newly identified prodromal symptoms with high odds ratios for impending eclampsia, including twitching/jerking limbs, hearing loss, impaired speech, confusion, feelings of doom, severe vertigo, jitters, difficulty concentrating, weakness/paralysis, and altered mental status.
  • •Examine the patient: measure blood pressure with a validated automated device after 5 minutes of rest in a seated position, using an appropriately sized cuff. Confirm an elevated reading with a repeat measurement. Perform fundoscopic examination for arteriolar spasm, assess for hyperreflexia (≥3+ or clonus), and evaluate for peripheral edema (though not specific). Sustained clonus (≥5 beats) or any twitching/jerking should prompt immediate consideration of magnesium sulfate.
  • •Order laboratory studies: complete blood count (platelet count <100,000/μL indicates severe features), serum creatinine (>1.1 mg/dL or doubling from baseline), liver enzymes (AST/ALT >2× upper limit of normal), and urinalysis. If dipstick proteinuria is ≥1+, send a spot protein-to-creatinine ratio (≥0.3 mg/mg is diagnostic) or start a 24-hour urine collection (≥300 mg/24 h is gold standard).
  • •Obtain an sFlt-1/PlGF ratio if there is diagnostic uncertainty, especially at 24-36 weeks. A ratio ≤38 has a negative predictive value of 99.3% for ruling out preeclampsia within 1 week, allowing safe outpatient management. A ratio >38 mandates close surveillance or admission. The ratio also stratifies risk of adverse neonatal outcomes.
  • •Perform obstetric ultrasound to assess gestational age, fetal number, amniotic fluid volume, and fetal growth. For confirmed preeclampsia, initiate serial assessment of fetal biometry, umbilical artery Doppler (pulsatility index >95th percentile or absent/reversed end-diastolic flow defines placental insufficiency), middle cerebral artery Doppler, and cerebroplacental ratio. Abnormal findings indicate fetal hypoxemia and may prompt delivery consideration.
  • •Diagnostic criteria per ACOG/ISSHP: new-onset hypertension after 20 weeks plus either proteinuria (≥300 mg/24 h or protein/creatinine ratio ≥0.3) OR one or more of the following end-organ abnormalities: thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or new-onset cerebral/visual symptoms. Proteinuria is sufficient but not necessary.
  • •Classify severity: severe features include systolic BP ≥160 mmHg or diastolic ≥110 mmHg on two occasions, platelet count <100,000/μL, AST/ALT >2× upper normal, serum creatinine >1.1 mg/dL or doubling, pulmonary edema, or new-onset cerebral/visual disturbances. The presence of any one severe feature reclassifies the patient as having preeclampsia with severe features.
  • •Consider differential diagnoses: systemic lupus erythematosus with nephritis, hemolytic uremic syndrome/thrombotic thrombocytopenic purpura (profound thrombocytopenia, microangiopathic hemolysis), acute fatty liver of pregnancy (marked transaminase elevation), pheochromocytoma (paroxysmal hypertension), and chronic kidney disease exacerbation. Also consider gestational hypertension (hypertension without proteinuria or end-organ dysfunction).
  • •For women with chronic hypertension, suspect superimposed preeclampsia when there is new-onset proteinuria or a sudden increase in blood pressure or end-organ dysfunction after 20 weeks. The sFlt-1/PlGF ratio may be less discriminatory in this population because baseline sFlt-1 levels are already elevated.

Management

  • •Admit all patients with preeclampsia with severe features to a labor and delivery unit or high-dependency unit for continuous maternal and fetal monitoring. ICU admission is indicated for persistent severe hypertension despite first-line therapy, eclampsia, pulmonary edema, or need for mechanical ventilation.
  • •Initiate antihypertensive therapy within 30-60 minutes of confirmed severe hypertension (systolic ≥160 mmHg or diastolic ≥110 mmHg) to prevent maternal stroke. First-line agents: intravenous labetalol 20 mg, repeat every 10-20 minutes up to 80 mg per episode (total 300 mg); intravenous hydralazine 5 mg, repeat every 20 minutes up to 10 mg per episode (total 20 mg); or immediate-release oral nifedipine 10 mg, repeat every 20-30 minutes up to 20 mg per episode (total 50 mg).
  • •If blood pressure remains uncontrolled after two doses of one agent, switch to an alternative first-line agent. Failure to achieve control after three agents or persistent severe hypertension despite maximal doses warrants emergent consultation with maternal-fetal medicine, anesthesiology, and/or critical care.
  • •Administer magnesium sulfate for seizure prophylaxis in all patients with preeclampsia with severe features, eclampsia, or HELLP syndrome. Standard regimen: 4-6 g IV loading dose over 15-20 minutes, followed by a maintenance infusion of 1-2 g/h for 24 hours postpartum. The Cochrane review (11,444 women) showed magnesium sulfate halves the risk of eclampsia (RR 0.41, 95% CI 0.29-0.58; NNT = 100).
  • •Monitor for magnesium toxicity: respiratory depression (<12 breaths/min), loss of deep tendon reflexes, oliguria. Keep calcium gluconate 1 g IV readily available as an antidote. Discontinue magnesium if signs of toxicity occur. For women who have received a minimum 8-hour predelivery infusion, discontinuation immediately after delivery is safe and reduces time to ambulation and lactation initiation.
  • •For term pregnancies (≥37 weeks) with preeclampsia without severe features, recommend induction of labor immediately. The HYPITAT trial demonstrated that induction reduces composite poor maternal outcome from 44% to 31% (RR 0.71, 95% CI 0.59-0.86; NNT = 8). For preeclampsia with severe features at term, deliver promptly regardless of gestational age.
  • •For late preterm preeclampsia (34 to <37 weeks), planned delivery reduces maternal composite outcome (PHOENIX trial: 65% vs 75%; aRR 0.86, 95% CI 0.79-0.94) but increases neonatal unit admissions (42% vs 34%). Discuss the trade-off with the patient. Administer antenatal corticosteroids (betamethasone 12 mg IM × 2 doses 24 hours apart) if delivery is anticipated before 34 weeks.
  • •For early-onset preeclampsia (<34 weeks), consider expectant management in stable women without severe features, with daily maternal and fetal surveillance. Use the fullPIERS model to predict adverse maternal outcome within 48 hours: gestational age, chest pain/dyspnea, oxygen saturation, platelet count, creatinine, AST. Score ≥30 indicates risk >20% and prompts expeditious delivery.
  • •Route of delivery: vaginal delivery is appropriate when the cervix is favorable and fetal status is reassuring. Cesarean section is reserved for standard obstetric indications (malpresentation, non-reassuring fetal status, failed induction). No randomized trial has shown that cesarean improves maternal outcomes in preeclampsia per se.
  • •Postpartum care: continue antihypertensive therapy to maintain BP <150/100 mmHg (per ACOG). Blood pressure often peaks 3-6 days after delivery. Continue magnesium sulfate for 24 hours postpartum. For women who develop postpartum preeclampsia de novo (new-onset hypertension 48 hours to 6 weeks after delivery), treat similarly with antihypertensives and magnesium if severe features are present.
  • •What NOT to do: do not use ergometrine for postpartum hemorrhage prophylaxis or treatment in women with preeclampsia (causes severe vasoconstriction and hypertensive crisis). Do not use ACE inhibitors or ARBs during pregnancy (fetal nephrotoxicity). Do not use vitamins C and E for prevention or treatment (no benefit, possible harm). Do not use pravastatin for treatment of early-onset preeclampsia (no reduction in sFlt-1 levels).
  • •For long-term prevention in subsequent pregnancies, initiate low-dose aspirin (81-162 mg daily) starting between 12 and 16 weeks of gestation and continue until delivery for all women with prior preeclampsia. The ASPRE trial showed that 150 mg daily reduces preterm preeclampsia by 62% (OR 0.38, 95% CI 0.20-0.74). ACOG recommends 81 mg daily; NICE recommends 75-150 mg daily.
  • •Discharge criteria: stable blood pressure <150/100 mmHg on oral antihypertensives, no severe features, no signs of end-organ dysfunction, adequate diuresis, and fetal status reassuring if undelivered. Arrange postpartum follow-up: blood pressure check within 72 hours, at 1 week, and then annually for all women following a preeclamptic pregnancy to monitor for chronic hypertension and cardiovascular risk.
  • •Refer to maternal-fetal medicine for early-onset preeclampsia (<34 weeks), preeclampsia with severe features, superimposed preeclampsia on chronic hypertension, HELLP syndrome, eclampsia, or when delivery timing is uncertain. Also refer for first-trimester combined screening for preterm preeclampsia using the Fetal Medicine Foundation algorithm.

Board Review — High Yield

  • •Definition, New-onset hypertension (≥140/90 mmHg) after 20 weeks with proteinuria or end-organ dysfunction.
  • •Pathophysiology, Defective trophoblast invasion → placental ischemia → antiangiogenic factors (sFlt-1, sEng) → endothelial dysfunction.
  • •sFlt-1/PlGF ratio, ≤38 rules out preeclampsia for 1 week (NPV 99.3%); >655 predicts delivery within 2 weeks.
  • •Severe features, BP ≥160/110, platelets <100K, AST/ALT >2× ULN, Cr >1.1, pulmonary edema, cerebral/visual symptoms.
  • •Magnesium sulfate, Halves eclampsia risk (RR 0.41; NNT 100); standard dose 4-6 g IV load then 1-2 g/h for 24 h.
  • •Acute hypertension, Treat within 30-60 min with IV labetalol, IV hydralazine, or oral nifedipine.
  • •Delivery timing, Term: immediate induction (HYPITAT NNT 8). Late preterm: planned delivery reduces maternal morbidity but increases NICU admissions. Early preterm: expectant management if stable.
  • •Aspirin prophylaxis, 81-150 mg/day started ≤16 weeks reduces preterm preeclampsia by 62% (ASPRE trial).
  • •HELLP syndrome, Hemolysis, elevated liver enzymes, low platelets; severe variant requiring prompt delivery.
  • •Long-term risks, Recurrence rate ~40%; increased lifetime cardiovascular disease risk; annual BP monitoring recommended.

Deep Dive — Evidence Details

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