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Management of Hypertension Before, During, and After Pregnancy
Management of Hypertension Before, During, and After Pregnancy
MANAGEMENT OF HYPERTENSION
BEFORE, DURING, AND AFTER
PREGNANCY 1499
P Rachael James, Catherine Nelson-Piercy
Heart 2004; 90:14991504. doi: 10.1136/hrt.2004.035444
H
ypertension is the most common medical problem encountered in pregnancy and remains
an important cause of maternal, and fetal, morbidity and mortality. It complicates up to
15% of pregnancies and accounts for approximately a quarter of all antenatal admissions.
The hypertensive disorders of pregnancy cover a spectrum of conditions, of which pre-eclampsia
poses the greatest potential risk and remains one of the most common causes of maternal death
in the UK.
Early in the first trimester there is a fall in blood pressure caused by active vasodilatation,
achieved through the action of local mediators such as prostacyclin and nitric oxide. This
reduction in blood pressure primarily affects the diastolic pressure and a drop of 10 mm Hg is
usual by 1320 weeks gestation.1 Blood pressure continues to fall until 2224 weeks when a nadir
is reached. After this, there is a gradual increase in blood pressure until term when pre-pregnancy
levels are attained. Immediately after delivery blood pressure usually falls, then increases over the
first five postnatal days.w1 Even women whose blood pressure was normal throughout pregnancy
may experience transient hypertension in the early post partum period, perhaps reflecting a
degree of vasomotor instability.
Correspondence to:
Dr Catherine Nelson-Piercy, Chronic hypertension
Department of Obstetrics, Chronic hypertension complicates 35% of pregnancies4 although this figure may rise, with the
Guys and St Thomas trend for women to postpone childbirth into their 30s and 40s. The diagnosis of chronic
Hospitals, North Wing, St
Thomas Hospital, Lambeth hypertension is based on a known history of hypertension pre-pregnancy or an elevated blood
Palace Road, London pressure > 140/90 mm Hg before 20 weeks gestation.5 However, there are several caveats to this
SE1 7EH, UK; diagnosis. Undiagnosed hypertensive women may appear normotensive in early pregnancy
catherine.nelson-piercy@
gstt.sthames.nhs.uk because of the normal fall in blood pressure, commencing in the first trimester. This may mask
_________________________ the pre-existing hypertensionw5 w6 and when hypertension is recorded later in the pregnancy it
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may be interpreted as gestational. Sometimes the diagnosis is Table 1 Risk factors for developing pre-eclampsia
only made several months post partum, when the blood
pressure fails to normalise as would be expected with c Nulliparity
gestational hypertension. Furthermore, pre-eclampsia can c Multiple pregnancy
rarely present before 20 weeks gestation and may be c Family history of pre-eclampsia
c Chronic hypertension
misinterpreted as chronic hypertension.w7
c Diabetes
1500 The presence of mild pre-existing hypertension approxi-
c Increased insulin resistance
mately doubles the risk of pre-eclampsia but also increases c Increased body mass index
the risk of placental abruption and growth restriction in the c Hypercoagulability (inherited thrombophilia)
fetus.w8 In general, when blood pressure is controlled, such c Renal disease even without significant impairment
women do well and have outcomes not dissimilar to normal c Low socioeconomic status
women.w6 However, when chronic hypertension is severe c Antiphospholipid syndrome (acquired thrombophilia)
(a diastolic blood pressure . 110 mm Hg before 20 weeks c Previous pre-eclampsia
gestation) the risk of pre-eclampsia is as high as 46%6 with c Hydatidiform mole
resultant raised maternal and fetal risks. c Black race
Gestational hypertension
Hypertension occurring in the second half of pregnancy in a
previously normotensive woman, without significant protein- abnormal placentation. In the first trimester, in a healthy
uria or other features of pre-eclampsia, is termed gestational pregnancy, the trophoblast invades the uterine decidua and
or pregnancy induced hypertension. It complicates 67% of reaches the inner layer of the myometrium. This migration
pregnancies7 and resolves post partum. The risk of super- transforms the small, musculo-elastic spiral arteries into
imposed pre-eclampsia is 1526%,8 but this risk is influenced large (fourfold increase in diameter) sinusoidal vessels
by the gestation at which the hypertension develops. When resulting in a high capacitance, low resistance blood supply
gestational hypertension is diagnosed after 36 weeks of to the intervillous space. Although commencing in the first
pregnancy, the risk falls to 10%.8 With gestational hyperten- trimester, the change is completed in the second trimester
sion, blood pressure usually normalises by six weeks post when another wave of trophoblast migration alters the
partum. myometrial segments of the arteries.w10 In pre-eclampsia,
these vascular alterations do not occur or they are limited to
Pre-eclampsia and eclampsia vessels in the decidua.w11 w12 In addition to the failure of
Pre-eclampsia usually occurs after 20 weeks gestation and is demuscularisation, the arteries maintain their response to
a multi-system disorder. It was classically defined as a triad vasomotor influencesw13 and undergo accelerated athero-
of hypertension, oedema, and proteinuria, but a more sclerosis, which further impairs perfusion to the intervillous
modern definition of pre-eclampsia concentrates on a space.
gestational elevation of blood pressure together with The secondary stage of pre-eclampsia involves the conver-
. 0.3 g proteinuria per 24 hours. Oedema is no longer sion of this uteroplacental maladaption to the maternal
included because of the lack of specificity.5 Pre-eclampsia
systemic syndrome, which has protean manifestations
may also manifest, with few maternal symptoms and signs,
(table 2). Failure of the normal cardiovascular changes of
as isolated intrauterine growth restriction (IUGR). Eclampsia
pregnancy to take place results in hypertension, reduction in
is defined as the occurrence of a grand mal seizure in
plasma volume, and impaired perfusion to virtually every
association with pre-eclampsia, although it may be the first
organ of the body. There is vasospasm and activation of
presentation of the condition.
platelets and the coagulation system, resulting in micro-
The incidence of pre-eclampsia is very much influenced by
thrombi formation. The link between the placenta and the
the presence of existing hypertension, although other risk
systemic disorder appears to involve endothelial dysfunction
factors are recognised (table 1).9 Overall pre-eclampsia
and oxidative stress.1113 w14 The management of pre-
complicates 56% of pregnancies,w9 but this figure increases
eclampsia essentially focuses on recognition of the condition
to up to 25% in women with pre-existing hypertension.w6 w9
and ultimately the delivery of the placenta, which is curative.
Eclampsia complicates 12% of pre-eclamptic pregnancies in
Since pre-eclampsia may arise with few symptoms, all
the UK. An estimated 50 000 women die annually from pre-
eclampsia worldwide9 and morbidity includes placental women are screened during pregnancy through regular
abruption, intra-abdominal haemorrhage, cardiac failure, antenatal care. Those women who are recognised to be at
and multi-organ failure. In the last confidential enquiry into increased risk have additional screening and more intensive
maternal deaths there were 15 confirmed deaths from monitoring.
pre-eclampsia or eclampsia, the majority as a result of intra-
cerebral haemorrhage.10 The risks to the fetus from pre-
eclampsia include growth restriction secondary to placental Table 2 Symptoms and signs of severe pre-eclampsia
insufficiency, and premature delivery. Indeed, pre-eclampsia
c Left upper quadrant/epigastric pain due to liver oedema hepatic
is one of the most common causes of prematurity (account- haemorrhage
ing for 25% of all infants with very low birth weight, c Headache visual disturbance (cerebral oedema)
, 1500 g). c Occipital lobe blindness
c Hyperreflexia clonus
Pathogenesis of pre-eclampsia c Convulsions (cerebral oedema)
The pathogenesis and manifestations of pre-eclampsia can be
considered in a two stage model. The primary stage involves
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1502
Figure 1 Doppler uterine artery assessment showing (A) normal flow velocity waveform with low resistance, and (B) abnormal flow velocity
waveform with an early diastolic notch (arrow) and a high resistance index.
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both conditions are associated with dyslipidaemia, insulin 9 Broughton Pipkin F. Risk factors for pre-eclampsia. N Engl J Med
2001;344:9256.
resistance, and endothelial dysfunction.w3740 It is of interest c An excellent editorial on the multiple risk factors for developing pre-
that the lipid abnormalities which occur in pre-eclampsia eclampsia.
10 Royal College of Obstetricians and Gynaecologists. Confidential enquiry into
(raised low density lipoprotein (LDL), VLDL, free fatty acid, maternal deaths in the United Kingdom. Why mothers die. London: Royal
and triglyceride values) pre-date the clinical appearance of College of Obstetricians and Gynaecologists, 2001.
c Death from cardiac disease is now the joint most common cause of
the conditionw39 w41 and endothelial dysfunction continues maternal death in the UK. This latest report is highly informative.
1504 to be impaired post partum.27 11 Roberts J. Endothelial dysfunction in preeclampsia. Semin Reprod Endocrinol
Although there are methodological concerns with some of 1998;16:515.
12 Roberts JM, Hubel CA. Is oxidative stress the link in the two-stage model of
the data in this area, these apparent late sequelae may have pre-eclampsia? Lancet 1999;354:7889.
important public health implications given the relative 13 Dekker GA, Sibai BM. Etiology and pathogenesis of preeclampsia: current
concepts. Am J Obstet Gynecol 1998;179:135975.
frequency of pregnancy induced hypertension and may, in 14 Caritis S, Sibai BM, Hauth J, et al. Low-dose aspirin to prevent pre-eclampsia
future, dictate screening for cardiovascular disease in in women at risk. N Engl J Med 1998;338:7015.
previously affected women. At the very least, it would seem 15 Chappell LC, Seed PT, Briley AL, et al. Effects of antioxidants on the occurrence
of pre-eclampsia in women at increased risk: a randomised trial. Lancet
prudent for such women to have an annual blood pressure 1999;354:81016.
measurement. Interestingly, women who go through a 16 Von Dadelszen P, Ornstein MP, Bull SB, et al. Fall in mean arterial pressure
and fetal growth restriction in pregnancy hypertension: a meta-analysis.
pregnancy without developing hypertension are at a reduced Lancet 2000;355:8792.
risk of becoming hypertensive in later life, when compared to 17 Homuth V, Dechend R, Luft FC. When should pregnant women with an
elevated blood pressure be treated? Nephrol Dial Transplant
nulliparous women.25 Pregnancy may offer a window into the 2003;18:14567.
future cardiovascular health of women, which is unavailable c An up to date evaluation of the evidence for treatment of hypertension
in men.28 in pregnancy.
18 Cockburn J, Moar VA, Ounsted M, et al. Final report of study on hypertension
during pregnancy: the effects of specific treatment on the growth and
.................. development of the children. Lancet 1982;i:6479.
19 Briggs GG, Freeman RK, Yaffe SJ. In Mitchell CW, ed. Drugs in pregnancy
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P R James, Department of Cardiology, Royal Sussex County Hospital, Philadelphia: Lippincott Williams and Wilkins, 2002.
Brighton, West Sussex, UK c A comprehensive, up to date text, solely on the safety of drugs in
C Nelson-Piercy, Department of Obstetrics, Guys and St Thomas pregnancy and breastfeeding.
Hospitals, London, UK 20 Committee on Drugs, American Academy of Pediatrics. The transfer of drugs
and other chemicals into human milk. Pediatrics 1994;93:13750.
21 Hargood JL, Brown MA. Pregnancy-induced hypertension; recurrence rate in
second pregnancies. Med J Austral 1991;154:37687.
22 Zhang J, Troendle JF, Levine RJ. Risks of hypertensive disorders in the second
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c A broad overview of the epidemiology, pathophysiology, and
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management of pre-eclampsia.
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