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RESEARCH ARTICLE
SA JOURNAL OF DIABETES & VASCULAR DISEASE
8
VOLUME 16 NUMBER 1 • JULY 2019
pregnancy, are generally held to be contra-indicated in the
management of chronic hypertension during pregnancy because
pregnancy reliesuponvolumeexpansion tosecureanaccelerated rate
of delivery of oxygenated blood to the peripheral tissues, including
the placental bed. ACE inhibitors are also contra-indicated because
they may interfere with the physiological regulation of uterine
blood flow through local uterine mechanisms. More seriously, they
are associated with neonatal renal failure in children of women
treated with them during pregnancy. Of the other categories of
antihypertensive drugs, beta-blockers are also relatively contra-
indicated, being considered to be an independent risk factor for
the development of intra-uterine growth restriction.
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Antihypertensive therapy during pregnancy in chronically
hypertensive women is usually secured through the use of
alphamethyldopa or calcium channel blockers. The aim of treatment
is to reduce the occurrence of severe hypertension to safer levels of
blood pressure. Practically, the threshold for introducing treatment
is a sustained increase in blood pressure to above 160/110 mmHg
to levels below this without seeking to reduce the pressure to
normotensive levels.
The complications of chronic hypertension during pregnancy may
extend to various forms of cardiac decompensation, depending on
the severity of the condition. Hence, hypertensive cardiomyopathy
is rarely seen in relatively young women with chronic hypertension,
although it may develop and can give rise tomaternal mortality.
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More
commonly, diastolic dysfunction caused by changes in left ventricular
morphology may result in the onset of increasing dyspnoea in the
third trimester as the volume expansion peaks out. Patients in this
category are otherwise well, without any signs of superimposed pre-
eclampsia. This is one circumstance where diuretic therapy may result
in rapid clinical improvement and resolution of symptoms that will
allow the pregnancy to continue to term.
Obstetric intervention is not commonly required in chronically
hypertensive women. However, some mild degree of foetal growth
restriction may be present and the risk of superimposed pre-
eclampsia cannot be excludedwith absolute certainty. Consequently,
induction of labour is usually recommended for women who do
not labour spontaneously before 40 weeks’ gestation.
Latent hypertension
Pregnancy may render overt hypertension that is not yet clinically
manifest outside of pregnancy. Women who have a strong familial
history of hypertension, whose genetic predisposition will manifest
as essential hypertension in later life, may become hypertensive
during pregnancy. The mechanism is thought to be related to
subnormal pregnancy vasodilatation in vessels, with a hereditary
defect in vasoregulation. In this circumstance, the increased
intravascular volume of pregnancy cannot be accommodated by
adequate vasodilatation, with a rise in blood pressure developing in
the late second to third trimester of pregnancy.
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This condition should be managed according to the same
principles as those outlined for women with chronic hypertension.
The outcome of the pregnancy is usually unaffected and the only
consideration might be the need for induction of labour in women
not yet delivered by 40 weeks’ gestation.
Physiological hypertension
Hypertension does not always indicate disease. Pregnancy is
characterised by massive plasma volume expansion, and the
cardiovascular adaptation needed to accommodate this increased
intravascular volume is that of equally massive peripheral
vasodilatation. The net consequence of this is a fall in blood pressure
during the second trimester, with increasing levels of blood pressure
closer to term. The entire adaptation is mediated by the placenta,
and the adequacy of the pregnant physiological change depends on
the amount of biochemically active trophoblast in the uterus. Hence
women with multiple pregnancies or those who have singleton
pregnancies with a large placenta will have a greater degree of
volume expansion than those with a smaller placental mass. The
consequences of this may be a supraphysiological increase in plasma
volume that exceeds the degree of compensatory vasodilatation
close to term. These individuals have normal pregnancies in every
respect, with normally grown babies and no other signs of pre-
eclampsia. This is not a condition requiring treatment or intervention
and should be recognised as a variant of normal.
3
The difficulty of managing these patients lies in being certain
that the distinction can be safely made between physiological
hypertension and pre-eclampsia. For this reason, many of these
women would be allowed to continue to term but induction of
labour would be justified at 40 weeks’ gestation
General evaluation of patients with hypertensive
disorder of pregnancy
Determining whether high blood pressure identified during
pregnancy is due to pre-eclampsia or chronic hypertension is
sometimes a challenge to the physician, especially if there are
no recorded blood pressures available from the first half of the
gestation. Clinical characteristics obtained through a good history,
physical examination and some laboratory investigations may be
used to help clarify the diagnosis.
Relevant history the physician must take
The time of detection of hypertension is very important. Hypertension
occurring before 20 weeks’ gestation is almost always due to
chronic hypertension, while new-onset hypertension after 20 weeks’
gestation should lead to a suspicion of gestational hypertension.
Worsening hypertension after 20 weeks of gestation should lead to
careful evaluation for the manifestations of pre-eclampsia.
Patients with pre-eclampsia may describe new-onset headache
that is frontal, throbbing or similar to migraine headache. They may
also have visual disturbances, including scintillations and scotoma,
which has been linked to cerebral vasospasm. Gastrointestinal
complaints, such as epigastric pain, may be moderate to severe in
intensity and due to hepatic swelling and inflammation, with stretch
of the liver capsule. Rapidly increasing or non-dependant oedema
may be a symptom of developing pre-eclampsia. In addition, rapid
weight gain as a result of oedema due to capillary leak, as well as
renal sodium and fluid retention could be a pointer to pre-eclampsia.
New-onset seizures in pregnancy suggest pre-eclampsia–eclampsia,
but primary neurological disorders must always be excluded.
Signs the physician must look out for
Pre-eclampsia is a multi-systemic disease with various physical signs.
Oedema can be seen in non-dependent areas such as the face and
hands, apart from the dependent areas. Maternal systolic blood
pressure above 160 mmHg or diastolic blood pressure above 110
mmHg can occur and denote severe disease.
In measuring the blood pressure, women should be made