Preeclampsia

Jan 25, 2020
14 min read

Updated: Nov 7

Preeclampsia remains a leading cause of maternal and neonatal morbidity worldwide, marked by hypertension, endothelial injury, and progressive organ dysfunction. Though advances in prenatal surveillance and antihypertensive therapy have improved outcomes, the condition’s unpredictable onset continues to challenge clinicians. Current research focuses on early biomarkers, placental pathology, and preventive strategies such as low-dose aspirin, aiming to reduce preventable deaths and long-term cardiovascular complications in mothers who survive the disorder.

Overview

What is preeclampsia?

Preeclampsia is a hypertensive disorder of pregnancy that emerges after 20 weeks of gestation, characterized by elevated blood pressure (≥140/90 mmHg) and proteinuria (≥300 mg/24 hours) or signs of organ dysfunction. It represents one of the leading causes of maternal and perinatal morbidity and mortality worldwide and is unique to pregnancy, resolving only after delivery of the placenta.

In preeclampsia, the body’s vascular system—particularly the endothelium—undergoes widespread dysfunction. This process restricts blood flow to vital organs, including the kidneys, liver, brain, and placenta, producing a cascade of inflammation, oxidative stress, and coagulation abnormalities. The result is a disease that can appear deceptively mild at onset but progress rapidly to eclampsia (seizures), HELLP syndrome, pulmonary edema, stroke, or multi-organ failure.

In the United States, preeclampsia complicates 5–8% of pregnancies, accounting for roughly 15% of all preterm births and contributing to 10–20% of maternal deaths annually. Globally, the condition is estimated to kill over 70,000 women and 500,000 infants every year, figures that underscore its public-health urgency.

Real-World Outcomes

Is preeclampsia a medical emergency?

Preeclampsia is a medical emergency and one of the most dangerous hypertensive disorders of pregnancy. Once blood pressure reaches or exceeds 140/90 mmHg, or 160/110 mmHg in severe presentations, endothelial injury has already begun. The vascular system becomes destabilized, triggering a cascade of microclot formation, capillary leakage, and organ ischemia that can escalate within hours.

As the condition progresses, uteroplacental blood flow declines, restricting oxygen and nutrient delivery to the fetus. The placenta, deprived of adequate perfusion, may shear away from the uterine wall—a complication known as placental abruption, which endangers both maternal and fetal survival. The same process that starves the fetus begins to damage the mother’s liver and kidneys, evident through elevated liver enzymes, proteinuria, and edematous swelling. Left untreated, this endothelial crisis evolves into HELLP syndrome or eclampsia, characterized by hemolysis, hepatic rupture, cerebral hemorrhage, and seizure.

Globally, preeclampsia and related hypertensive disorders account for 10–15% of maternal deaths, claiming over 70,000 women and 500,000 infants each year, according to the World Health Organization. However, these numbers represent only a rough outline of the truth. In today’s medical environment, obtaining a formal diagnosis is increasingly difficult, as systemic bias, inadequate screening, and diagnostic hesitancy obscure the real scope of disease. Many women are dismissed or sent home without essential testing—told their swelling, headaches, or shortness of breath are “normal” parts of pregnancy—until their condition progresses to organ failure or seizure.

The reality is that global preeclampsia statistics underestimate both prevalence and mortality. Without consistent diagnostic criteria, mandatory reporting, or standardized postpartum surveillance, tens of thousands of cases remain uncounted every year. Effective treatment depends entirely on early detection and decisive intervention, including initiating antihypertensives, administering magnesium sulfate to prevent seizures, and, when necessary, expedited delivery to save both lives. Every hour of delay increases the likelihood of irreversible damage.

Symptoms

What are the most common symptoms associated with preclampsia?

Preeclampsia often develops silently, detected only during routine prenatal screening. For many women, the first indication is an elevated blood pressure reading or the detection of protein on urinalysis. However, others experience subtle warning signs that should never be dismissed.

Common early symptoms include:

Persistent or severe headaches unrelieved by hydration or rest.
Blurred vision, light sensitivity, or seeing dark spots (scotomata).
Rapid weight gain or swelling in the hands, face, and ankles from fluid retention.
Right upper-quadrant or epigastric pain due to hepatic congestion.
Shortness of breath or chest heaviness from early pulmonary fluid accumulation.

Because these signs can mimic normal pregnancy changes, clinical vigilance is critical. Even mild edema or fatigue may precede dangerous rises in blood pressure.

Severe preeclampsia involves end-organ dysfunction and requires urgent management.

Diagnostic indicators include:

Severe hypertension (≥160/110 mmHg)
Oliguria (marked reduction in urine output)
Thrombocytopenia (platelet count <100,000/mm³)
Elevated serum creatinine or transaminases
Pulmonary edema or cerebral symptoms such as confusion or visual disturbance

Patients meeting these criteria are typically hospitalized for continuous monitoring, with magnesium sulfate administered for seizure prevention and antihypertensive therapy to lower pressure without compromising uteroplacental flow. Delivery, often by induction or cesarean, is the definitive treatment, as symptoms generally resolve within days of placental removal.

Pathophysiology

What cellular mechanisms drive the development of preeclampsia?

At the cellular level, preeclampsia is rooted in defective placentation. In normal pregnancy, trophoblasts remodel uterine arteries to ensure high-volume, low-resistance blood flow. In preeclampsia, this remodeling fails, leading to placental ischemia and the release of antiangiogenic factors (such as sFlt-1 and endoglin) that damage maternal endothelium. The result is vasoconstriction, leaky capillaries, and coagulation activation, all hallmarks of systemic vascular injury.

This dysfunction extends beyond pregnancy. Women with a history of preeclampsia face twice the lifetime risk of heart failure, ischemic heart disease, and stroke, highlighting that preeclampsia is not only an obstetric complication but also a cardiovascular red flag for future health.

Causes

What causes preeclampsia?

The exact cause of preeclampsia remains complex and multifactorial, but research converges on one central mechanism: abnormal placentation leading to systemic endothelial dysfunction. During early pregnancy, the placenta normally remodels the maternal spiral arteries to create low-resistance channels for high-volume blood flow. In preeclampsia, this remodeling is incomplete or shallow.

The resulting placental hypoxia triggers the release of antiangiogenic and inflammatory mediators—notably soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng)—which enter the maternal circulation and disrupt vascular signaling. These molecules neutralize proangiogenic factors such as VEGF and PlGF, leading to widespread vasoconstriction, capillary leak, and microthrombus formation.

This is not a simple blood pressure disorder, but a vascular injury syndrome affecting nearly every organ system. The placenta becomes both the source and the casualty of this dysfunction, often resulting in growth restriction, hypoxia, and premature delivery.

Psychosocial Determinants of Health

Does stress contribute to preeclampsia?

Psychological stress alone does not directly cause preeclampsia, but chronic stress can exacerbate hypertensive and inflammatory pathways that worsen endothelial injury. Elevated cortisol and catecholamines influence vascular tone, platelet aggregation, and immune balance, all of which intersect with the biology of preeclampsia. While stress reduction cannot prevent the condition, stress regulation and social support improve overall maternal cardiovascular stability and may reduce disease severity.

Risk Factors

Who is most at risk for preeclampsia?

While preeclampsia can strike without warning, clinicians have identified well-established risk categories based on epidemiologic and genetic data.

High-risk factors include:

Chronic hypertension, kidney disease, or diabetes mellitus
Autoimmune conditions such as lupus or antiphospholipid syndrome (APS)
History of preeclampsia or HELLP syndrome in a prior pregnancy is associated with a recurrence risk of 15–25%
Multiple gestation, including twins, triplets, or higher order
Use of assisted reproductive technologies increases placental implantation abnormalities

Moderate-risk factors include:

First pregnancy (nulliparity)
Maternal age over 35
Obesity (BMI ≥30)
Family history of preeclampsia (mother or sister affected)
History of fetal growth restriction or low-birth-weight infant

The American College of Obstetricians and Gynecologists (ACOG) recommends low-dose aspirin (81 mg daily) beginning between 12–16 weeks’ gestation for anyone with one high-risk or two moderate-risk factors.

Foundations

When is preeclampsia most likely to present itself during pregnancy?

Preeclampsia most often develops after 20 weeks of gestation, typically during the third trimester (after 27 weeks). Early-onset preeclampsia, diagnosed before 34 weeks, accounts for about 10–20% of cases and carries the highest risk of severe complications for both mother and fetus.

Postpartum preeclampsia can emerge within 48 hours to 7 days after delivery, sometimes later, and is equally dangerous. Many cases are missed because symptoms mimic normal postpartum recovery. Persistent headache, visual changes, or swelling after childbirth always warrant evaluation.

Complications

What are the most common complications associated with preeclampsia?

Untreated preeclampsia is life-threatening. It can progress rapidly to eclampsia (seizures), cerebral hemorrhage, liver rupture, or multi-organ failure. Severe endothelial injury leads to HELLP syndrome—hemolysis, elevated liver enzymes, and low platelet count—which occurs in roughly 10–20% of severe preeclampsia cases.

Maternal complications include:

Stroke or intracerebral hemorrhage due to severe hypertension
Pulmonary edema and respiratory compromise
Renal insufficiency or acute kidney failure
Placental abruption (premature detachment of the placenta)
Disseminated intravascular coagulation (DIC) and postpartum hemorrhage

Fetal complications include:

Premature birth accounts for 15% of all preterm deliveries in the U.S
Low birth weight and intrauterine growth restriction (IUGR) due to poor placental perfusion
Stillbirth or neonatal death in severe, untreated cases

Long-Term Health Risks

Are there long-term health risks associated with a preeclampsia diagnosis?

The effects of preeclampsia reach far beyond pregnancy. Decades of research confirm that it is not an isolated obstetric event but a systemic vascular disorder — one that reveals underlying endothelial fragility and future cardiovascular risk. Women who experience preeclampsia face a two to fourfold increase in long-term morbidity from chronic hypertension, ischemic heart disease, stroke, and kidney disease. This risk persists even when blood pressure normalizes postpartum, signaling the need for lifelong follow-up and prevention.

Survivors of preeclampsia have an elevated risk of developing the following conditions:

Chronic Hypertension

Up to half of women with a history of preeclampsia develop sustained high blood pressure within 5 to 10 years of delivery. The endothelial injury and vascular remodeling that occur during preeclampsia can permanently alter arterial elasticity and resistance, predisposing to chronic hypertension. Early-onset preeclampsia confers the greatest risk, highlighting the importance of routine blood pressure monitoring beginning as early as the postpartum period.

Ischemic Heart Disease

Preeclampsia increases the lifetime risk of ischemic heart disease by approximately twofold. The same inflammatory and prothrombotic mechanisms that drive placental dysfunction — including endothelial activation, oxidative stress, and microvascular thrombosis — later contribute to coronary artery disease. Women with this history are more likely to develop atherosclerotic plaque at a younger age, often decades before traditional risk factors appear.

Heart Failure

Studies show that women with prior preeclampsia have a fourfold increased risk of heart failure, even in the absence of coronary obstruction. This form, known as diastolic or heart failure with preserved ejection fraction (HFpEF), is thought to arise from microvascular injury and chronic hypertension sustained during pregnancy. The risk is particularly high in women with recurrent or severe disease, making early cardiac imaging and echocardiographic surveillance advisable.

Stroke

Preeclampsia roughly doubles the risk of both ischemic and hemorrhagic stroke. The vascular endothelial dysfunction, heightened coagulation, and arterial stiffness that characterize the disorder persist long after delivery, increasing cerebrovascular vulnerability. Women under 45 with prior preeclampsia are disproportionately represented in stroke registries — an alarming signal that this condition accelerates vascular aging.

Chronic Kidney Disease (CKD)

Preeclampsia causes glomerular endotheliosis and microangiopathy, which can evolve into chronic kidney disease (CKD) or even end-stage renal disease (ESRD). Longitudinal data show that up to 30% of women exhibit reduced glomerular filtration rates within 15 years of diagnosis. Annual renal function tests, including serum creatinine and urine albumin-to-creatinine ratios, are recommended for early detection.

Recurrent Preeclampsia in Future Pregnancies

The risk of recurrence ranges from 15% to 65%, depending on disease severity and gestational onset during the prior pregnancy. Early-onset or severe preeclampsia predicts higher recurrence rates, particularly when underlying conditions such as chronic hypertension, diabetes, or thrombophilia are present. Preconception counseling and early prenatal surveillance with a maternal-fetal medicine specialist are strongly recommended.

Long-term management should extend beyond routine postpartum care. Regular assessment of blood pressure, lipid profiles, renal function, glucose metabolism, and vascular inflammation can help identify early warning signs. According to the American Heart Association (2024), preeclampsia should be viewed as a sentinel cardiovascular event — one that, when recognized early, offers a unique opportunity for prevention of future heart disease, kidney failure, and stroke.

Diagnosis

How is preclampsia diagnosed?

Preeclampsia is typically identified during routine prenatal surveillance, often before the patient feels unwell. Diagnosis relies on objective clinical and laboratory criteria rather than symptoms alone, as many women remain asymptomatic until late in the disease process.

At each prenatal visit, healthcare providers monitor blood pressure, weight gain, and urine protein levels. When preeclampsia is suspected, diagnostic evaluation expands to include laboratory and imaging studies to confirm organ involvement and assess fetal well-being.

Key diagnostic assessments include:

Blood pressure monitoring: Sustained readings ≥140/90 mmHg on two occasions at least four hours apart.
Proteinuria: ≥300 mg per 24-hour urine collection or a protein-to-creatinine ratio ≥0.3.
Renal and hepatic function tests: Elevated serum creatinine (>1.1 mg/dL) or liver transaminases (AST/ALT) ≥2× the upper limit of normal indicate systemic involvement.
Platelet count: <100,000/mm³ signals thrombocytopenia and risk for HELLP syndrome.
Ultrasound and fetal assessment: Evaluation of fetal growth, placental perfusion (via Doppler flow studies), and amniotic fluid volume to identify intrauterine growth restriction (IUGR).

Preeclampsia is classified as mild or severe based on the degree of hypertension and organ dysfunction:

Classification	Key Diagnostic Features
Mild Preeclampsia	BP ≥140/90 mmHg, proteinuria ≥300 mg/24 hr, no systemic symptoms
Severe Preeclampsia	BP ≥160/110 mmHg and/or evidence of end-organ injury (elevated creatinine or liver enzymes, pulmonary edema, visual disturbances, or headache unresponsive to medication)

Severe preeclampsia constitutes a medical emergency. Patients with neurologic symptoms (headache, vision changes), pulmonary edema, or abnormal labs require immediate hospital admission for continuous monitoring, as progression to eclampsia or multi-organ failure can occur within hours.

Management and Treatment

How is preeclampsia treated?

There is no curative therapy for preeclampsia other than delivery of the placenta. Management focuses on balancing maternal stabilization with fetal maturity, prolonging pregnancy safely when possible without compromising maternal health. Treatment strategies depend on disease severity and gestational age.

For pregnancies ≥37 weeks (term)

For pregnancies <34–36 weeks (preterm)

Women with severe preeclampsia are managed in tertiary centers with access to intensive care, neonatology, and blood products. Magnesium sulfate remains the gold standard for seizure prophylaxis, and studies show it reduces eclampsia risk by 50–60% compared with placebo or diazepam.

Long-Term Management

How is preeclampsia managed long-term and after delivery?

While preeclampsia usually resolves after delivery, hypertension and laboratory abnormalities may persist for days or weeks. Close postpartum monitoring is crucial, as postpartum preeclampsia—including new-onset seizures—can develop up to two weeks after birth.

Women with a history of preeclampsia should undergo:

Follow-up blood pressure checks within 3–10 days and again at 6 weeks postpartum.
Renal and hepatic function re-evaluation, if previously abnormal.
Long-term cardiovascular screening is necessary for these women, who face 2–4× higher lifetime risk of hypertension, ischemic heart disease, and stroke.

Preventive counseling—including lifestyle modification, weight management, and aspirin prophylaxis in future pregnancies—is essential to lower recurrence risk.

Frequently Asked Questions (FAQ)

Frequently Asked Questions

Can I deliver naturally with preeclampsia?

Yes, vaginal delivery remains possible and is often preferred when maternal and fetal conditions are stable. The decision depends on disease severity, gestational age, cervical readiness, and fetal tolerance to labor. When blood pressure is controlled and no immediate complications exist, induction can safely lead to vaginal birth. However, if there are signs of maternal instability—such as severe hypertension, HELLP syndrome, or nonreassuring fetal heart patterns—cesarean delivery may be the safest course. Continuous monitoring and access to rapid intervention are essential in either case.

Will my baby survive preclampsia?

Does preeclampsia resolve after delivery?

Women require close postpartum monitoring for persistent hypertension, renal dysfunction, or neurologic symptoms. Some may temporarily need antihypertensive medications such as labetalol or nifedipine. The condition usually resolves fully, but its occurrence is a strong predictor of future cardiovascular disease and warrants lifelong blood pressure surveillance.

Prevention

What can I do to reduce my risk of developing preeclampsia?

Preeclampsia prevention focuses on modifying known risk factors, optimizing vascular health before conception, and identifying early endothelial dysfunction during pregnancy. For women with established or emerging risk factors, the following interventions are supported by robust clinical evidence:

Low-Dose Aspirin Therapy

Initiating low-dose aspirin therapy (81 mg daily) between 12–16 weeks of gestation reduces the incidence of preeclampsia by 10–24% in high-risk populations, according to large-scale meta-analyses from the U.S. Preventive Services Task Force and the World Health Organization.

Weight Management Before Conception

Maintaining or achieving a BMI within the healthy range (18.5–24.9) lowers the risk of endothelial inflammation and oxidative stress—key precursors to preeclampsia.

Control of Chronic Conditions

Tight regulation of preexisting hypertension, renal disease, insulin resistance, or autoimmune disorders decreases placental stress and improves perfusion.

Nutrient-Dense, Low-Sodium Diet

Emphasis on whole grains, lean proteins, leafy vegetables, and foods rich in calcium, magnesium, and omega-3 fatty acids supports endothelial integrity and modulates vascular tone

Moderate Physical Activity

At least 150 minutes per week of low- to moderate-intensity activity (such as walking or prenatal yoga) has been shown to improve vascular elasticity and reduce blood pressure variability.

Sleep and Stress Regulation

Consistent 7–9 hours of nightly sleep and the use of stress-reduction techniques such as mindfulness or breathing therapy can mitigate sympathetic overactivation, a key driver of hypertension in pregnancy.

While no single intervention can eliminate the risk entirely, low-dose aspirin prophylaxis combined with vigilant prenatal monitoring and early blood pressure screening remains the most effective preventive strategy. The evidence is unequivocal: timely recognition and proactive management can prevent many of the most catastrophic outcomes of preeclampsia.

Seeking Care

When should patients contact their provider or seek urgent medical care?

Every case of preeclampsia demands strict follow-up. Women diagnosed during pregnancy should never miss prenatal or postpartum appointments, as disease progression can be unpredictable.

Seek immediate emergency care (call 911 in the U.S.) if you experience:

Seizures, convulsions, or sudden unresponsiveness (possible eclampsia)
Shortness of breath or chest pressure
Severe right-sided abdominal pain or shoulder pain
Blurry vision, persistent headache, or flashing lights in vision

Even after delivery, postpartum preeclampsia can emerge suddenly within 48 hours to several weeks, often misinterpreted as normal postpartum fatigue. Any new neurological or respiratory symptom requires urgent evaluation.

Patient-Provider Communication

What questions should you ask your doctor about your diagnosis and care plan?

Effective care begins with informed conversations. In complex conditions like preeclampsia, the difference between early intervention and critical deterioration often lies in what questions are asked and how directly they’re answered. Patients who understand their risk profile, treatment plan, and warning signs are far more likely to receive timely care and avoid preventable complications. The following questions are designed to help patients advocate for themselves and ensure that their healthcare team addresses every aspect of risk management.

Open, informed dialogue with your care team is essential for safety, trust, and shared decision-making. Questions to discuss include:

What is my target blood pressure, and how will it be monitored?

Your outpatient target is generally below 140/90 mmHg. Severe hypertension is 160 systolic or 110 diastolic or higher and requires treatment within 30 to 60 minutes.

Home Monitoring: Use an upper-arm automated cuff validated for pregnancy. Measure twice daily, morning and evening, seated for five minutes, arm at heart level. Record two readings one minute apart and use the average.
Clinic Monitoring: At every visit, with repeat measurements if the first is elevated.
Action Thresholds: If home readings are 160/110 or higher on two checks 15 minutes apart, seek urgent care. If persistent readings are 150s/100s with symptoms, call the on-call clinician the same day.

Do I need medication, activity changes, or hospitalization at this stage?

How often will my labs and fetal growth be checked?

Which warning signs require immediate evaluation?

How will this affect future pregnancies and long-term health?

Asking precise, evidence-based questions transforms the clinical relationship from reactive to preventative. Preeclampsia is not a condition that can afford passive management. Every woman deserves full transparency about her care plan, her risks, and her right to rapid medical attention when warning signs emerge.

Clinical Clarifications

Why is preeclampsia so misunderstood?

Preeclampsia and its related hypertensive disorders remain among the most misunderstood and mismanaged conditions in obstetric medicine. Despite clear diagnostic criteria and decades of research, early signs are often minimized, delayed in recognition, or dismissed as “normal pregnancy symptoms.” When left unchecked, these conditions can escalate rapidly into multi-organ failure, seizures, and maternal death. The following clinical clarifications outline the core distinctions, presentations, and critical timeframes for detection and intervention.

Early Signs of Preeclampsia

The earliest indicators of preeclampsia often emerge subtly but require immediate attention. Elevated blood pressure (≥140/90 mmHg), proteinuria (≥300 mg/24 hours), and rapid-onset edema—particularly of the face, hands, or ankles—are the cardinal warning signs. Patients may also experience persistent headaches, visual disturbances, or upper right quadrant pain, which reflect early vascular and hepatic involvement. Timely recognition and laboratory confirmation are critical, as preeclampsia can progress rapidly even in previously healthy women.

Difference Between Preeclampsia and Eclampsia

Eclampsia represents the most severe and life-threatening progression of preeclampsia, defined by the onset of generalized seizures or coma in the absence of other neurologic disease. Pathophysiologically, eclampsia results from cerebral edema, vasospasm, and endothelial dysfunction leading to loss of cerebral autoregulation and intracranial hypertension. It can occur without preceding hypertension or proteinuria, underscoring the need for vigilance in all symptomatic pregnant and postpartum women. Despite modern interventions, eclampsia remains responsible for 10–15% of maternal deaths worldwide.

Postpartum Preeclampsia

Postpartum preeclampsia develops after childbirth, most commonly between 2 and 7 days postpartum, though cases have been documented up to six weeks after delivery. It carries the same risk profile as antepartum disease—stroke, pulmonary edema, seizure, renal failure, and hepatic rupture—and is frequently missed because patients are no longer under continuous obstetric surveillance. Women presenting with headache, blurred vision, swelling, or chest pain after delivery should have immediate blood pressure and urine evaluation. Delayed recognition remains a leading cause of preventable maternal readmission and mortality in the United States and globally.

Preeclampsia, eclampsia, and postpartum preeclampsia are predictable, identifiable vascular disorders that demand immediate clinical action. Every case begins with a missed opportunity: a symptom uninvestigated, a pressure unrecorded, a mother sent home too soon. Recognizing these early signs and applying consistent diagnostic vigilance are not acts of caution, but acts of prevention that save lives.

The International Women’s Blood Clot Advocates (IWBCA) provides the information and materials on this site for educational and informational purposes only. The content is not a substitute for professional medical evaluation, diagnosis, or treatment. Always consult your physician or another qualified healthcare provider regarding any questions you may have about a medical condition, diagnosis, or course of treatment. Do not disregard, delay, or alter medical advice based on information obtained from this site. If you believe you are experiencing a medical emergency, call 911 or your local emergency services immediately.