⚕️ Target audience: This clinical review is intended for physicians and healthcare professionals; It is a summary of current literature and guidelines for educational purposes. Clinical decisions should be made based on patient-specific evaluation and applicable institutional protocols.

Definition, Classification and Epidemiology

Preeclampsia is a progressive multisystem disorder in which new-onset hypertension after the 20th week of pregnancy (or in the postpartum period) is accompanied by proteinuria or significant maternal end-organ dysfunction without proteinuria. Pathogenesis includes both abnormal placentation and maternal systemic vascular dysfunction (UpToDate, “Preeclampsia: Clinical features and diagnosis,” 2026). Approximately 90% of cases occur in the late preterm (≥34–<37 weeks), term or postpartum period and generally have a good prognosis; The remaining ~10% in the early-onset (<34 weeks) group is associated with serious perinatal morbidity/mortality.

In a systematic review, 4.6% (95% CI 2.7–8.2) of pregnancies worldwide were complicated by preeclampsia; The US incidence is approximately 5% (UpToDate 2026). Late-onset preeclampsia (2.7%) is more common than early-onset (0.3%). Hypertensive disorders of pregnancy, along with hemorrhage and venous thromboembolism, are directly responsible for 10–15% of maternal deaths worldwide.

Spectrum of hypertensive pregnancy disorders

ACOG Practice Bulletin No. The basic diagnoses according to the 222 (June 2020) and ISSHP 2021 classification are:

Gestational hypertension: Hypertension that develops after the 20th week in a previously normotensive patient without proteinuria or other signs of preeclampsia. Up to 50% of these patients progress to preeclampsia over time; True gestational hypertension resolves within 12 weeks after birth.
Preeclampsia (severe feature ±): Hypertension + proteinuria or hypertension + significant end-organ dysfunction.
Preeclampsia superimposed on chronic hypertension: Worsening/resistant hypertension, new proteinuria, or new end-organ dysfunction after the 20th week in a patient with chronic hypertension.
HELLP syndrome (Hemolysis, High Liver enzymes, Low Platelets): Considered a subtype of preeclampsia with severe features. 82–88% of patients have hypertension and 86–100% have proteinuria; ~15% may present without hypertension.
Eclampsia: Development of tonic-clonic convulsion in a patient with preeclampsia, when there is no other neurological condition that would explain the seizure.

Diagnostic Criteria and Thresholds

Hypertension in pregnancy is defined as systolic blood pressure (SBP) ≥140 mmHg and/or diastolic blood pressure (DBP) ≥90 mmHg; severe hypertension is SBP ≥160 mmHg and/or DBP ≥110 mmHg (ACOG PB 222, 2020). Measurements must be repeated to verify the threshold — non-severe values are re-verified every few hours/days, severe values are re-verified within 15 minutes (as they require urgent treatment).

Table 1. Preeclampsia diagnostic criteria (ACOG PB 222, 2020)
Component	Criterion
Hypertension	SBP ≥140 and/or DBP ≥90 mmHg, on two measurements at least 4 hours apart (after week 20, previously normotensive)
Proteinuria (diagnostic if present)	≥300 mg / 24-hour urine or protein/creatinine ratio ≥0.3 mg/mg or (only if there is no quantitative method) dipstick ≥2+
If there is no proteinuria — one of the following is sufficient	Thrombocytopenia (<100,000/µL) · creatinine >1.1 mg/dL or twice baseline · transaminases ≥2× ULN · pulmonary edema · headache unresponsive to treatment · visual disturbance

Severe features (organ criteria)

Approximately 25% of patients with preeclampsia develop one or more of the following criteria indicating the severe end of the disease (alarm findings) (ACOG PB 222, 2020; UpToDate 2026):

SBP ≥160 mmHg and/or DBP ≥110 mmHg (at least twice, repeated measurement)
Thrombocytopenia: platelets <100,000/µL
Liver dysfunction: elevation of transaminases to twice the ULN and/or severe right upper quadrant/epigastric pain unresponsive to treatment
Renal failure: serum creatinine >1.1 mg/dL (97 µmol/L) or doubling of baseline creatinine in the absence of other renal disease
Pulmonary edema
New onset headache that does not respond to medication and cannot be explained by another diagnosis
Visual disturbances (scotoma, photopsia, temporary blindness)

Note: The degree of proteinuria threshold or the amount of proteinuria does not predict maternal/perinatal outcome after diagnosis; therefore, repeated urine protein measurement is not recommended after the threshold is exceeded (UpToDate, "Antepartum management", 2026).

Pathophysiology: Abnormal Placentation and Angiogenic Imbalance

The key event in the pathogenesis of preeclampsia is inadequate spiral artery remodeling (defective trophoblast invasion) in early pregnancy. As a result, relative placental hypoperfusion, hypoxia, ischemia and oxidative stress develop; this leads to the release of anti-angiogenic factors into the maternal circulation (UpToDate, “Preeclampsia: Pathogenesis”, 2026).

The central molecular mechanism is the imbalance between sFlt-1 (soluble fms-like tyrosine kinase-1) and PlGF (placental growth factor). sFlt-1 is a decoy receptor that binds and neutralizes VEGF and PlGF; Excessive secretion causes widespread maternal endothelial dysfunction, vasoconstriction and increased capillary permeability. This explains hypertension, proteinuria (glomerular endotheliosis) and other end-organ findings. According to ISSHP, angiogenic imbalance (PlGF <5th percentile or increase in sFlt-1:PlGF ratio, e.g. >38 by Roche test) may strengthen the clinical diagnosis, but should not be used as a sole diagnostic criterion (ISSHP 2021).

In the USA, the FDA approved the sFlt-1:PlGF ratio in May 2023 only for singleton pregnancies at 23+0–34+6 weeks of gestation hospitalized for a hypertensive disorder of pregnancy, to predict progression to severe features within two weeks (based on the PRAECIS study). In this population, a ratio <40 indicates low risk with a two-week negative predictive value of ~96% (UpToDate 2026). ACOG has specified that the test should be used only in patients who meet PRAECIS inclusion criteria.

Risk factors and screening

Traditional risk factors are screened at the first prenatal visit. Those with the highest relative risk (RR) were: previous history of preeclampsia (RR 8.4), chronic hypertension (RR 5.1), pregestational diabetes (RR 3.7), multiple pregnancy (RR 2.9), chronic kidney disease, and antiphospholipid syndrome (RR 2.8). Recurrence after second trimester preeclampsia with severe features reaches 25–65% (UpToDate, "Clinical features", 2026). Blood pressure measurement is the primary screening method at all visits.

Prevention: Low-Dose Aspirin Prophylaxis

Low-dose aspirin is the best-studied and most useful pharmacological intervention in preventing preeclampsia. It protects vascular prostacyclin synthesis while reducing platelet thromboxane synthesis. Meta-analyses show that it reduces preeclampsia and related outcomes (preterm birth, growth restriction) by approximately 10–20% in intermediate-high risk patients (USPSTF 2021 meta-analysis, RR 0.85, 95% CI 0.75–0.95). The effect is particularly pronounced in preterm preeclampsia (RR 0.62); The effect on term preeclampsia is minimal.

The cornerstone of this evidence is the ASPRE study (Rolnik et al., NEJM 2017; PMID 28657417): in 1776 singleton pregnancies identified as high risk by the first-trimester multivariable screening algorithm, aspirin 150 mg daily from weeks 11–14 until week 36 reduced preterm preeclampsia at <37 weeks by 62% (1.6% versus 4.3%; OR 0.38, 95% CI 0.20–0.74; P=0.004). There was no significant difference in neonatal adverse outcomes.

💊 Aspirin prophylaxis — practical summary:

Candidate: ≥1 high-risk factor (prior preeclampsia, chronic HT, type 1/2 diabetes, multiple pregnancy, kidney disease, autoimmune disease) or ≥2 intermediate-risk factors (nulliparity, obesity [BMI >30], family history, age ≥35, IVF, etc.) — USPSTF/ACOG criteria.
Dose: 81 mg/day in the USA (USPSTF 2021); 100–150 mg/day in the European/ASPRE regimen. UpToDate finds 100–162 mg reasonable in select subgroups.
Initiation: at ≥12 weeks, ideally before 16 weeks. Starting after 16 weeks (before symptoms develop) may also be effective.
Duration: Until birth (some recommend discontinuation at 36 weeks or 5–10 days before birth; aspirin alone is not a contraindication to neuraxial anesthesia).

Other proven/possible interventions: Treatment of chronic hypertension with a target of <140/90 mmHg (CHAP study, 2022—reduced any preeclampsia by RR 0.79); WHO recommended elemental calcium supplementation of 1500–2000 mg per day in populations with low dietary calcium intake. On the contrary; Vitamin C/E, fish oil, and folic acid are ineffective in preventing preeclampsia (UpToDate, “Prevention,” 2026).

Management: Magnesium Sulfate and Acute Antihypertensive Therapy

Five key principles of preeclampsia management: (1) treat severe hypertension, (2) monitor mother and fetus closely, (3) optimize timing of birth, (4) prevent maternal seizure (eclampsia), (5) maintain close postpartum monitoring (UpToDate, "Antepartum management", 2026). Antihypertensive treatment does not stop disease progression but prevents stroke and detachment; Magnesium sulfate prevents seizures.

Magnesium sulfate — seizure prophylaxis

Magnesium sulfate is the preferred anticonvulsant in the setting of preeclampsia/eclampsia. The MAGPIE study (Lancet 2002; PMID 12057549; 10,141 patients in 33 countries) showed a 58% reduced risk of eclampsia (95% CI 40–71%) compared to placebo. In the treatment of eclampsia, it is superior to phenytoin and diazepam and reduces recurrent seizures by half to two-thirds and maternal death by one-third (Cochrane; Eclampsia Trial Collaborative Group, Lancet 1995).

⚠️ Magnesium sulfate dosage:

Loading: 4–6 g IV over 15–20 minutes (UpToDate prefers 6 g; lower limit may delay reaching peak level in obese patients). IM alternative: 5 g into each buttock, 10 g total.
Maintenance: 1–2 g/h continuous IV infusion (if renal function is normal; UpToDate prefers 2 g/h).
Safety monitoring: Maintenance is continued only if patellar reflex is present, breathing is >12/min and urine output is >100 mL/4 hours. In renal failure, the dose is reduced and the magnesium level is monitored (therapeutic range 4.8–8.4 mg/dL).
Antidote: Calcium gluconate 1 g IV (in magnesium toxicity).
Contraindication: Myasthenia gravis.
Duration: 24–48 hours after birth.

Treatment of acute severe hypertension (≥160/110 mmHg)

Confirmed severe hypertension (SBP ≥160 and/or DBP ≥110 mmHg) should be treated as soon as possible—ideally within 30–60 minutes of diagnosis—to prevent stroke (ACOG; UpToDate, "Treatment of hypertension in pregnant and postpartum patients," 2026). ACOG considers labetalol, hydralazine, and immediate-release oral nifedipine similarly safe and effective for first-line therapy. Goal: reduce mean arterial pressure by no more than 25% over 2 hours; target BP 130–150/80–100 mmHg (avoid an aggressive drop <120/80 mmHg to preserve uteroplacental perfusion).

Table 2. First-line antihypertensives for acute severe hypertension (pregnancy/postpartum)
Medicine	Dosing schedule	Onset of effect / notes
Labetalol (IV)	20 mg IV (2 min); if there is no response, 20 → 40 → 80 → 80 → 80 mg every 10 minutes; max. cumulative 300 mg. Alternative: 1–2 mg/min infusion.	5–10 min; effect 3–6 hours. Contraindication: asthma requiring medication, maternal pulse <60/min. It is preferred if the pulse is >110.
Hydralazine (IV)	5 mg IV (1–2 min); If the target is not reached within 20 minutes, 5–10 mg bolus; per treatment max. 20–30mg.	10–30 min; effect 2–4 hours. Max. If the dose or pulse is >100/min, switch to another agent.
Nifedipine (oral, rapid-acting capsule 10 mg)	10 mg PO; If the target is not reached within 20 minutes, 10–20 mg, if necessary, 10–20 mg again after 20 minutes; Then switch to another agent.	~20 min. Particularly useful if IV access is not available; caution due to risk of rapid/excessive decline (UpToDate author limits IR form).
Resistant case	Nicardipine 5 mg/hour IV infusion (max. 15 mg/hour) or esmolol infusion.	Unresponsive to three first-line agents.

Treatment of non-severe hypertension (SBP <160 and DBP <110 mmHg) with antihypertensives in preeclampsia does not change the course of the disease; It is avoided in most patients (except for chronic hypertension). Sodium restriction and diuretics (except for pulmonary edema) have no routine place.

Birth Timing and Antenatal Follow-up

The definitive treatment for preeclampsia is delivery; timing is based on disease severity, maternal-fetal status and gestational age (UpToDate, "Antepartum management", 2026):

Without severe feature

≥37+0 weeks: Delivery is indicated (HYPITAT study: induction reduced composite maternal outcome by 30%, without increasing caesarean section).
34+0–36+6 weeks (late preterm): If the mother and fetus are stable, expectant management is reasonable until the 37th week. PHOENIX study: planned preterm birth reduces maternal composite outcome (RR 0.86) but increases neonatal NICU admission (RR 1.26).
<34+0 weeks: If the mother and fetus are stable and there is no end-organ dysfunction, expectant management with close monitoring for fetal maturation is appropriate.

With severe feature

≥34+0 weeks: Delivery is generally indicated — the risk of maternal complications (stroke, liver rupture, AKI, pulmonary edema, seizure, detachment) is unpredictable and may occur suddenly.
<34+0 weeks: Deliver if there is maternal/fetal instability or the gestational age is below viability. Otherwise, in selected stable cases, expectant management is reasonable in a tertiary center, under the supervision of a maternal-fetal medicine specialist, to allow time for antenatal corticosteroid administration and fetal maturation (UpToDate, "Delaying delivery remote from term").

Antenatal corticosteroid: A course of lung maturation is recommended for patients with a viable fetus and <34+0 weeks preeclampsia (Grade 1A); However, birth should not be delayed just for steroids. Follow-up: In expectant management, platelet + liver/kidney function tests are performed at least twice a week; blood pressure at least twice a day; twice weekly NST + amniotic fluid or biophysical profile; fetal growth ultrasound for diagnosis and repeat every 3–4 weeks if normal. Umbilical artery Doppler reduces perinatal death by 29% in cases of suspected growth restriction (RR 0.71).

HELLP Syndrome and Eclampsia

HELLP syndrome is a laboratory-predominant variant of preeclampsia with severe features: microangiopathic hemolysis (schistocytes/helmet cells on peripheral smear, increased indirect bilirubin/LDH), transaminase elevation and thrombocytopenia. Right upper quadrant pain, nausea/vomiting are common; Be alert for rare but life-threatening hepatic hematoma/rupture. Management is the same as for preeclampsia with severe features (MgSO4 + antihypertensive + delivery).

Eclampsia is a tonic-clonic seizure on the basis of preeclampsia and is an absolute contraindication to expectant management. Management priorities: airway/aspiration protection (left lateral position, O₂ 8–10 L/min), treatment of severe hypertension, termination of prolonged seizure and prevention of recurrent seizure with MgSO4. In active seizures lasting >5 minutes, lorazepam 4 mg IV (max. 2 mg/min) or diazepam 5 mg IV can be given. MgSO4 regime is the same as above (6 g loading + 2 g/h). Post-seizure fetal bradycardia is common and usually transient; Maternal stabilization mostly provides intrauterine recovery. If this does not improve within 10-15 minutes, detachment should be considered. In eclampsia, vaginal delivery (induction) is a reasonable option at ≥32–34 weeks or appropriate Bishop score.

Postpartum Follow-up and Long Term

The disease resolves within days to weeks after birth; however, end-organ dysfunction may worsen in the first 1–3 days. Mobilization of third space fluid and diuresis usually begins within 48 hours. Hypertension worsens in the first (sometimes second) postpartum week and normalizes within 4 weeks in most patients. In ~5% of cases, preeclampsia is first recognized postpartum (usually within 48 hours); Late postpartum preeclampsia (2 days–6 weeks after birth) most commonly presents with headache—these patients are at risk for eclampsia. If MgSO4 is started before birth, it is continued for 24–48 hours. Severe postpartum hypertension is treated according to the same objectives with drugs compatible with breastfeeding (labetalol, nifedipine).

In the long term, a history of preeclampsia increases the risk of recurrence in future pregnancies as well as the lifetime risk of cardiovascular and renal disease; these patients should be followed for cardiovascular risk modification.

Controversial Points and Current Changes

Aspirin dosage (81 mg vs 150 mg): There is no consensus on the optimal dose. In the US, 81 mg is standard; ASPRE has shown striking benefit with 150 mg. A meta-analysis of small studies found 150–162 mg superior to 75–81 mg in preterm preeclampsia (RR 0.34), but a national cohort from Sweden found no difference (aRR 1.07). Multicenter RCTs are ongoing.
Clinical role of sFlt-1:PlGF: Despite its high negative predictive value, randomized trials (PARROT, INSPIRE, PARROT-2) have failed to consistently demonstrate that the test improves perinatal outcome; It has not become routine in most of the United States.
Late preterm (34–37 weeks) timing: In PHOENIX, planned preterm birth provided maternal benefit but increased neonatal NICU admission; The decision should be shared.
Timed delivery in high-risk pregnancies: The PREVENT-PE study showed that risk-based early-term delivery reduces preeclampsia diagnoses but adds uncertainty of maternal/fetal benefit.

Clinical Summary

Preeclampsia = new hypertension (≥140/90) after week 20 + proteinuria or end-organ dysfunction; The severe feature threshold is ≥160/110 and organ criteria.
Pathogenesis: inadequate spiral artery remodeling → sFlt-1/PlGF imbalance → maternal endothelial dysfunction.
Aspirin: in high-risk candidates, 81 mg (US) / 100–150 mg (Europe/ASPRE), starting at ≥12 weeks, ideally <16 weeks, until birth.
MgSO4: 4–6 g IV loading + 1–2 g/h maintenance; antidote calcium gluconate 1 g IV; 24–48 hours after birth.
Acute antihypertensive (≥160/110): Labetalol 20→80 mg IV (max 300 mg), hydralazine 5–10 mg IV (max 20–30 mg), or nifedipine 10 mg PO; Initiate within 30–60 minutes.
Birth: ≥37 weeks in mild preeclampsia/gestHTN; ≥34 weeks in severe cases (earlier if instability is present).

🔄 Current Developments (2026)

ACOG Practice Bulletin 222 (2020) remains the principal practice bulletin in effect through 2026; A comprehensive replacement guide has not been published. However, with the addition of a Clinical Practice Update (blood pressure monitoring and biomarker) in 2024, the bulletin has been layered with updates. The titles that changed or were newly added in the 2024–2026 period are summarized below.

sFlt-1:PlGF — From FDA approval to institutional ACOG guidance

Following the FDA's May 2023 approval, ACOG institutionalized the topic with a formal Clinical Practice Update in June 2024 (Raghuraman et al., Obstet Gynecol 2024). According to the update, the sFlt-1:PlGF ratio is a complementary risk-stratification test added to diagnostic evaluation to predict progression to preeclampsia with severe features within 2 weeks in singleton pregnancies with clinical signs/symptoms hospitalized for a hypertensive disorder at 23+0–34+6 weeks. It does not make a diagnosis on its own. The PRAECIS-based Roche Elecsys threshold of ≥40 indicates impending severe preeclampsia (sensitivity ~94%, specificity ~75%), while ≤38 distinguishes the low-risk group with a high negative predictive value. It should be emphasized that the thresholds are population and assay specific: cut-off points validated in Chinese singleton pregnant women with hypertension (≥74 for gestational age <34 weeks and ≥95 for gestational age ≥34 weeks) were found to be significantly higher than European standards (Pan et al., Ultrasound Obstet Gynecol 2025; DOI 10.1002/uog.70075).

Discontinuing aspirin at 24–28 weeks — a new option

In pregnant women who were found to be high risk by the first trimester screening and were started on 150 mg/day aspirin, discontinuing aspirin at 24–28 weeks when sFlt-1:PlGF is ≤38 was found to be non-inferior to continuing until the 36th week (preterm preeclampsia: discontinuation 1.48% vs continuation 1.73%; absolute difference 0.25%), and minor antepartum bleeding was significantly lower in the discontinuation arm (StopPRE; Mendoza et al., JAMA 2023;329:542-550). Two post-hoc analyzes reinforced the finding: discontinuation was also non-inferior in the PlGF ≥100 pg/mL subgroup (Acta Obstet Gynecol Scand 2024; PMID 39171611) and placental biomarker trajectories did not change when aspirin was stopped (BJOG 2025; PMID 41017450). In practice, early discontinuation of aspirin has become defensible in selected pregnant women with a normal angiogenic profile at 24–28 weeks.

Aspirin dosage and calcium debate

Obesity and aspirin dosage: 162 mg versus 81 mg failed to demonstrate superiority in preeclampsia with severe features in the ASPREO trial (n=220; BMI ≥30 + ≥1 risk factor) (35% vs 40%; posterior RR 0.88; 95% CI 0.64-1.22, not significant)—with call for large multicenter RCT 81 mg remains standard (Amro/Sibai et al., Am J Obstet Gynecol 2024; PMID 38977068).

The landscape of calcium prophylaxis has also shifted: two large RCTs from India and Tanzania showed that low-dose calcium at 500 mg per day was non-inferior to 1500 mg (NEJM 2024; DOI 10.1056/NEJMoa2307212), leading the WHO to consider a low-dose option; Solid evidence syntheses in 2025 also called into question the preeclampsia-preventing benefit of calcium. While aspirin remains the cornerstone of prophylaxis, the role and dose of calcium are being re-evaluated.

Statin and metformin prophylaxis is not yet routinely recommended: pravastatin meta-analysis failed to show significant benefit (RR 0.62; 95% CI 0.33-1.14; trial sequential analysis "insufficient evidence"; AJOG MFM 2024; PMID 38109997). These agents are in the investigational phase, although ongoing large RCTs are expected.

Guidance status: ACOG PB 222 (2020) + June 2024 CPU in effect. RCOG Green-top Guideline No. 10A has been archived and the RCOG refers it to NICE for updated guidance; In the UK the current source is NICE NG133 (with 2019, 2023 and 2025 PlGF updates). ISSHP 2021 and USPSTF 2021 recommendations remain unchanged.

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Preeclampsia and Hypertensive Disorders of Pregnancy