Preeclampsia, HELLP syndrome and eclampsia

• Pre-eclampsia is new high blood pressure after 20 weeks of pregnancy in someone who was previously normotensive, together with proteinuria or another sign of maternal organ or uteroplacental dysfunction. ^[2]
• It is not just a blood pressure problem: it is a disease of the placenta that secondarily affects the mother's vessels, brain, liver, kidneys, blood and the baby's growth.
• HELLP syndrome is a severe form of pre-eclampsia (haemolysis, raised liver enzymes and a low platelet count), not a separate disease.
• Eclampsia is pre-eclampsia with a generalised tonic-clonic seizure and is an obstetric emergency.
• The cure is delivery of the placenta, but timing depends on gestation and severity; before then we control blood pressure, prevent seizures with magnesium sulfate and monitor mother and baby closely.
• Low-dose aspirin, started between 12 and 28 weeks in women at increased risk, is the only drug with strong evidence for preventing the disease. ^[5]

By the end of this page you should be able to:

1. Define and classify pre-eclampsia, eclampsia, HELLP and the other hypertensive disorders of pregnancy.
2. Explain how abnormal placentation leads to the clinical picture of pre-eclampsia.
3. Recognise the history, examination findings, diagnostic cut-offs and severe features, and apply them in a case.
4. Manage acute severe hypertension and eclampsia, including intravenous magnesium sulfate with the correct regimen.
5. Choose the timing of delivery for pre-eclampsia at different gestations and apply NICE, ACOG and WHO guidance.
6. Provide postpartum care for women after pre-eclampsia and counsel them about future risk.

Hypertension in pregnancy is defined by most international guidelines as a systolic blood pressure of 140 mmHg or higher, or a diastolic of 90 mmHg or higher. ^[2] The disorders overlap in blood pressure but differ in timing and in whether there is organ involvement:

• Chronic (pre-existing) hypertension: blood pressure present or first diagnosed before 20 weeks (or not resolved after birth). In a large series of 795,221 pregnancies, women with chronic hypertension had superimposed pre-eclampsia in about 25.9%, caesarean birth in 41.4%, preterm birth under 37 weeks in 28.1%, birth weight under 2,500 g in 16.9%, neonatal unit admission in 20.5% and perinatal death in 4.0%. ^{[2] [1]}
• Gestational hypertension: new hypertension at or after 20 weeks without proteinuria or other organ dysfunction; up to 35% of these women develop pre-eclampsia. ^[2]
• Pre-eclampsia: new hypertension at or after 20 weeks with proteinuria or another maternal or uteroplacental sign.
• Eclampsia: pre-eclampsia with a generalised tonic-clonic seizure.
• HELLP syndrome: a severe form of pre-eclampsia with haemolysis, raised liver enzymes and a low platelet count (see below).
• Superimposed pre-eclampsia on chronic hypertension: chronic hypertension with a sudden rise or new features of pre-eclampsia after 20 weeks.
• White-coat and masked hypertension: differing clinic and out-of-office readings; suspected when fits occur without apparent risk factors.

An important diagnostic clarification is that under NICE (United Kingdom), ISSHP and other international bodies, hypertension with fetal growth restriction or an abnormal umbilical artery Doppler counts as pre-eclampsia even without proteinuria, because uteroplacental dysfunction is treated as an end-organ feature. The American College of Obstetricians and Gynecologists (ACOG) does not count isolated uteroplacental dysfunction as pre-eclampsia, so the same woman may carry a different label in the United States. ^[2]

Globally, hypertensive disorders of pregnancy complicate up to about 10% of pregnancies and are a leading cause of maternal death. ^[2] At least 12% of maternal deaths worldwide are attributed to pre-eclampsia. ^[3] The American College of Obstetricians and Gynecologists estimates that pre-eclampsia complicates 2 to 8% of pregnancies globally, and that 16% of maternal deaths are attributable to hypertensive disorders of pregnancy. ^[4] In Latin America and the Caribbean, hypertensive disorders account for almost 26% of maternal deaths, and in Africa and Asia for 9%. ^[4]

Where data exist, women with pre-eclampsia have a 20% risk of any hypertensive disorder of pregnancy in a future pregnancy, up to a 16% risk of recurrent pre-eclampsia, and a 6 to 12% risk of gestational hypertension. ^[2]

The cause is not fully settled. The dominant view is a two-stage placental disease: poor invasion of the decidua and spiral arteries by trophoblast produces a shallow placental bed; the resulting hypoxic placenta releases factors that injure maternal endothelium. Pre-eclampsia is therefore a disease in which the placenta (and hence the conceptus) is central, which is why delivery cures it.

Risk factors divide into those you are born with or acquire before pregnancy and those of the pregnancy itself:

High risk (NICE NG133 lists these as reasons to offer aspirin): ^[1]

• hypertensive disease in a previous pregnancy
• chronic kidney disease
• autoimmune disease (systemic lupus erythematosus, antiphospholipid syndrome)
• type 1 or type 2 diabetes
• chronic hypertension
• multifetal pregnancy (added in later ACOG guidance) ^[5]

Moderate risk (offer aspirin if more than one): ^[1][5]

• nulliparity
• age 40 years or older (35 years or older in ACOG 2021) ^[5]
• pregnancy interval longer than 10 years
• BMI of 35 kg per m2 or more (ACOG: 30 kg per m2 or more) ^[1][5]
• family history of pre-eclampsia
• Black race or lower income, which ACOG identifies as markers of underlying racism and structural disadvantage, not biological risk ^[5]
• in vitro fertilisation ^[5]
• personal history factors (low birth weight, previous adverse pregnancy outcome) ^[5]

Pre-existing chronic hypertension is one of the most important risk factors for pre-eclampsia, and roughly a quarter of women with chronic hypertension develop superimposed pre-eclampsia. ^[2]

• A normal pregnancy is a low-resistance, high-flow state. Systemic vascular resistance falls, plasma volume and cardiac output rise, and renal blood flow and glomerular filtration increase. Blood pressure normally falls in the first trimester and returns toward baseline by term. ^[2]

In pre-eclampsia, trophoblast invasion of the spiral arteries is inadequate and their muscular walls are retained. Uteroplacental perfusion falls. The stressed placenta releases anti-angiogenic factors, notably soluble fms-like tyrosine kinase-1 (sFlt-1), which neutralise the protective placental growth factor (PlGF). The resulting imbalance produces widespread maternal endothelial dysfunction: vasoconstriction, leaky capillaries, platelet activation and organ ischaemia. ^[2]

As a beginner, it is useful to trace every symptom to one of four mechanisms:

1. Vasoconstriction of resistance vessels produces rising blood pressure and its neurological consequences (headache, scotoma, seizure).
2. Endothelial leak produces oedema, proteinuria and cerebral and pulmonary oedema.
3. Platelet activation and endothelial injury in the liver produce haemolysis, raised transaminases and low platelets (HELLP).
4. Uteroplacental insufficiency produces fetal growth restriction, abnormal Doppler waveforms and an increased risk of stillbirth.

The diagnostic tools map onto these mechanisms: blood pressure for the first, urine protein for the second, platelet count and transaminases for the third, and ultrasound plus Doppler for the fourth.

Pre-eclampsia often presents with no symptoms and is found on routine antenatal blood pressure measurement. When severe, ask about and warn about: ^[1]

• severe headache
• problems with vision (blurring, flashing lights, scotomata)
• severe pain just below the ribs or in the upper abdomen
• vomiting
• sudden swelling of the face, hands or feet, or weight gain over a few days
• breathlessness, chest pain or neurological change
• reduced fetal movement.

Late presentation with one of these is the commonest way serious disease is missed. A woman can have severe disease with a blood pressure of "only" 150 systolic, so symptoms matter as much as numbers. ^[2]

• Blood pressure: seated, arm supported at heart level, appropriate cuff, after rest, validated device; two readings at least four hours apart (or sooner if severe). Automated oscillometric devices may underestimate blood pressure in pregnancy, so auscultatory measurement with sphygmomanometry is preferred. ^[2]
• Oedema: sudden swelling of the face or hands is more worrying than ankle oedema, which is common.
• Reflexes and clonus: hyperreflexia is common and non-specific; sustained clonus is a warning sign.
• Fundoscopy: papilloedema or haemorrhage denotes severe disease.
• Uterus and fetal status: fundal height, fetal movement, lie and heart rate, looking for growth restriction.
• Respiration and liver area tenderness: right upper quadrant or epigastric tenderness is a severe feature.

Pre-eclampsia must be separated from conditions that look like it and from other hypertensive disorders of pregnancy.

The following table collects the tests the NICE, ACOG and review sources above use in the workup of pre-eclampsia, with their thresholds.

HELLP is a severe form of pre-eclampsia in which the placental factors produce a thrombotic microangiopathy centred on the liver: Haemolysis (from mechanical red-cell damage in small vessels), Elevated Liver enzymes (sinusoidal obstruction) and Low Platelets (consumption). It is not a separate disease, so it is managed as severe pre-eclampsia. ^[2]

Clinically the woman may have right upper quadrant or epigastric pain, nausea and vomiting, and sometimes bleeding tendencies from liver haematoma or rupture (rare but lethal). Notably, about 30% of HELLP cases begin or progress after birth, so the postpartum review must be as careful as the antepartum one. ^[2]

Management points from the NICE and summarised guidelines: ^[1][3]

• Do not use dexamethasone or betamethasone to treat HELLP syndrome. Corticosteroids are still offered if early birth before 37 weeks is planned, for fetal lung maturity, in line with the NICE guideline on preterm labour and birth. ^[1]
• Suspected liver haematoma or rupture (sudden pain, shock, falling haematocrit) needs urgent imaging and surgical review.
• Platelet transfusion before delivery or other procedures is guided by local protocol and the clinical situation. ^[1]

Eclampsia is a pre-eclamptic woman (antepartum, intrapartum or up to several weeks postpartum) who has a generalised tonic-clonic seizure that cannot be attributed to another cause. Seizures occur most often in late pregnancy and the early puerperium, and eclampsia may be the first presentation of disease. ^[2]

Immediate management: ^[1]

1. Turn the woman onto her left side, clear the airway, give oxygen.
2. Give intravenous magnesium sulfate (regimen below).
3. Control severe hypertension with intravenous labetalol, oral (or immediate-release) nifedipine or intravenous hydralazine.
4. Arrange delivery once the mother is stabilised: eclampsia at term or persisting despite treatment is an indication for birth.
5. Magnesium sulfate is the anticonvulsant of choice: diazepam, phenytoin and other anticonvulsant drugs should not replace it. ^[1]

A blood pressure of 160 systolic or 110 diastolic mmHg or higher, confirmed on two occasions at least four hours apart (or persistent), is severe hypertension and needs urgent same-day assessment. ^[2] Severe features of pre-eclampsia include: ^[1][2]

• inability to control blood pressure despite three or more classes of antihypertensive in appropriate doses ^[1]
• maternal oxygen saturation under 90% ^[1]
• progressive deterioration in liver, renal, haemolysis or platelet parameters
• ongoing neurological features (severe intractable headache, repeated visual scotomata, eclampsia)
• placental abruption
• reversed end-diastolic flow in the umbilical artery, a non-reassuring cardiotocograph, or stillbirth.

Severe or eclamptic women need critical care admission. NICE's criteria suggest level 2 (high-dependency or step-down) or level 3 (intensive) care according to ventilation need, organ support and complications such as eclampsia, HELLP syndrome, haemorrhage, severe oliguria or abnormal neurology. ^[1]

• Position, monitoring: high-dependency unit with blood pressure measured every 15 to 30 minutes until it is under 160 systolic and 110 diastolic, then at least four times a day as an inpatient; urine output; reflexes and clonus; daily weights or fluid balance. ^[1]
• Severe hypertension: treat immediately with one of labetalol (oral or intravenous), oral nifedipine or intravenous hydralazine. ^[1]
• Crystalloid: consider up to 500 mL before or with the first intravenous hydralazine dose; otherwise do not use volume expansion unless hydralazine is the antihypertensive, and limit maintenance fluids to 80 mL per hour in severe pre-eclampsia, unless there is ongoing haemorrhage. ^[1]
• Steroids: offer antenatal corticosteroids when early birth before 37 weeks is likely within 7 days, including magnesium sulfate, in line with the NICE guideline on preterm labour and birth. ^[1]
• Decision-making: involve a senior obstetrician in timing-of-birth decisions; discuss with the anaesthetic and neonatal teams. ^[1]

NICE recommends labetalol first line for chronic and gestational hypertension and for pre-eclampsia, with nifedipine when labetalol does not suit the woman and methyldopa as the third option, choosing on the basis of pre-existing treatment, side effects, fetal effects and the woman's preference. ^[1] Review sources summarise the same agents: first-line oral drugs for non-severe hypertension are nifedipine, labetalol and methyldopa; second-line or alternatives include hydralazine, clonidine, and (with limited evidence) amlodipine, prazosin, doxazosin or beta-blockers other than atenolol. ^{[2] [3]}

Drugs that must be avoided in pregnancy: ^[2]

• ACE inhibitors and angiotensin receptor blockers are strictly contraindicated because of fetal renal damage and death.
• Thiazide and thiazide-like diuretics are generally avoided (may worsen volume and are not recommended in pre-eclampsia).
• Atenolol and some beta-blockers are associated with fetal growth restriction and should be avoided, particularly in early pregnancy.

Graduated targets for non-severe hypertension: keep blood pressure at 135 over 85 mmHg or less under NICE; the International Society for the Study of Hypertension in Pregnancy (ISSHP) uses a diastolic of 85 mmHg regardless of systolic. Under ACOG, non-severe disease in the United States is managed with a systolic target of 120 to 140 and a diastolic of 80 to 110 mmHg. ^[1][2] For severe hypertension, blood pressure should be brought below 160 over 110, and preferably to 130 to 150 over 80 to 100 for severe episodes in monitored settings. ^[3]

For the acute severe episode, use in critical care: ^[1]

• hydralazine: intravenous, for severe hypertension when indicated
• labetalol: intravenous or oral, for severe hypertension when indicated
• nifedipine: oral, for severe hypertension when indicated

These acute dosing figures from formulary tables should always be checked against your local formulary and the product information before prescribing. ^[1]

Magnesium sulfate is the anticonvulsant of choice both to prevent fits in severe pre-eclampsia and to treat eclampsia. It is recommended by NICE, ACOG, WHO and all major guidelines as first-line treatment of eclampsia and prophylaxis in women with pre-eclampsia and severe hypertension or other adverse features. ^[1][3][6]

NICE specifies the Collaborative Eclampsia Trial regimen: ^[1]

• loading dose of 4 g intravenously over 5 to 15 minutes
• infusion of 1 g per hour maintained for 24 hours
• if a fit has occurred, continue the infusion for 24 hours after the last fit ^[1]
• recurrent fits: a further 2 to 4 g intravenously over 5 to 15 minutes.

Monitor for toxicity: respiratory rate, oxygen saturation, tendon reflexes, urine output and serum magnesium where available. Magnesium sulfate should be withheld if urine output falls markedly or reflexes disappear. ^[1]

This is the central decision in pre-eclampsia, balancing maternal safety against gestation.

NICE timing table: ^[1]

• Before 34 weeks: keep monitoring and plan early birth only for a specific indication; if early birth is planned, offer magnesium sulfate and antenatal corticosteroids.
• From 34 weeks to 36 weeks plus 6 days: keep monitoring unless an indication arises; take into account maternal and fetal condition, comorbidities, multifetal pregnancy and neonatal unit capacity, and consider corticosteroids. ^[1]
• From 37 weeks: initiate birth within 24 to 48 hours.

Indications for planned early birth before 37 weeks (NICE): inability to control blood pressure despite three or more drug classes, maternal oxygen saturation under 90%, progressive deterioration in liver, renal, haemolysis or platelet parameters, ongoing neurological features, placental abruption, reversed end-diastolic flow in the umbilical artery, non-reassuring cardiotocograph, or stillbirth. ^[1]

For chronic or gestational hypertension without severe features, NICE advises not to bring birth forward before 37 weeks (below 160 over 110) and to agree timing with a senior obstetrician from 37 weeks, generally not before term unless other indications arise. ^[1]

The NICE guideline on preterm labour and birth governs corticosteroids, and the 2022 CHAP trial supported treating chronic hypertension to 140 over 90 mmHg instead of waiting for severe hypertension. ^[2]

Blood pressure often rises again in the first week after birth and pre-eclampsia can worsen, or appear for the first time, postpartum. ^[2][3]

NICE postpartum schedule for pre-eclampsia: ^[1]

• blood pressure at least four times a day while an inpatient; then every 1 to 2 days for up to 2 weeks once she is at home, if she has been on treatment.
• at every blood pressure check, ask whether she has had a severe headache or epigastric pain.
• if she did not take antihypertensives, measure at least four times a day as an inpatient, at least once between days 3 and 5, and on alternate days until normal.
• start antihypertensives when blood pressure is persistently elevated after birth.
• platelet count, transaminases and creatinine at 48 to 72 hours after birth or step-down; repeat if abnormal.
• urinary dipstick at 6 to 8 weeks; if proteinuria persists (1+ or more), review at 3 months and consider a kidney assessment. ^[1]
• transfer to community care only when there are no symptoms, blood pressure (with or without treatment) is controlled, and blood tests are stable or improving. ^[1]
• continue methyldopa is stopped within 2 days of birth and switched to an alternative if it was used.
• reduce treatment once pressure falls under 140 over 90 and under 130 over 80; review at 2 weeks if still treated, and offer a medical review at 6 to 8 weeks for all.

NICE also advises that women who took magnesium sulfate should have the neonatal team consider magnesium monitoring if treatment was prolonged or repeated, because prolonged or repeated exposure has been associated with neonatal skeletal and calcium-magnesium abnormalities. ^[1]

Beyond blood pressure, the International Society for the Study of Hypertension in Pregnancy recommends treating women with pre-eclampsia as high risk for at least 3 days postpartum, with blood pressure and clinical status assessed at least every 4 hours while awake in the early postpartum period, and continuing antenatal antihypertensives, tapering them over several days rather than stopping abruptly. Women should be reviewed within a week if still medicated and all should be seen at 3 months. ^{[2] [1]}

Up to 8% of women without antepartum hypertension develop postpartum hypertension, and up to 50% of those who had pre-eclampsia are hypertensive 6 to 12 weeks after birth. Thirty percent of HELLP cases begin or progress after birth, and eclamptic seizures may occur for the first time in the early puerperium. ^[2]

Breastfeeding: the drugs used in pregnancy are generally compatible with breastfeeding; enalapril, captopril and related ACE inhibitors are introduced postpartum (with very low milk concentrations), while methyldopa is usually withdrawn because of depression risk. Diuretics can reduce milk supply. ^{[2] [3]}

• Central nervous system: severe headache, cortical blindness, stroke, eclampsia. Cerebral autoregulation fails and women may bleed at relatively low pressures. ^[2]
• Cardiovascular: severe hypertension, pulmonary oedema (a leading cause of maternal death with pre-eclampsia), myocardial dysfunction.
• Renal: acute kidney injury, proteinuria that may persist.
• Hepatic: raised transaminases, subcapsular haematoma and rupture (rare), HELLP.
• Haematological: thrombocytopenia, disseminated intravascular coagulation.
• Placental and fetal: placental abruption, fetal growth restriction, oligohydramnios, stillbirth. About 35% of women with gestational hypertension develop pre-eclampsia. ^[2]
• Postpartum: stroke from postpartum hypertension, postpartum eclampsia, HELLP beginning or worsening after delivery.
• Long term: a two to four fold increase in cardiovascular disease, including hypertension, ischaemic heart disease, stroke and chronic kidney disease. In one meta-analysis of over 198,000 women with previous pre-eclampsia, relative risks were 3.70 for hypertension (14.1 years of follow-up), 2.16 for ischaemic heart disease (11.7 years), 1.81 for stroke (10.4 years) and 1.79 for venous thromboembolism (4.7 years). ^[2]

Mild pre-eclampsia at term, treated with timely birth, has an excellent maternal prognosis. Outcomes worsen with earlier onset, higher pressures and lower platelets. In chronic hypertension cohorts, about 28% deliver preterm and 4% have a perinatal death; in pre-eclampsia the perinatal risk includes growth restriction and stillbirth, which monitoring is designed to detect. ^[2]

Beyond pregnancy, all women who have had pre-eclampsia should receive lifelong cardiovascular counselling: annual review of blood pressure, lipids and glucose, weight optimisation, exercise and no smoking, with a blood pressure goal under 120 over 80 mmHg. ^[2][3]

• First-trimester risk assessment using maternal risk factors, blood pressure and, where available, placental growth factor and uterine artery Doppler. ^[2][3]
• Low-dose aspirin is the only preventive drug with strong evidence. NICE advises 75 to 150 mg daily from 12 weeks until birth for women at high risk or with more than one moderate risk factor. ^[1] ACOG and the Society for Maternal-Fetal Medicine recommend 81 mg daily, initiated between 12 and 28 weeks (optimally before 16 weeks) and continued daily until delivery. ^[5] WHO and updated guidance follow the same risk-based approach. ^[6]
• Calcium supplementation reduces hypertensive disorders where intake is low; use the dose recommended by your guideline or the WHO update for your setting. ^[6]
• Exercise (moderate intensity 150 minutes a week) cuts gestational hypertension and pre-eclampsia risk by roughly 30 to 40%. ^[2]
• Weight: in obese women (BMI over 30 kg per m2) weight gain of 5 to 9 kg is advised. ^[3]
• Do not use for prevention: salt restriction alone, strict bed rest, diuretics, antioxidants, fish oils, garlic, magnesium, folic acid alone or nitric oxide donors. ^[1][3]
• PlGF-based testing helps rule out pre-eclampsia when suspected. ^[1]

• Pregnancy: all of the above. This page is the pregnancy-specific management.
• Children (fetal/neonatal): pre-eclampsia is a leading cause of iatrogenic preterm birth; magnesium sulfate exposure of a prolonged or repeated course carries risks to neonatal calcium and bone metabolism and should be limited. ^[1]
• Older women and those with chronic disease: treat thresholds may be lower and nephrology, cardiology or rheumatology input added; high-risk women benefit from aspirin and preconception optimisation. ^[1][2]
• Postpartum women: see above.
• Women planning another pregnancy: offer preconception review, optimise blood pressure, counsel on recurrence (up to 16% pre-eclampsia, and 6 to 12% gestational hypertension) and lifelong cardiovascular risk. ^[2]

• One written protocol. Low- and middle-income settings often use 150 over 100 mmHg to start treatment and to define severe disease, while high-income guidelines use 160 over 110. Adopt one protocol and audit it; mixing them causes harm. ^{[2] [1]}
• Oral and inexpensive drugs work: labetalol, nifedipine, methyldopa and hydralazine given orally can control acute severe hypertension, but stocks and cold chains must be secured. ^{[2] [1]}
• Magnesium sulfate is the priority seizure drug. NICE's intravenous loading regimen (4 g over 5 to 15 minutes, then 1 g per hour for 24 hours, with 2 to 4 g intravenously for recurrent fits) is preferred where infusion pumps are available; where staffing permits intramuscular protocols (as in WHO practice), they are life-saving. ^[1][6]
• Basic surveillance is better than none: blood pressure technique, an appropriate cuff, symphysis-fundal height, fetal movement awareness and handheld Doppler, with ultrasound where available. ^[2]
• Postpartum vigilance matters most where monitoring is limited: counsel all women to return urgently for severe headache, visual change, epigastric pain, vomiting or sudden swelling in the six weeks after birth. ^[1][2]
• Send any delivered placenta or liver sample for histopathology if available, and arrange follow-up of hypertension.

• Pre-eclampsia is pre-existing normotension turned hypertension after 20 weeks, with proteinuria or other maternal or uteroplacental dysfunction. ^[2]
• HELLP syndrome is a severe form of the same disease, with haemolysis, raised liver enzymes and low platelets. ^[2]
• Eclampsia is a generalised tonic-clonic seizure in pre-eclampsia; it may be the first sign. ^[2]
• The primary disease process is failed placental vascular remodelling, producing an imbalance of angiogenic factors and maternal endothelial dysfunction. ^[2]
• Hypertensive disorders of pregnancy complicate up to 10% of pregnancies, and pre-eclampsia complicates 2 to 8% of pregnancies globally. ^[2][4]
• At least 12% of maternal deaths worldwide are due to pre-eclampsia. ^[3]
• Optimally, treat non-severe hypertension to under 135 over 85 mmHg with labetalol first line, avoiding ACE inhibitors, angiotensin receptor blockers and thiazides. ^[1][2]
• Magnesium sulfate is the anticonvulsant of choice (4 g intravenous loading dose over 5 to 15 minutes, then 1 g per hour for 24 hours; 2 to 4 g intravenously for recurrent fits). ^[1]
• Severe hypertension (at least 160 over 110) and severe features require same-day critical care. ^[1][2]
• Birth is the cure: at or beyond 37 weeks initiate within 24 to 48 hours; before that, follow NICE indications and gestation bands. ^[1]
• Postpartum surveillance matters: rising blood pressure, eclampsia and HELLP can begin or worsen after birth; up to half of women who had pre-eclampsia are hypertensive at 6 to 12 weeks. ^[2]
• Prevention is low-dose aspirin (75 to 150 mg, NICE; 81 mg, ACOG) started between 12 and 28 weeks, optimally before 16, and continued to delivery, for women at increased risk. ^[1][5]
• Long-term cardiovascular risk rises two to four fold after pre-eclampsia; offer annual follow-up and lifestyle advice. ^[2][3]

Plain-text related MedGrasp topics: gestational and chronic hypertension in pregnancy; hypertensive disorders of pregnancy; pregnancy diagnosis and physiology; obstetric exam and fetal heart rate monitoring; adult hypertension; stroke in pregnancy; low back pain in pregnancy.