Hypertension in Pregnancy

Introduction

Hypertensive disorders complicate around 8-10% of pregnancies and remain among the leading causes of maternal and perinatal morbidity worldwide. In the UK, deaths from eclampsia have fallen dramatically, but deaths from intracranial haemorrhage in women whose severe hypertension was not treated promptly still occur, and this is the single most avoidable element of the whole subject.^1,2

The framework that makes this topic manageable is chronological. Blood pressure is measured at booking and at every subsequent antenatal contact for exactly this reason: to establish a baseline and then to detect deviation from the expected trajectory. Whether hypertension appears before or after 20 weeks determines its name, its cause, its investigation and its outcome.

This article covers chronic and gestational hypertension. Pre-eclampsia, eclampsia and HELLP syndrome are covered in detail separately, but they cannot be entirely separated here, because the main task in managing any hypertensive pregnancy is watching for progression to pre-eclampsia.

Physiology of blood pressure in pregnancy

From early in the first trimester, systemic vascular resistance falls by around 30% under the influence of progesterone, prostacyclin and nitric oxide. Cardiac output rises by 30-50% and plasma volume by around 40%, but the vasodilatation predominates, so blood pressure falls. The diastolic pressure falls more than the systolic, reaching a nadir of roughly 10 mmHg below baseline at 20-24 weeks, before climbing back towards pre-pregnancy values by term.

Two clinically important consequences follow. First, a woman with mild pre-existing hypertension may have an entirely normal booking blood pressure and appear to develop hypertension in the third trimester, when in fact her pressure is simply returning to its true baseline. Second, a blood pressure of 140/90 mmHg recorded before 20 weeks is essentially never new-onset pregnancy-related disease, and should be treated as chronic hypertension requiring investigation for a secondary cause.

Classification

Severe hypertension, defined as 160/110 mmHg or above, is a category that cuts across all of these and always demands urgent treatment regardless of the underlying label, because it is the level at which the risk of maternal intracranial haemorrhage rises steeply.

Chronic hypertension

Chronic hypertension complicates 1-5% of pregnancies and is becoming more common with rising maternal age and BMI. Most is essential hypertension, but a young woman presenting with hypertension deserves consideration of secondary causes: renal parenchymal and renovascular disease, primary hyperaldosteronism, phaeochromocytoma, coarctation of the aorta and Cushing's syndrome.

Pre-conception and booking

• Stop ACE inhibitors and angiotensin receptor blockers, ideally before conception and certainly within two working days of a positive test, and switch to a safe alternative
• Stop thiazide and thiazide-like diuretics, which are associated with congenital anomaly and neonatal complications
• Stop statins, which are not recommended in pregnancy
• Advise dietary sodium reduction, which lowers blood pressure and reduces the need for treatment
• Assess for end-organ damage: urinalysis for proteinuria, U&E, and consider echocardiography if long-standing
• Start aspirin 75-150 mg daily from 12 weeks until birth, as chronic hypertension is a high-risk factor for pre-eclampsia

Antenatal management

The target blood pressure is below 135/85 mmHg. Treatment is not withheld for fear of impairing placental perfusion; the CHIPS and CHAP trials showed that tighter control reduces severe hypertension without increasing fetal growth restriction. Women are seen more frequently than the routine schedule allows, with blood pressure and urinalysis at each visit. Placental growth factor-based testing can be used between 20 and 35 weeks to help rule out pre-eclampsia in women with suspected disease.¹

Fetal growth is monitored with ultrasound at 28, 32 and 36 weeks, with umbilical artery Doppler, because chronic hypertension is associated with placental insufficiency and fetal growth restriction. Birth before 37 weeks is not offered on the basis of chronic hypertension alone; after 37 weeks the timing is agreed with the woman, taking account of blood pressure control and any complications.

Gestational hypertension

Gestational hypertension is new hypertension after 20 weeks without proteinuria or other features of pre-eclampsia. It affects around 6% of pregnancies. It is best regarded as a provisional diagnosis rather than a benign endpoint, because between 15% and 25% of these women will progress to pre-eclampsia, and the earlier the hypertension appears the higher that risk: onset before 32 weeks carries a risk of progression approaching 40%.

Significant proteinuria is defined as a urinary albumin:creatinine ratio of 8 mg/mmol or more, or a protein:creatinine ratio of 30 mg/mmol or more, on a spot sample. Automated reagent-strip reading is used for initial screening; a dipstick result of 1+ or more should be quantified rather than acted on directly. If significant proteinuria appears, the diagnosis becomes pre-eclampsia and management changes accordingly.

Antihypertensive treatment is offered to all women with gestational hypertension, aiming for a blood pressure below 135/85 mmHg. Birth is not offered before 37 weeks for gestational hypertension alone; from 37 weeks, timing is discussed and agreed, taking into account blood pressure, treatment burden, and maternal and fetal condition. Fetal growth scans with umbilical artery Doppler and an assessment of amniotic fluid volume are arranged at diagnosis and then every 2-4 weeks.¹

Investigations

Investigation of hypertension in pregnancy serves three purposes: to quantify proteinuria, to detect maternal organ dysfunction that would reclassify the woman as having pre-eclampsia, and in chronic hypertension to look for a secondary cause and for pre-existing end-organ damage.

Serum creatinine deserves particular attention because pregnancy shifts the normal range. Glomerular filtration rate rises by around 50%, so creatinine falls to a typical range of 40-70 micromol/L. A value of 90 micromol/L, entirely normal in a non-pregnant woman, represents meaningful renal impairment at 32 weeks. The same principle applies to urate, which rises in pre-eclampsia but is too non-specific to be used diagnostically on its own.¹

Antihypertensive drugs in pregnancy

Acute severe hypertension

A blood pressure of 160/110 mmHg or above requires treatment within an hour, in a monitored setting, with a senior clinician informed. Options are oral nifedipine, intravenous labetalol or intravenous hydralazine, chosen according to what has already been given and any contraindications. The aim is to bring the pressure below 135/85 mmHg without precipitous falls, since abrupt reductions compromise placental perfusion and may produce fetal distress. Continuous fetal monitoring is used while intravenous agents are being titrated.^1,2

Postnatal management

Blood pressure characteristically rises for the first three to five days after birth, peaking around day 3-5 when the physiological diuresis occurs, and women can develop severe hypertension or even eclampsia after apparently uncomplicated deliveries. Monitoring must therefore continue after birth rather than stopping at delivery.

• Measure blood pressure daily for the first two days, at least once between days 3 and 5, and then as clinically indicated
• Continue antenatal antihypertensives, but stop methyldopa within two days of birth and substitute an alternative
• Reduce treatment if blood pressure falls below 130/80 mmHg
• Drugs compatible with breastfeeding include labetalol, nifedipine, enalapril, amlodipine and atenolol
• Women with gestational hypertension should be reviewed at 6-8 weeks; if still hypertensive, or still requiring treatment, arrange specialist review
• Women who remain hypertensive beyond 6 weeks postpartum have chronic hypertension by definition and need lifelong follow-up

Every woman who has had a hypertensive disorder of pregnancy should be told that it identifies her as being at increased long-term cardiovascular risk. The relative risk of later chronic hypertension, ischaemic heart disease and stroke is roughly doubled, and higher again after early-onset pre-eclampsia. Annual blood pressure measurement, weight and lifestyle advice, and attention to conventional cardiovascular risk factors should be part of the discharge plan and communicated to the GP.^1,4

Red flags

Prognosis

Gestational hypertension resolves within six weeks of birth in the large majority of women, and often much sooner. Around one in six will have hypertension in a subsequent pregnancy, and a similar proportion will develop pre-eclampsia next time, which is why previous hypertensive disease of pregnancy is a high-risk factor triggering aspirin prophylaxis in the next pregnancy.

Perinatal outcomes in well-controlled gestational hypertension without progression to pre-eclampsia are close to those of normotensive pregnancy. The risks accrue from progression, from placental insufficiency and from iatrogenic preterm birth, which is why the monitoring schedule is intensive and the threshold for growth surveillance is low.¹