Clinical overview
The hypertensive disorders of pregnancy are, alongside obstetric haemorrhage and non-pregnancy-related infection, one of the leading direct causes of maternal death in South Africa, recurring triennium after triennium in the Saving Mothers (NCCEMD) reports. The tragedy of the SA picture is that most hypertensive deaths are judged avoidable — the recurring lessons are failure to measure blood pressure properly, failure to recognise severity, delay in giving magnesium sulphate and antihypertensives, delay in delivery, and inappropriate transfer of unstable women. A registrar must therefore treat hypertension in pregnancy not as a benign antenatal label but as a condition that kills mothers and babies through stroke, eclampsia, pulmonary oedema, abruption, HELLP, acute kidney injury and iatrogenic prematurity.
This chapter covers the classification and management of all forms of pregnancy hypertension — chronic hypertension, gestational (pregnancy-induced) hypertension, pre-eclampsia, and chronic hypertension with superimposed pre-eclampsia — and the drills for the two emergencies they generate: severe hypertension and eclampsia. The pathophysiology and detailed management of pre-eclampsia and HELLP are developed further in pre-eclampsia-and-hellp; the intrauterine growth restriction that frequently accompanies placental hypertensive disease is covered in intrauterine-growth-restriction; and resuscitation of the collapsed or convulsing mother in resuscitation-in-pregnancy.
Core knowledge
Definitions and classification
Hypertension in pregnancy is defined as a systolic blood pressure ≥140 mmHg and/or diastolic ≥90 mmHg, confirmed on repeat measurement, using a correctly sized cuff with the woman seated and the arm supported at heart level. The standard classification (aligned across NICE NG133 and the SA Maternity Guideline) is:
- Chronic hypertension — present before pregnancy or before 20 weeks' gestation, or persisting beyond 6 weeks postpartum. May be essential or secondary (renal, endocrine, coarctation).
- Gestational hypertension — new hypertension arising after 20 weeks without proteinuria or other features of pre-eclampsia. A proportion progress to pre-eclampsia, so it is not a benign endpoint.
- Pre-eclampsia — new hypertension after 20 weeks with proteinuria or other maternal organ dysfunction (renal, hepatic, neurological, haematological) or uteroplacental dysfunction (fetal growth restriction). Note the contemporary definition no longer requires proteinuria if other organ involvement is present.
- Chronic hypertension with superimposed pre-eclampsia — the highest-risk group; suspected when a woman with chronic hypertension develops new/worsening proteinuria, a sudden rise in BP needing escalation of treatment, or new organ dysfunction.
Severe hypertension is a sustained systolic ≥160 mmHg and/or diastolic ≥110 mmHg — the threshold above which the risk of maternal stroke rises sharply and which mandates urgent treatment regardless of the underlying category. This is the single most important number on the page.
Figure J19.1 — Classification, severe BP threshold and major complications of hypertension in pregnancy.
Pathophysiology in brief
Pre-eclampsia is a disorder of abnormal placentation: failure of trophoblast to fully remodel the spiral arteries leaves them high-resistance, producing placental ischaemia and the release of anti-angiogenic factors (notably soluble fms-like tyrosine kinase-1, sFlt-1) that antagonise placental growth factor (PlGF) and vascular endothelial growth factor. The result is a systemic maternal endothelial dysfunction causing vasoconstriction (hypertension), increased capillary permeability (oedema, proteinuria, pulmonary oedema), a procoagulant state and end-organ ischaemia. This explains why the only definitive cure is delivery of the placenta, and why disease can still worsen for 24–48 hours postpartum. The mechanistic detail is expanded in pre-eclampsia-and-hellp.
Figure J19.2 — Placenta-driven endothelial dysfunction explains the multisystem complications of pre-eclampsia.
Why it matters: the complications
- Maternal: eclampsia (seizures), intracerebral haemorrhage/stroke (the commonest mode of hypertensive death — usually from uncontrolled systolic pressure), HELLP syndrome, pulmonary oedema, acute kidney injury, hepatic rupture, DIC, and placental abruption.
- Fetal/neonatal: fetal growth restriction, oligohydramnios, hypoxia, abruption, iatrogenic prematurity and its sequelae, and stillbirth.
Assessment
History and risk stratification
At booking, identify women at high risk of pre-eclampsia: previous pre-eclampsia (especially early or severe), chronic hypertension, chronic kidney disease, diabetes (type 1 or 2), and autoimmune disease (SLE, antiphospholipid syndrome). Moderate-risk factors include first pregnancy, age ≥40, BMI ≥35, pregnancy interval >10 years, family history of pre-eclampsia, and multiple pregnancy. Risk factors drive aspirin prophylaxis (below) and the schedule of antenatal surveillance — see antenatal-booking and high-risk-pregnancy-risks.
Symptoms of severe/imminent disease must be actively sought at every contact: severe headache, visual disturbance (flashing lights, blurring), epigastric or right-upper-quadrant pain, vomiting, and rapid swelling of face/hands. Reduced fetal movements warrant assessment (see decreased-fetal-movements).
Examination
- Blood pressure — correct technique, correct cuff, Korotkoff V for diastolic. Repeat to confirm. An automated oscillometric device may under-read in pre-eclampsia; verify with a validated device.
- Proteinuria — urine dipstick is a screen; quantify with a spot urine protein:creatinine ratio (PCR ≥30 mg/mmol is significant) or 24-hour collection where available. Dipstick alone over-/under-calls and must not be the sole arbiter.
- General — hyperreflexia and clonus (neurological irritability), epigastric tenderness, basal crepitations (pulmonary oedema), oedema, fundal height (growth restriction).
Investigations
In suspected pre-eclampsia, baseline and serial bloods are essential: full blood count (platelets — thrombocytopenia, haemoconcentration or haemolysis), urea, creatinine and electrolytes (renal impairment), liver enzymes (ALT/AST — transaminitis points to HELLP), and where indicated LDH and a peripheral smear for haemolysis, plus coagulation if platelets are low or abruption suspected. Fetal assessment — symphysis-fundal height, ultrasound for estimated fetal weight and liquor, and umbilical artery Doppler to assess placental function (see intrauterine-growth-restriction and placental-insufficiency-response). Where available, a low PlGF-based test / sFlt-1:PlGF ratio has a strong negative predictive value to rule out pre-eclampsia in the short term (NICE DG49); it is not yet routine in most SA public settings.
Management
Management has four pillars: control the blood pressure, prevent and treat seizures with magnesium sulphate, monitor mother and fetus, and time delivery — the only cure. The level of care matters: a woman with severe disease must be stabilised before transfer and managed at a facility able to deliver her and care for a preterm neonate. Do not transfer an unstable, uncontrolled or convulsing woman without first giving magnesium and an antihypertensive.
Prevention
For women at high or multiple-moderate risk, give low-dose aspirin (NICE NG133 advises 75–150 mg daily from 12 weeks until delivery); the SA Maternity Guideline recommends low-dose aspirin for at-risk women. Calcium supplementation is recommended in populations with low dietary calcium intake — relevant to much of South Africa — and is endorsed for reducing pre-eclampsia risk.
Chronic and gestational hypertension (non-severe)
Aim for a target around ≤135/85 mmHg (NICE NG133). First-line oral agents are labetalol, nifedipine (modified-release), and methyldopa; these are the EML-available agents in SA. ACE inhibitors, ARBs and direct renin inhibitors are contraindicated in pregnancy (fetal renal toxicity, oligohydramnios) and must be switched pre-conceptually or as soon as pregnancy is recognised. Women with chronic hypertension need aspirin, closer surveillance for superimposed pre-eclampsia, and serial growth scans. Gestational hypertension is monitored for progression with regular BP, proteinuria checks and bloods.
Treatment of SEVERE hypertension — an emergency
DRILL — sustained BP ≥160/110 mmHg is a hypertensive emergency. Treat urgently to prevent maternal stroke. Do NOT wait for proteinuria, bloods or transfer.
- Oral nifedipine (immediate-release, swallowed — not sublingual), OR IV labetalol, OR IV hydralazine are the standard first-line agents (NICE NG133; SA Maternity Guideline). Use the agent and protocol stocked at your facility and repeat at the protocol interval until target is reached.
- Target: lower BP in a controlled way to roughly 140–150 / 90–100 mmHg — avoid precipitous drops that compromise placental perfusion.
- Give magnesium sulphate in severe pre-eclampsia/eclampsia (below) — antihypertensives prevent stroke, magnesium prevents seizures; they are complementary, not alternatives.
- Avoid fluid overload — restrict maintenance fluids (commonly ~80 mL/h total) because these women are prone to pulmonary oedema; do not "run fluids" to chase oliguria.
- Insert a urinary catheter, monitor input/output, repeat BP frequently, and escalate to a doctor able to plan delivery.
Magnesium sulphate — seizure prophylaxis and treatment
DRILL — Magnesium sulphate is the drug of choice to prevent and treat eclamptic seizures (MAGPIE trial; NICE NG133; SA Maternity Guideline). It is on the SA EML and must be immediately available wherever pre-eclampsia is managed.
- Indications: eclampsia (treatment), and severe pre-eclampsia (prophylaxis), and consideration in women with signs of imminent eclampsia.
- Regimen (standard teaching, per protocol): a loading dose followed by a maintenance infusion, continued for 24 hours after delivery or after the last seizure, whichever is later. Use your facility's exact protocol doses — verify the milligram/gram figures against the current SA Maternity Guideline or EML before administering; do not give from memory.
- Monitoring for toxicity: hourly respiratory rate, deep tendon reflexes (loss of patellar reflex is an early warning), and urine output (magnesium is renally cleared — reduce/withhold in oliguria/renal impairment).
- Antidote: calcium gluconate must be drawn up and available at the bedside for magnesium toxicity (respiratory depression).
Eclampsia — the convulsing mother
DRILL — ECLAMPSIA: this is an obstetric emergency. Call for help.
- Airway, Breathing, Circulation — left lateral position, protect the airway, high-flow oxygen, secure IV access.
- Magnesium sulphate — loading dose, then maintenance infusion (per protocol); treat recurrent seizures with a further magnesium bolus per protocol.
- Control the blood pressure if severe — labetalol/hydralazine/nifedipine.
- Stabilise the mother first, then deliver — eclampsia is not in itself an indication for immediate caesarean; the mother must be stabilised (seizure controlled, BP controlled) before delivery is undertaken.
- Restrict fluids, catheterise, monitor, and arrange delivery at an appropriate level of care.
Management of the acutely collapsed or persistently convulsing woman, including the place of advanced airway support, is detailed in resuscitation-in-pregnancy.
Figure J19.3 — Emergency drill for severe hypertension, magnesium sulphate safety and eclampsia stabilisation.
Timing and mode of delivery
Delivery is the only cure. In pre-eclampsia at term, delivery is generally advised. In gestational hypertension, delivery is usually planned from around term. Below 34–37 weeks, the decision balances maternal stability against prematurity, ideally with antenatal corticosteroids for fetal lung maturation when preterm delivery is anticipated (see preterm-birth-and-pprom) and, where indicated, magnesium sulphate for fetal neuroprotection in very preterm delivery. Severe, uncontrollable disease, eclampsia, HELLP, deteriorating organ function, abruption or a non-reassuring fetal status mandate delivery irrespective of gestation once the mother is stabilised. Mode of delivery depends on gestation, fetal condition, cervix and urgency — vaginal birth is not contraindicated, but severe early disease with an unfavourable cervix often ends in caesarean. Beware regional anaesthesia in thrombocytopenia (HELLP) — check the platelet count.
Postpartum
Disease can worsen in the first 24–48 hours postpartum — continue magnesium for 24 hours, continue BP monitoring and antihypertensives, watch for pulmonary oedema, and avoid NSAIDs in women with hypertension, renal impairment or poor urine output. Provide effective contraception (see postpartum-contraception) and counsel on the recurrence risk and lifelong cardiovascular risk associated with a history of pre-eclampsia, with arrangements for postnatal BP review and de-escalation of treatment.
Red flags / pitfalls
- Treating the diastolic and ignoring the systolic. Maternal stroke is driven by uncontrolled systolic pressure; a systolic ≥160 mmHg is an emergency in its own right.
- Sublingual nifedipine — never; immediate-release capsules are swallowed. Sublingual administration causes precipitous, uncontrolled drops.
- Giving fluids to "treat" oliguria. These women are intravascularly constricted but leak into the lungs — fluid loading causes pulmonary oedema, a recurring avoidable cause of death. Restrict fluids.
- Relying on dipstick proteinuria to confirm or exclude pre-eclampsia, or waiting for proteinuria before treating severe hypertension. Quantify with PCR; treat severe BP immediately.
- Forgetting that magnesium and antihypertensives do different jobs — magnesium prevents seizures, antihypertensives prevent stroke. Severe pre-eclampsia needs both.
- Transferring an unstable woman. Stabilise first — magnesium, BP control — then transfer with an escort and a clear handover.
- Stopping monitoring after delivery. The most dangerous window can be postpartum; eclampsia occurs postnatally too.
- Missing superimposed pre-eclampsia in a woman already labelled "chronic hypertension" — a new rise in BP, new proteinuria or new symptoms is the warning.
- Continuing ACE inhibitors/ARBs into pregnancy — switch immediately to a pregnancy-safe agent.
- No calcium gluconate at the bedside when magnesium is running.
Evidence anchors
- South African National Integrated Maternal and Perinatal Care Guideline (NDoH, 2024) — the SA source of truth for thresholds, EML antihypertensives (labetalol, nifedipine, methyldopa), magnesium sulphate protocol, and level-of-care/referral pathways.
- Saving Mothers / NCCEMD (latest triennium) — hypertensive disorders among the leading direct causes of maternal death in SA; recurring avoidable factors (BP measurement, recognition of severity, magnesium/antihypertensive delay, delivery delay, inappropriate transfer).
- NICE NG133 — Hypertension in Pregnancy: Diagnosis and Management (2019) — classification, BP targets (~≤135/85), low-dose aspirin 75–150 mg from 12 weeks for at-risk women, choice of antihypertensives, severe-hypertension treatment, magnesium sulphate, and timing of birth.
- NICE DG49 — PlGF-based testing (sFlt-1:PlGF ratio) to help rule out pre-eclampsia.
- MAGPIE trial — magnesium sulphate more than halves the risk of eclampsia in women with pre-eclampsia; basis for magnesium as the drug of choice.
- South African EML — Hospital Level (Adults) — confirms the locally available antihypertensive and magnesium sulphate formulations; verify exact doses against the current EML/Maternity Guideline before administration.
Author's note on hedged facts: the specific magnesium sulphate loading/maintenance doses and the nifedipine/labetalol/hydralazine dosing intervals are deliberately written as "per protocol" and not quoted as numbers — these must be read directly from the current SA Maternity Guideline / EML at the point of care, as exact figures were not line-itemed in the verified-sources reference.