Pre-Eclampsia — Symptoms, Causes & Treatment | MyMedicPlus

Pre-eclampsia is a multisystem hypertensive disorder of pregnancy defined as new-onset hypertension (blood pressure at or above 140/90 mmHg on two occasions at least 4 hours apart) after 20 weeks of gestation, accompanied by significant proteinuria (protein-to-creatinine ratio above 30 mg/mmol) or evidence of end-organ damage — renal (rising creatinine, oliguria), hepatic (elevated transaminases or severe right upper quadrant pain), neurological (eclamptic seizures, severe headache, or persistent visual disturbances), haematological (thrombocytopaenia below 150,000, haemolysis), or feto-placental (intrauterine growth restriction or abnormal umbilical artery Doppler). Pre-eclampsia affects 5-8% of all pregnancies globally and is a leading cause of maternal and perinatal mortality, responsible for approximately 70,000 maternal deaths and 500,000 perinatal deaths per year worldwide — disproportionately affecting women in low- and middle-income countries where monitoring and access to magnesium sulphate are limited. There are two distinct clinical subtypes: early-onset pre-eclampsia (before 34 weeks, more severe, associated with pronounced placental dysfunction and higher maternal-fetal morbidity) and late-onset pre-eclampsia (after 34 weeks, more common but with lower maternal morbidity). The pathophysiological origin lies in abnormal early placentation — failure of trophoblast invasion causing placental ischaemia — which leads to systemic endothelial dysfunction through release of anti-angiogenic factors (sFlt-1, soluble endoglin) into the maternal circulation, causing hypertension, proteinuria, and multi-organ involvement. Delivery of the placenta is the only definitive cure; all other treatment is supportive and aimed at preventing stroke and eclampsia while prolonging pregnancy to an acceptable gestational age.

Pre-eclampsia originates from impaired first-trimester placentation ('two-stage model'): in stage one (clinically silent, before 20 weeks), inadequate cytotrophoblast invasion of the maternal spiral arteries fails to convert them from narrow, muscular, vasoconstricted vessels into the wide, dilated, low-resistance conduits needed for adequate placental perfusion — this causes chronic placental ischaemia and hypoxia. In stage two (clinical disease, after 20 weeks), the ischaemic placenta releases excessive anti-angiogenic factors into the maternal circulation: soluble Fms-like tyrosine kinase-1 (sFlt-1 — binds and inactivates VEGF and PlGF, depleting circulating pro-angiogenic factors), and soluble endoglin — producing widespread maternal endothelial dysfunction. Endothelial injury drives hypertension (vasospasm and loss of vascular smooth muscle relaxation), proteinuria (glomerular endotheliosis — capillary endothelial swelling obstructing filtration), and multi-organ ischaemia underlying HELLP and eclampsia. Risk factors: nulliparity (2x risk — parous women have greater immunological tolerance to paternal antigens); prior pre-eclampsia (the strongest risk factor — 7x increased risk overall, rising to 25-65% recurrence for early-onset or severe disease); multiple pregnancy (twin or higher-order gestation — 3x risk from greater placental mass and ischaemic stimulus); chronic hypertension (5x risk); chronic kidney disease; type 1 or 2 diabetes mellitus; antiphospholipid syndrome (15-30% pre-eclampsia rate — all women with APS should receive aspirin from 12 weeks); obesity (BMI above 30 — dose-dependent increased risk from adipose-derived inflammation and insulin resistance); maternal age above 40; interpregnancy interval above 10 years; and family history in mother or sister.

Hypertension (blood pressure at or above 140/90 mmHg on two separate occasions at least 4 hours apart after 20 weeks of gestation) — women with pre-eclampsia are often entirely asymptomatic with elevated blood pressure, making regular antenatal blood pressure measurement at every visit the most important diagnostic intervention. Proteinuria (PCR above 30 mg/mmol, 24-hour urine protein above 300 mg, or automated validated dipstick 2+) — indicates glomerular endothelial damage from pre-eclampsia. Warning symptoms of severe or deteriorating pre-eclampsia, all warranting immediate obstetric assessment: severe frontal or occipital headache not relieved by paracetamol (from cerebral vasospasm and raised intracranial pressure — the most common premonitory symptom before an eclamptic fit); visual disturbances (flashing lights, photopsia, blurring of vision, or visual field loss — from retinal vasospasm and occipital cortical oedema); epigastric or right upper quadrant pain and tenderness (hepatic capsule distension from subcapsular haematoma or hepatic ischaemia — the dominant symptom of HELLP syndrome in 90% of cases); sudden, severe, or rapidly worsening swelling of the face, hands, or periorbital area; nausea and vomiting associated with other severe features (not isolated morning sickness); and reduced fetal movements (from uteroplacental insufficiency). Eclampsia: generalised tonic-clonic seizures in a woman with pre-eclampsia or within 24 hours of delivery — a life-threatening obstetric emergency requiring immediate IV magnesium sulphate (4 g loading dose), airway protection, and urgent delivery. HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets): right upper quadrant pain, malaise, nausea, vomiting, and rapidly rising liver transaminases combined with thrombocytopaenia — a severe pre-eclampsia variant requiring emergency delivery regardless of gestational age.

Blood pressure measurement using validated equipment (korotkoff phase V for diastolic). Urinalysis and spot urine PCR (protein:creatinine ratio) for proteinuria confirmation. FBC (thrombocytopenia in HELLP), liver function tests (elevated transaminases in HELLP), renal function (rising creatinine), LDH and blood film (hemolysis in HELLP). Fetal monitoring: CTG, Doppler ultrasound (umbilical artery, middle cerebral artery for fetal compromise). PlGF (placental growth factor) biomarker testing: low PlGF (below 100pg/mL after 20 weeks) is highly predictive of pre-eclampsia requiring delivery within 14 days. sFlt-1:PlGF ratio guides risk stratification. A systematic diagnostic approach that carefully combines a thorough clinical history, detailed physical examination findings, and appropriately targeted laboratory and imaging investigations is essential to accurately distinguish this condition from closely mimicking disorders and to guide safe and effective treatment selection. Early specialist referral — particularly when the diagnosis is uncertain or when initial treatments fail — optimises diagnostic accuracy and reduces unnecessary delays to effective management.

Antihypertensive therapy is used to control severe hypertension and prevent stroke — it does not treat the underlying disease. First-line antihypertensives in pregnancy: labetalol (oral or IV — preferred; 200mg oral or 50mg IV bolus), nifedipine (calcium channel blocker, oral modified-release), methyldopa (first-line in some guidelines). Target BP 135/85 mmHg. Magnesium sulfate is the standard treatment for eclampsia prevention and eclampsia management: 4g IV loading dose followed by 1g/hour infusion for 24 hours. Monitor for toxicity (reduced reflexes, respiratory rate). Aspirin 150mg nocte from 12-16 weeks until 36 weeks reduces pre-eclampsia incidence by 10-20% in high-risk women. Delivery is the only cure: for term pre-eclampsia (over 37 weeks), deliver promptly. Below 37 weeks, balance risks of prematurity against severity — NICE advises delivery at 34 weeks or below if severe, after steroids for fetal lung maturity.

Eclampsia (seizures): maternal mortality 2%, fetal mortality up to 9% — prevented by magnesium sulfate. HELLP syndrome: intravascular hemolysis, hepatic failure, DIC, placental abruption, and subcapsular liver haematoma (risk of rupture). Abruption: placenta separates prematurely causing fetal compromise and maternal haemorrhage. Fetal growth restriction and prematurity from placental insufficiency. Long-term maternal risk: women with pre-eclampsia have 4x lifetime risk of hypertension, 2x risk of cardiovascular disease, and 2x risk of stroke — cardiovascular risk reduction counseling should be given at postnatal follow-up.

Low-dose aspirin (150mg nightly from 12-16 weeks until 36 weeks) is recommended for all women with one major risk factor or two or more moderate risk factors for pre-eclampsia — reduces risk by 10-20%. Combined first-trimester screening (maternal factors, uterine artery Doppler, mean arterial pressure, PlGF at 11-14 weeks) identifies high-risk women most likely to benefit from aspirin prophylaxis. Calcium supplementation (1.5-2g/day) reduces pre-eclampsia incidence in women with low dietary calcium intake (mainly in low-income countries). Regular blood pressure monitoring throughout pregnancy enables early detection.

Attend all antenatal appointments — blood pressure measurement and urine dipstick testing at every appointment are how pre-eclampsia is detected early, often before symptoms develop. Contact your midwife or maternity unit immediately (the same day) for: a blood pressure reading at home of 140/90 mmHg or above at any point from 20 weeks; sudden severe facial, hand, or foot swelling (oedema); and persistent headache not relieved by paracetamol. Call 999 or go directly to the maternity emergency unit for: severe headache with visual disturbances (flashing lights, blurring, scotomata); upper abdominal or epigastric pain; a seizure or convulsion during pregnancy or within 4 weeks of delivery (eclampsia — a life-threatening emergency); or any sudden severe deterioration. Seek postnatal follow-up for: blood pressure check at 6-8 weeks postnatally (pre-eclampsia resolves after delivery but hypertension can persist); and cardiovascular risk counselling — women who have had pre-eclampsia have a 4x lifetime risk of hypertension and 2x risk of stroke and cardiovascular disease.