17.3 Hypertension in pregnancy

The hypertensive disorders of pregnancy cause many of the developing world’s maternal deaths. They kill mothers by causing cerebrovascular accidents: heart failure, respiratory failure and kidney failure, postpartum haemorrhage, DIC (disseminated intravascular coagulation), and abruption of the placenta.

When you find that a mother’s blood pressure is high during pregnancy, she is likely to have one of four conditions:

(A) She might have had essential hypertension before she became pregnant.

(B) She might have had renal hypertension before she became pregnant (uncommon, see Section 17.6).

Figure 17.2: DANGER SIGNS in gestational hypertension, as seen by a community health worker. From David Werner’s ‘Where there is no doctor’.

(C) She might have developed essential hypertension during pregnancy. This typically happens to an older multip who doesn’t get much, if any, proteinuria with her hypertension. Her blood pressure is usually raised before 28 weeks, so that she may need antihypertensive treatment early in pregnancy. Her long-term risks are those normally associated with essential hypertension.

(D) She might have developed the disease that has been traditionally known as ’pre-eclampsia’, and which is more common than hypertension developing during pregnancy. ’Pre-eclampsia’ typically happens to a young primigravida whose blood pressure rises after 28 weeks, and who has a significant proteinuria. Her blood pressure is normal when she is not pregnant, and her long term prognosis is normal in respect of her blood pressure.

So far so good. But: (1) You are unlikely to know what a mother’s blood pressure was before she became pregnant. (2) What about the hypertensive primigravida without proteinuria, and the hypertensive multip with it? (3) (C) and (D), have many features in common, and babies in both of them are at increased risk from IUGR. (4) Two rival international societies dispute the classification and terminology of hypertension in pregnancy, so it is in great confusion. In practice, however, (C) and (D) are inseparable, so we have put them together and called all hypertension arising during pregnancy ’gestational hypertension’. This is WHO’s term, which strictly refers only to (D). Other terms include ’pregnancy-induced hypertension’, or ’PIH’.

Detecting gestational hypertension early is one of the main aims of antenatal care. If the staff of your clinics are hard pressed, the most important occasion on which to measure a mother’s blood pressure is when she first attends early in pregnancy. If it is normal then, the risks of it rising are small until the second half of pregnancy, when she may develop gestational hypertension.

If a mother has gestational hypertension, aim to monitor her blood pressure, to test her urine for protein, and to bring her as near to term as you can. The value of bed-rest, and particularly phenobarbitone, are disputed. We don’t use the latter for treating mild hypertension.

If her gestational hypertension is severe enough to cause eclampsia (fits), or severe pre-eclampsia (signs or symptoms which indicate that fits are imminent), aim to: (1) Deliver her baby; this is the definitive cure. (2) Prevent or treat her fits as soon as possible with magnesium sulphate, or one of the forms of sedation described below. (3) Control her blood pressure with hydralazine.

Magnesium sulphate: (1) Has a curariform action on the neuromuscular junction which stops convulsions. (2) Has no central action, so it does not sedate her, with the result that she remains fully alert, and can co-operate better during labour. (4) Does not sedate her baby, although it can affect him. (5) Is cheap. (6) Will depress her respiration, perhaps fatally, if you give her too much. However, although the margin of safety of magnesium sulphate is small, you can assess its anticonvulsant effect quite easily by testing her knee-jerks—it will abolish these before it depresses her respiration. You will not overdose her if you are very careful and if: (a) you test her knee jerks before each intramuscular dose, and (b) you keep her urinary output above 25 ml per hour—her kidneys are the only way she can excrete it.

If you are going to use sedation instead of magnesium sulphate, it has to be deep enough to control her convulsions. She should be semiconscious, so that she can only just be aroused, but not unconscious. You can produce this deep sedation with:

(1) Chlormethiazole (’Heminevrin’). This is a sedative and anticonvulsant; it has a wide margin of safety and controls eclampsia rapidly. It normally requires an intravenous drip, but you can give it without one; it is also comparatively expensive. Chlormethiazole is available as a powder for adding to a drip, as tablets, and as capsules in arachis oil.

(2) An intramuscular ’lytic cocktail’ of pethidine, chlorpromazine, and promethazine, which has the advantage of not needing a drip.

(3) Diazepam has two uses: (a) As a bolus intravenous injection to control fits urgently at the start of any anticonvulsant regime. (b) Orally, or with an intravenous drip, to maintain constant sedation and a constant anticonvulsive effect. But: (i) the intravenous infusion of diazepam ideally needs an infusion pump; (ii) if you give diazepam for more than 36 hours before delivery, the baby will be ’floppy’, and liable to neonatal cyanotic attacks. Diazepam is thus best avoided, except to control fits urgently.

(4) You can use phenytoin (’Epanutin’), which is widely used for epilepsy.

(5) Sodium amytal and (6) paraldehyde can be used but are not so effective. (7) Thiopentone will control fits, but has all the risks associated with its use as an anaesthetic (A 12.1).

There is no agreement as to which is the best method, especially under difficult circumstances like yours. Magnesium sulphate gives good results in centres of excellence, but needs particularly careful monitoring. An alert patient on magnesium sulphate is easier to nurse than a heavily sedated one. However, if your midwives cannot be relied on to monitor the administration of magnesium sulphate, their patients may be safer sedated, even if nursing them is more difficult. Under difficult conditions, chlormethiazole is probably the best of the sedative methods.

The methods above may fail to control a mother’s blood pressure, so after you have controlled her fits with magnesium sulphate or sedation, you may have to use hydralazine to bring her systolic blood pressure down to less than 170 mm. If it is less than this, and she is also sedated, she should have no more fits. But if she is unsedated on magnesium sulphate, they can occur at systolic pressures of less than 160 mm.

If she has imminent eclampsia (visual disturbances, and exaggerated reflexes, etc., or severe proteinuria), deliver her baby early, whatever the duration of pregnancy.

If she has mild or moderate proteinuria, and no symptoms of imminent eclampsia, management depends on the duration of pregnancy: (1) If her baby is more than 36 weeks deliver him, regardless of the quality of your neonatal care, because he will probably survive. (2) If he is less than 36 weeks, balance the risk of death in utero with that of induction followed by death in your neonatal nursery. If your nursery is very good (unlikely), consider delivering him at 32 weeks. If it is poor, continue to 36 weeks.

Induce her on the above indications, or if this is impractical, section her. Provided you don’t section her too late, it will improve her chances. If however, she is already in extremis (unusual), a Caesarean section will speed her death.

She will usually improve rapidly after delivery. Unfortunately, delivery sometimes fails to control gestational hypertension, and fits may occur for the first time during labour, or soon afterwards. Occasionally, her blood pressure starts to rise for the first time after delivery. She will not be out of danger from eclampsia until at least 48 hours after her baby is born.

There are problems: some patients have a high blood pressure and no eclamptic symptoms; a few have eclampsia with a normal blood pressure.

Some common errors: (1) Don’t use thiazides or other diuretics in the attempt to treat her oedema. (2) Don’t use morphine unless you have no other way of treating her. Don’t use heparin. (3) Don’t nurse her in the dark—this is old-fashioned, unnecessary, and may lead to lack of attention.