Hypertensive disorders of pregnancy: pre-eclampsia, eclampsia and HELLP

Overview

Hypertensive disorders complicate many pregnancies and are among the top killers of mothers in poorer countries, including Pakistan. Pre-eclampsia complicates about 2-3% of pregnancies and kills tens of thousands of women worldwide each year, mostly from stroke. It also causes fetal growth restriction, abruption and preterm birth.

Classification

Degrees of hypertension

Pre-eclampsia

Definition

Blood pressure of 140/90 mmHg or more, on two occasions at least 4 hours apart, arising after 20 weeks in a previously normotensive woman, with proteinuria of 300 mg or more in 24 hours, and resolving by 6 weeks after delivery. Newer guidelines also accept maternal organ dysfunction (kidney, liver, platelets, neurological) or placental dysfunction in place of proteinuria. Oedema is not part of the definition: ankle oedema is common in normal pregnancy, but rapid swelling of the face and hands is suspicious.

Risk factors

• First pregnancy (and a first pregnancy with a new partner).
• Pre-eclampsia in a previous pregnancy.
• 10 years or more since the last baby.
• Age 40 or over.
• BMI 35 or more.
• Family history (mother or sister).
• Multiple pregnancy.
• Booking diastolic BP 80 mmHg or more; booking proteinuria.
• Medical: chronic hypertension, renal disease, pre-existing diabetes, antiphospholipid syndrome.
• Molar pregnancy (pre-eclampsia before 20 weeks).

Pathophysiology: a two-stage disease

1. Placental stage (early pregnancy): normally, trophoblast invades the spiral arteries and turns them into wide, low-resistance channels. In pre-eclampsia this invasion is patchy and shallow; the arteries keep their muscle walls, and the placenta becomes ischaemic.
2. Maternal stage: the ischaemic placenta releases factors that cause oxidative stress, inflammation and widespread endothelial dysfunction, leading to vasospasm, leaky vessels and activation of clotting.

Because the endothelium is everywhere, pre-eclampsia is a multisystem disorder. It needs trophoblast, not a fetus: it occurs in molar pregnancy and in abdominal pregnancy.

Organ effects

Clinical features

• Most women have no symptoms; pre-eclampsia is found at routine BP and urine checks.
• Symptoms of severe disease: frontal headache, visual disturbance (flashing lights), epigastric pain, nausea and vomiting, sudden swelling.
• Signs: hypertension, proteinuria, epigastric tenderness (liver involvement), brisk reflexes and clonus, papilloedema (rare).

Investigations

• Urine: dipstick, then quantify proteinuria (24-hour collection or protein:creatinine ratio).
• FBC: falling platelets, rising haematocrit.
• Renal function including uric acid; liver function (ALT, AST, LDH).
• Clotting studies if platelets are low.
• Fetus: ultrasound for growth, liquor and umbilical artery Doppler; CTG.

Management

There is no cure except delivery of the baby and placenta. Management keeps the mother safe while the baby gains maturity.

1. Where to manage: mild hypertension with minimal protein and normal bloods may be followed closely as an outpatient; women with higher BP, heavy proteinuria or abnormal blood results are admitted.

2. Control blood pressure (to prevent cerebral haemorrhage, the commonest cause of death):

Avoid: ACE inhibitors and angiotensin receptor blockers (fetal kidney damage), and atenolol (FGR); stop them before or as soon as pregnancy is confirmed.

3. Prevent and treat fits: magnesium sulphate

• Drug of choice for eclampsia and for prevention of fits in severe pre-eclampsia.
• Regimen (Ten Teachers): 4 g IV loading dose, then 1 g per hour infusion, usually continued for 24 hours after delivery (or after the last fit).
• Narrow therapeutic range: toxicity causes loss of tendon reflexes, respiratory depression and cardiac arrest. Monitor reflexes, respiratory rate and urine output (magnesium is excreted by the kidney).
• Antidote: 10 ml of 10% calcium gluconate IV, given slowly.
• Magnesium works better than diazepam or phenytoin for eclampsia.

4. Timing of delivery

• Severe or worsening disease, eclampsia, HELLP, abruption, fetal compromise: deliver once the mother is stabilised, whatever the gestation.
• Before 34 weeks: give IM corticosteroids to the mother if time allows; transfer to a centre with neonatal care.
• Mode: induction if feasible; caesarean often needed when preterm or severe.
• Epidural is useful in labour (helps BP control) if clotting is normal.
• Avoid ergometrine (and Syntometrine) in the third stage; use oxytocin.
• Give thromboprophylaxis (heparin and stockings).

5. After delivery

• Fits and severe hypertension can still occur in the first days postpartum; BP often rises again around days 3-4.
• Continue antihypertensives and wean gradually; switch to breastfeeding-safe drugs.
• Hypertension or proteinuria persisting beyond 6 weeks suggests chronic hypertension or renal disease.
• Counsel about recurrence and later cardiovascular risk.

Prevention

• Low-dose aspirin (75 mg daily) from early pregnancy (about 12 weeks) in high-risk women modestly lowers the risk.
• Calcium supplements help women with low dietary calcium.
• Uterine artery Doppler (a "notch" and high resistance) can flag high-risk women but is not useful as a screen in low-risk women.
• Placental growth factor (PlGF) is low in pre-eclampsia and is being used to help diagnosis.

HELLP syndrome

• Haemolysis, Elevated Liver enzymes, Low Platelets.
• Occurs in about 2-4% of women with pre-eclampsia; fetal loss can reach 60%.
• Presents with epigastric or right upper quadrant pain, nausea and vomiting; BP may be only mildly raised or even normal.
• Complications: DIC, acute kidney injury, liver haematoma or rupture, abruption, stillbirth, stroke.
• Management: stabilise, correct clotting, magnesium sulphate, control BP and deliver.

Eclampsia

• One or more generalised tonic-clonic fits (or coma) in a woman with pre-eclampsia when no other cause is found.
• Can occur before, during or after delivery; fits may come with little warning, and not all women have severe hypertension beforehand.
• Warning signs: severe headache, visual disturbance, epigastric pain, hyperreflexia and clonus, uncontrolled BP, falling urine output.
• Risk factors: uncontrolled hypertension, few antenatal visits, first pregnancy, age under 20, obesity, diabetes.

Management of an eclamptic fit

1. Call for help; protect the airway, place her in the left lateral position, give oxygen.
2. Magnesium sulphate loading dose then infusion (repeat bolus for a recurrent fit per local protocol).
3. Control BP (labetalol or hydralazine IV).
4. Monitor fluids carefully (risk of pulmonary oedema) and urine output.
5. Deliver once the mother is stable; the fit itself is not an indication for immediate caesarean.

Chronic hypertension in pregnancy

• About 90% is essential; exclude secondary causes (renal disease is the commonest secondary cause, then endocrine causes such as phaeochromocytoma, Conn's and Cushing's syndromes, and coarctation).
• Risks: superimposed pre-eclampsia (about one third), abruption, FGR, heart failure, stroke.
• Treat if BP stays above 150/100 mmHg; target systolic below 160 and diastolic 80-100 mmHg.
• Use labetalol, nifedipine or methyldopa; stop ACE inhibitors, ARBs and atenolol.
• Serial growth scans; delivery around 39 weeks if on treatment and well.

Quick revision

• Pre-eclampsia: 140/90 twice 4 hours apart, after 20 weeks, proteinuria 300 mg or more per 24 hours.
• Severe: 160 systolic or 110 diastolic or more.
• Cause: shallow spiral artery invasion, then endothelial dysfunction.
• HELLP: haemolysis, high liver enzymes, low platelets; epigastric pain; BP may be near normal.
• MgSO4: 4 g load, 1 g/hour for 24 hours after delivery; antidote 10 ml 10% calcium gluconate.
• BP drugs: labetalol (first-line), nifedipine, methyldopa; IV hydralazine for severe.
• Avoid ACE inhibitors, ARBs, atenolol, and ergometrine at delivery.
• Aspirin 75 mg from 12 weeks for high-risk women; delivery is the cure.

Written by The House Job from standard references (Obstetrics by Ten Teachers).

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