30/11/2019 Gestational hypertension - UpToDate

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Gestational hypertension
Authors: Lissa Magloire, MD, Edmund F Funai, MD
Section Editor: Charles J Lockwood, MD, MHCM
Deputy Editor: Vanessa A Barss, MD, FACOG

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2019. | This topic last updated: Jun 21, 2019.

INTRODUCTION

Gestational hypertension and preeclampsia/eclampsia are hypertensive disorders induced by

pregnancy; both disorders resolve postpartum. Gestational hypertension is the most common cause
of hypertension in pregnant women.

This topic will discuss gestational hypertension. Other hypertensive disorders of pregnancy are
reviewed separately:

● (See "Preeclampsia: Clinical features and diagnosis".)

● (See "Preeclampsia: Management and prognosis".)
● (See "Eclampsia".)
● (See "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)

DEFINITION/DIAGNOSIS

Gestational hypertension is a clinical diagnosis defined by the new onset of hypertension (defined as
systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg) at ≥20 weeks of
gestation in the absence of proteinuria or new signs of end-organ dysfunction [1]. The blood pressure
readings should be documented on at least two occasions at least four hours apart.

Gestational hypertension is severe when systolic blood pressure is ≥160 mmHg and/or diastolic blood
pressure is ≥110 mmHg: It is not necessary, and undesirable, to wait hours before confirming and
treating severe hypertension. In the 2019 American College of Obstetricians and Gynecologists'
practice bulletin on Gestational Hypertension and Preeclampsia, gestational hypertension is
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considered "preeclampsia with severe features" when blood pressures are at this level and/or when
other signs/symptoms of preeclampsia with severe features are present (table 1) [1]. This change in
nomenclature from severe gestational hypertension to severe preeclampsia underscores the potential
for serious adverse events when pregnancy-related blood pressures are severely elevated, even in
the absence of proteinuria.

Gestational hypertension is a temporary (provisional) diagnosis for hypertensive pregnant women

who do not meet criteria for preeclampsia (table 2) or chronic hypertension (hypertension first
detected before the 20th week of pregnancy). The diagnosis is changed to:

● Preeclampsia, if proteinuria or new signs of end-organ dysfunction develop (ie, criteria for
preeclampsia are met)

● Chronic hypertension, if blood pressure elevation persists ≥12 weeks postpartum. Of note, in
2017, the definition of hypertension in nonpregnant adults was revised as follows (see "Overview
of hypertension in adults", section on 'Definitions'):

• Normal blood pressure – Systolic <120 mmHg and diastolic <80 mmHg

• Elevated blood pressure – Systolic 120 to 129 mmHg and diastolic <80 mmHg

• Hypertension:

- Stage 1 – Systolic 130 to 139 mmHg or diastolic 80 to 89 mmHg

- Stage 2 – Systolic at least 140 mmHg or diastolic at least 90 mmHg
● Transient hypertension of pregnancy, if blood pressure returns to normal by 12 weeks
postpartum

An important consideration is the availability of prepregnancy blood pressures for comparison with
blood pressures during pregnancy. Some women may have had undiagnosed prepregnancy
hypertension, which may be in the severe range. When such women present for prenatal care early in
gestation, they may have normal or mildly elevated blood pressures because of normal early
pregnancy physiology. Development of isolated severe hypertension later in pregnancy may reflect
return to their baseline blood pressure level rather than preeclampsia with severe features. Similarly,
if they present late in gestation for prenatal care and have isolated severe hypertension, it is difficult
to determine whether this reflects chronic hypertension or development of preeclampsia with severe
features. Since the management and pregnancy outcome of chronic hypertension is different from the
management and pregnancy outcome of preeclampsia with severe features, the distinction is
clinically relevant but not always possible during pregnancy.

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All patients require postpartum follow up at 12 weeks to establish whether they had pregnancy-
related hypertension or have chronic hypertension, with or without superimposed preeclampsia, as all
of these diagnoses have long-term health implications. (See "Preeclampsia: Management and
prognosis", section on 'Long-term maternal risks of pregnancy-associated hypertension' and
"Overview of hypertension in adults".)

PREVALENCE

Gestational hypertension is the most common cause of hypertension during pregnancy. It occurs in 6
to 17 percent of healthy nulliparous women and 2 to 4 percent of multiparous women [2-4]. The
prevalence is highest in women with preeclampsia in a previous pregnancy, women with multifetal
gestation, and overweight/obese women [5,6].

RISK FACTORS

Risk factors are similar to those for preeclampsia (see "Preeclampsia: Clinical features and
diagnosis", section on 'Risk factors'). However, epidemiologic studies report differences in the
magnitude of the associations for the two disorders [7].

DIAGNOSTIC EVALUATION

The main goals in the initial evaluation of pregnant women with newly developed hypertension are to
distinguish gestational hypertension from preeclampsia, which has a different course and prognosis,
and to determine whether hypertension is severe, which affects management and outcome.

As in other patients with newly diagnosed hypertension, white coat hypertension (also called isolated
clinic or office hypertension) should be excluded by repeating measurement of blood pressure when
the patient is relaxed. Results of home blood pressure monitoring can be useful to establish the
patient’s blood pressure profile. If an automated device is used in the home or office, it should have
been validated in a pregnant population [8]. (See "Ambulatory and home blood pressure monitoring
and white coat hypertension in adults".)

In addition, the following evaluation should be performed.

Measure protein excretion — Urinary protein excretion should be determined since the presence or
absence of proteinuria is a key clinical criterion that determines whether the patient will be given a
diagnosis of gestational hypertension or preeclampsia. A urine dipstick of negative to trace should not

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be used to definitively exclude significant proteinuria since false negative results occur with low
specific gravity (<1.010), high salt concentration, highly acidic urine, or with nonalbumin proteinuria. A
positive urine dipstick value, especially if only +1, also requires confirmation since false positives
occur. Urine protein can be quantitated using a urine protein-to-creatinine ratio ≥0.26 mg protein/mg
creatinine (30 mg/mmol) on a random urine sample or with a 24-hour urine collection. We prefer the
latter, as it conforms to the most widely accepted diagnostic criteria for preeclampsia. (See
"Evaluation of proteinuria in pregnancy and management of nephrotic syndrome".)

Even after this evaluation, it can be difficult to exclude preeclampsia conclusively. Studies have
shown that 10 percent of women with clinical and/or histological manifestations of preeclampsia have
no proteinuria and 20 percent of women with eclampsia (a form of severe preeclampsia) do not have
significant proteinuria prior to their seizure [9]. Therefore, when hypertension is accompanied by any
of the signs and symptoms of end-organ dysfunction (table 2), the patient should be managed as a
patient with preeclampsia, even if proteinuria is not present [1]. (See "Preeclampsia: Management
and prognosis".)

Evaluate for features of severe disease — Patients should be questioned about the presence of
severe features of preeclampsia, such as the new onset of cerebral or visual disturbances or
epigastric or right upper quadrant pain (table 1). The chest should be auscultated to assess for
pulmonary edema. The presence of any of these findings upgrades the diagnosis to preeclampsia
with severe features. (See "Preeclampsia: Clinical features and diagnosis".)

Rule out other causes of acute hypertension — Acute hypertension can also be caused by
medical disorders, such as pheochromocytoma and use of drugs that can produce a hyperadrenergic
state, such as cocaine, amphetamine(s), and phencyclidine. (See "Preeclampsia: Clinical features
and diagnosis", section on 'Differential diagnosis' and "Evaluation and treatment of hypertensive
emergencies in adults", section on 'Evaluation and diagnosis'.)

Perform laboratory evaluation — Laboratory evaluation helps to determine whether there is end
organ involvement, which occurs with preeclampsia but not gestational hypertension. Changes
consistent with preeclampsia with severe features include thrombocytopenia, increase in creatinine
concentration to >1.1 mg/dL, and doubling of hepatic transaminases (table 1).

Determine the severity of hypertension — Hypertension in pregnancy is defined as systolic blood

pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg. It is considered severe when
systolic blood pressure is ≥160 mmHg and/or diastolic blood pressure is ≥110 mmHg. (See
'Management' below.)

Assess fetal well-being — As with all hypertensive pregnancies, fetal well-being should be
assessed with a biophysical profile or nonstress test with amniotic fluid estimation. We also obtain a

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sonographic estimation of fetal weight; umbilical artery Doppler velocimetry is reserved for fetuses
with growth restriction [5]. (See "Overview of antepartum fetal surveillance".)

RISK OF PROGRESSION TO PREECLAMPSIA

Ten to 50 percent of women initially diagnosed with gestational hypertension go on to develop

preeclampsia in one to five weeks [10,11]. Progression from preeclampsia to preeclampsia with
severe features may occur more rapidly, within days.

It is not clear whether gestational hypertension and preeclampsia are independent diseases with a
similar phenotype (hypertension) or if gestational hypertension is an early mild stage of preeclampsia.
There is consistent evidence that preeclampsia develops in a substantial proportion of women initially
diagnosed with gestational hypertension, and that women who progress to preeclampsia have
characteristics different from those who continue to have nonproteinuric hypertension. Clinical
characteristics at presentation of gestational hypertension that predict an increased risk for
progression to preeclampsia include [12]:

● Gestational age less than 34 weeks at diagnosis (sensitivity 85 percent, specificity 60 percent)

● Mean systolic blood pressure >135 mmHg on 24 hour blood pressure monitoring (sensitivity 61
percent, specificity 76 percent)

● Elevated serum uric acid level (>5.2 mg/dL [0.309 mmol/L]) (sensitivity 88 percent, specificity 93
percent) [13,14]

Abnormal uterine artery Doppler velocimetry has also been found to be predictive (sensitivity 86
percent, specificity 90 percent); however, uterine artery Doppler is not routinely performed clinically.

Other characteristics have been reported to be predictive, but are not readily measureable: elevated
serum levels of anti-angiogenic markers (eg, sFlt- 1), reduced levels of proangiogenic placental
growth factor, and higher total vascular resistance (>1340 dyne seconds/cm5) [15-18].

Some data suggest preeclampsia and gestational hypertension are independent diseases. Although
they share many risk factors, epidemiologic studies report differences in the magnitude of the
associations for the two disorders. For example, primiparity is a stronger risk factor for preeclampsia
than for gestational hypertension (odds ratio 2.2 versus 1.2) [19] and multiple gestation and diabetes
mellitus are stronger risk factors for preeclampsia than gestational hypertension [7,19]. Prognosis is
also different: the recurrence rate for gestational hypertension is several-fold higher than that for
preeclampsia (>20 percent versus approximately 5 percent for preeclampsia at term) [20,21].

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Others have reported physiological and histological differences between the two disorders. Total
blood and plasma volumes are significantly higher in women with gestational hypertension (3139
mL/m2 and 2132 mL/m2, respectively) than in women with preeclampsia (mean 2660 mL/m2 and
1790 mL/m2, respectively) [22], Doppler measures of arterial and venous hemodynamics and
vascular endothelial function are normal in women with gestational hypertension and abnormal in
women with preeclampsia [15,23], and levels of microparticles associated with endothelial cell
damage are significantly lower in women with gestational hypertension than in women with
preeclampsia [24]. Histological signs of placental ischemia are less prominent in gestational
hypertension than in preeclampsia [25].

MANAGEMENT

The decision to deliver women with preterm gestational hypertension attempts to balance three
competing factors: (1) the fetal benefits from expectant management (ie, further growth and
maturation), (2) the maternal and fetal benefits from early intervention (ie, avoidance of complications
from progression of hypertensive disease over the remainder of pregnancy), and (3) the maternal and
fetal risks from expectant management (eg, progression of hypertensive disease and possible
sequelae, including stillbirth or asphyxia). We believe close surveillance of pregnancies with non-
severe gestational hypertension managed expectantly can mitigate the risk of development of serious
sequelae of gestational hypertension; therefore, we manage these patients expectantly and deliver
them when their clinical situation deteriorates or at term. (See 'Timing of delivery' below.)

This strategy is supported by the HYPITAT-II trial, which randomly assigned women with non-severe
hypertensive disorders of pregnancy at 34+0 to 36+6 weeks to immediate delivery or to expectant
management with delivery at term or upon development of features of severe preeclampsia [26].
Three percent of women with gestational hypertension (new hypertension with diastolic blood
pressure ≥100 mmHg and no proteinuria) managed expectantly developed one or more adverse
maternal outcomes (thromboembolic complications, HELLP syndrome, eclampsia, placental
abruption) versus no woman in the immediate delivery group, but immediate delivery also resulted in
more cases of neonatal respiratory distress syndrome (4.3 versus 1.1 percent). In addition, early
delivery resulted in poorer neurodevelopmental outcomes compared with expectant management
[27].

Blood pressure less than 160/110 mmHg — The management of gestational hypertension is similar
to that of preeclampsia without severe features.

Site of care — Most women with gestational hypertension without severe blood pressure elevation
(ie, systolic blood pressure is ≥160 mmHg and/or diastolic blood pressure is ≥110 mmHg) can be

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managed safely as outpatients with weekly or twice weekly office visits to assess maternal symptoms
and fetal well-being, and measure blood pressure, protein excretion, platelet count, serum creatinine,
and liver enzymes. Home blood pressure monitoring can be useful to determine the patient's average
and peak blood pressure during usual activity.

Patient education and counseling — Patient education and counseling are important
components of management since these patients are at increased risk of developing preeclampsia
and other pregnancy complications. We instruct patients to promptly report any symptoms suggestive
of preeclampsia (headache, visual changes, epigastric or right upper quadrant pain). We also review
signs suggestive of possible fetal impairment, such as decreased fetal movement and vaginal
bleeding, and signs of preterm labor. Patients should be given appropriate telephone numbers to call
care providers. Heavy vaginal bleeding, severe headache ("worse headache of my life"), stroke
symptoms, severe breathing problems, or sudden severe pain are considered medical emergencies
because they can be associated with a life-threatening condition.

Level of physical activity — Women may maintain most of their normal physical activities.
Bedrest at home or in the hospital does not prevent progression to preeclampsia or improve maternal
or fetal outcome, but reduces the frequency of worsening hypertension [28]. The decision to place a
patient on bedrest should be individualized and should take into consideration her blood pressures,
comorbidities, and social factors. Prolonged bedrest should be avoided because it increases the risk
of venous thromboembolism [29].

We advise against strength training and pure isometric exercise, such as weight lifting, as these
activities can acutely raise blood pressure to severe levels. Aerobic exercise can cause a modest rise
in systolic pressure, usually with no change or a slight reduction in diastolic pressure. In the absence
of information about a woman's blood pressure response to her usual aerobic exercise activities, we
advise against aerobic exercise.

Whether and how many hours the patient continues to work outside her home depends on multiple
factors, particularly her blood pressure at work. These decisions should be made on a case-by-case
basis. (See "Working during pregnancy", section on 'Work characteristics'.)

Low dose aspirin — Whether low dose aspirin prevents progression of gestational hypertension
to preeclampsia is unclear. We do not begin aspirin for prevention of preeclampsia after 20 weeks of
gestation and therefore do not prescribe it for women with gestational hypertension. Meta-analyses
have shown that beginning low dose aspirin in the second trimester to pregnant women at average or
high risk of developing preeclampsia is associated with a modest reduction in preeclampsia and its
sequelae (growth restriction, preterm birth) [30]. However, the included trials had a wide variety of
inclusion and exclusion criteria, with some including and others excluding women with gestational

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hypertension. Most women in these trials began low dose aspirin before 20 weeks of gestation.
Practice guidelines consistently recommend initiating low dose aspirin before 20 weeks for this
reason and because preeclampsia is known to affect placental development early in pregnancy [31].
(See "Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

Maternal blood pressure and laboratory monitoring — We agree with the American College of
Obstetricians and Gynecologists (ACOG) guidelines that suggest monitoring blood pressure serially
with at least one in-office measurement and weekly assessment of proteinuria, platelet count, serum
creatinine, and liver enzymes [1]. Proteinuria, thrombocytopenia, renal insufficiency, or elevated liver
enzymes change the diagnosis to preeclampsia, and these patients should be managed accordingly.
As discussed above, home blood pressure monitoring can be useful to determine the patient's
average and peak blood pressure serially during usual activity. (See "Preeclampsia: Management and
prognosis".)

Fetal assessment — In our practice, we ask patients with gestational hypertension to monitor
fetal movement daily and call if it is decreased or absent. We order either a nonstress test with
sonographic estimation of the amniotic fluid index or a biophysical profile weekly. Testing is begun at
32 weeks of gestation, or earlier if an increased risk of fetal demise is identified and delivery for
perinatal benefit would be considered if test results are abnormal.

We also perform serial ultrasound examinations to monitor fetal growth every three to four weeks, as
hypertension of any etiology may be associated with placental insufficiency [32,33]. (See "Overview
of antepartum fetal surveillance".)

The need for, type, and frequency of fetal assessment in women with gestational hypertension that is
not severe are controversial [5]. There is no evidence from large randomized trials that any routine
surveillance method results in a decreased risk of fetal death or neonatal morbidity in these patients.
Nevertheless, antepartum fetal monitoring of pregnancies deemed to be at increased risk of adverse
fetal outcome is a routine obstetrical practice in the United States.

Antihypertensive therapy — We do not prescribe antihypertensive drugs for antepartum

treatment of gestational hypertension, unless hypertension is severe or approaching the severe range
or the patient has preexisting end organ dysfunction (eg, renal, cardiac) that may be worsened by
hypertension. Data from randomized trials show that drug therapy of mild hypertension does not
improve maternal or neonatal outcome. These data are reviewed separately. (See "Management of
hypertension in pregnant and postpartum women", section on 'General principles'.)

For most women undergoing treatment of severe hypertension, the blood pressure goal is 130 to 150
mmHg systolic and 80 to 100 mmHg diastolic, similar to that in preeclampsia. (See "Management of

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hypertension in pregnant and postpartum women", section on 'Treatment of hypertension in

preeclampsia'.)

Antenatal corticosteroids — If the clinician believes that an individual patient is at increased risk
for delivery within seven days and before 34 weeks of gestation (eg, coexistent pregnancy
complications, development of preeclampsia), then corticosteroids should be administered. However,
a course of antenatal corticosteroids is not routinely administered to women with non-severe
gestational hypertension because preterm birth <34 weeks is uncommon. A review of pregnancy
outcomes in women with non-severe gestational hypertension found that delivery before 34 weeks
occurred in only 1 to 5 percent of cases [5]. (See "Antenatal corticosteroid therapy for reduction of
neonatal respiratory morbidity and mortality from preterm delivery".)

Timing of delivery — We recommend delivery at term for women with gestational hypertension,
in general agreement with guidelines from multiple major societies [31]. The optimum gestational age
between 37 and 40 weeks for intervention (induction, cesarean delivery) because of gestational
hypertension is controversial. We individualize these cases based on the degree of hypertension,
presence of comorbidities, and the presence of risk factors for adverse pregnancy outcome.

● For uncomplicated pregnancies with only an occasional blood pressure ≥140/90 mmHg and
<160/110 mmHg, we deliver at 38 to 39 weeks, since neonatal morbidity is lower than at 37 to 38
weeks [34,35].

● For pregnancies with frequent blood pressures ≥140/90 mmHg and <160/110 mmHg,
comorbidities, or other risk factors for adverse outcome, we deliver at 37 weeks.

A consensus opinion from a workshop held by the Eunice Kennedy Shriver National Institute of Child
Health and Human Development and the Society for Maternal-Fetal Medicine suggested delivery at
37+0 to 38+6 weeks for all women with any degree of gestational hypertension because of the risk of
progression to preeclampsia [35]. ACOG suggests delivery rather than expectant management for
women with uncomplicated gestational hypertension at ≥37+0 weeks [1]. Authors of a retrospective
cohort study from the Consortium on Safe Labor concluded induction of labor between 38 and 39
weeks of gestation achieved optimal balance of low maternal and low neonatal morbidity/mortality
[36].

Intrapartum management — During labor, we monitor women with gestational hypertension for
development of proteinuria, worsening hypertension, and symptoms of severe disease since
preeclampsia can manifest intrapartum. We do not administer magnesium sulfate seizure prophylaxis
unless the patient develops severe hypertension or symptoms or laboratory abnormalities associated
with severe preeclampsia. ACOG suggests use of magnesium sulfate seizure prophylaxis for women

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with gestational hypertension with severe features (table 1), preeclampsia with severe features, or
eclampsia [1].

Blood pressure greater than 160/110 mmHg — Women who develop severe gestational
hypertension have rates of pregnancy complications comparable to those with preeclampsia with
severe features, and thus ACOG recommends managing these patients similarly. (See
"Preeclampsia: Management and prognosis", section on 'Preeclampsia with features of severe
disease'.)

MATERNAL PROGNOSIS

Postpartum course — Most women with gestational hypertension become normotensive within the
first postpartum week [37]. If blood pressure returns to normal by 12 weeks postpartum, their
diagnosis is changed to transient hypertension of pregnancy. If they remain hypertensive at the 12th
postpartum week, they are given the diagnosis of chronic hypertension, which happens in
approximately 15 percent of cases [38].

The mean time to normalization of blood pressure postpartum after preeclamptic pregnancies is
approximately two weeks. The slower rate of recovery in preeclampsia may reflect the time required
for resolution of the endothelial injury, which may not be present in gestational hypertension.

The decision to use nonsteroidal anti-inflammatory agents for postpartum analgesia should be
individualized, as these drugs are known to cause elevations in blood pressure in nonpregnant
individuals with hypertension. If blood pressure is elevated in the postpartum period, we recommend
avoiding these drugs. (See "Management of hypertension in pregnant and postpartum women",
section on 'Postpartum analgesia'.)

Recurrence risk — A 2015 meta-analysis of individual patient data from almost 24,000 women with
gestational hypertension who became pregnant again reported that 22 percent developed
hypertension in a subsequent pregnancy (gestational hypertension: 15 percent, preeclampsia: 7
percent) [39]. Given these data and other data that women with a high risk factor or several moderate
risk factors for preeclampsia may benefit from low dose aspirin therapy in pregnancy, we offer women
with a history of gestational hypertension and blood pressures ≥160/110 mmHg low dose aspirin in
future pregnancies to reduce their risk of developing preeclampsia. (See "Preeclampsia: Prevention",
section on 'Candidates'.)

Long-term prognosis — Gestational hypertension is associated with development of hypertension

later in life, and also with development of diseases related to hypertension (cardiovascular disease,
hyperlipidemia, chronic kidney disease, diabetes mellitus) [38,40-46]. A prospective study of over

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15,000 women with a first singleton birth observed that women with gestational hypertension in three
consecutive pregnancies had significantly higher blood pressure later in life than women who
remained normotensive (systolic pressure 27 mmHg higher, diastolic pressure 12 mmHg higher) [41].
They also had more unfavorable lipid and glycemic profiles, but these differences appeared to be due
to higher body mass index at follow-up in women with a history of hypertension in pregnancy. In
another study, women with both gestational hypertension and gestational diabetes were at particularly
high risk for future diabetes (hazard ratio [HR] 36.9, 95% CI 26.0-52.3), hypertension (HR 5.7, 95% CI
4.9-6.7), and cardiovascular disease/mortality (HR 2.4, 95% CI 1.6-3.5) compared with women who
had neither disorder, but no information on maternal weight was available [47]. In a third study,
gestational hypertension was associated with a twofold increased risk of cardiovascular disease
during 14 years of postpartum follow-up, and the risk increased in those with small-for-gestational-
age infants and/or preterm delivery [46].

Gestational hypertension and preeclampsia appear to have similar long-term cardiovascular risks,
including chronic hypertension. Many long-term outcome studies evaluate outcomes among women
with a history of "pregnancy-associated hypertension," given some uncertainty in the distinction
between gestational hypertension and preeclampsia. The long-term risks of preeclampsia are
reviewed in detail separately. (See "Preeclampsia: Management and prognosis", section on 'Long-
term maternal risks of pregnancy-associated hypertension'.)

Clinical monitoring, risk factor evaluation, and early intervention might benefit women with a history of
hypertension of any etiology in pregnancy. (See "Overview of primary prevention of coronary heart
disease and stroke".)

PERINATAL OUTCOME

● Non-severe hypertension – Pregnancy outcomes of patients with non-severe gestational

hypertension are generally favorable [3-5,11,48-50]. Most studies report that the mean birth
weight and rates of fetal growth restriction, preterm birth, abruption, and perinatal death are
similar to those in the general obstetrical population. However, one population-based cohort
study reported that the risk of delivering a small for gestational age newborn at term increased by
2 percent for each mmHg rise in diastolic blood pressure from early to late pregnancy, even in
the absence of overt hypertension [51].

● Severe hypertension – Pregnancies associated with severe gestational hypertension appear to

be at increased risk of maternal and perinatal morbidity [3-5,11,19,48,49]. These pregnancies
have rates of preterm delivery, small for gestational age (SGA) infants, and abruptio placentae
significantly higher than the rates in the general obstetrical population, and similar to rates

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reported for women with severe features of preeclampsia. In a study that compared selected
outcomes in women who developed severe preeclampsia (n = 45), severe gestational
hypertension (n = 24), and women who remained normotensive or developed mild gestational
hypertension (n = 467), the rates of delivery <35 weeks were 36, 25, and 8 percent, respectively
[4]. The rates of delivery of a SGA infant were 11, 21, and 7 percent, respectively. The small
number of patients with severe gestational hypertension or severe preeclampsia limits the
generalizability of these results.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around
the world are provided separately. (See "Society guideline links: Hypertensive disorders of
pregnancy".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The
Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and
they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more
detailed. These articles are written at the 10th to 12th grade reading level and are best for patients
who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-
mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: High blood pressure and pregnancy (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Gestational hypertension is defined as the new onset of hypertension (defined as systolic blood
pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg) after the 20th week of
pregnancy in the absence of proteinuria, severe hypertension, or new signs of end-organ
dysfunction. These criteria distinguish gestational hypertension from preeclampsia (proteinuria or
signs of end-organ dysfunction must be present (table 2)) and chronic hypertension

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(hypertension antedates pregnancy or develops before the 20th week of pregnancy). (See
'Definition/diagnosis' above.)

● Gestational hypertension is the most common cause of hypertension during pregnancy, occurring
in 6 to 17 percent of healthy nulliparous women and 2 to 4 percent of multiparous women. (See
'Prevalence' above.)

● The main goals in the diagnostic evaluation of women with gestational hypertension are to
distinguish this disorder from preeclampsia, which has a different course and prognosis, and
determine whether hypertension is severe, which affects management and outcome. The
evaluation includes (see 'Diagnostic evaluation' above):

• Measurement of urine protein

• Evaluation for severe features of preeclampsia (table 1)
• Assessment of fetal status

● Ten to 50 percent of women initially diagnosed with gestational hypertension go on to develop

preeclampsia in one to five weeks, so frequent maternal monitoring for signs/symptoms of
preeclampsia is indicated. (See 'Risk of progression to preeclampsia' above.)

● Pregnancy outcomes of patients with gestational hypertension with blood pressure <160/110
mmHg are generally favorable, whereas pregnancies associated with higher blood pressures are
at increased risk for maternal and perinatal morbidity, similar to the rates reported for women with
preeclampsia with severe features. (See 'Perinatal outcome' above.)

● For women with gestational hypertension and blood pressure <160/110 mmHg, we measure
blood pressure once or twice weekly and measure urine protein, platelets, and liver enzymes
weekly (see 'Maternal blood pressure and laboratory monitoring' above). Blood pressure
≥160/110 mmHg upgrades the diagnosis to severe gestational hypertension; proteinuria,
thrombocytopenic, or elevated liver enzymes upgrades the diagnosis to preeclampsia. These
patients should be managed accordingly. (See 'Blood pressure greater than 160/110 mmHg'
above and "Preeclampsia: Management and prognosis".)

● We ask patients with gestational hypertension to monitor fetal movement daily and call if it is
decreased or absent. We order either a nonstress test with sonographic estimation of the
amniotic fluid index or a biophysical profile weekly starting at 32 weeks of gestation. We also
perform serial ultrasound examinations to monitor fetal growth every three to four weeks. (See
'Fetal assessment' above.)

● We do not prescribe antihypertensive drugs for treatment of gestational hypertension, unless

hypertension is severe or approaching the severe range or the patient has preexisting end organ
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dysfunction that may be worsened by hypertension. (See 'Antihypertensive therapy' above.)

● If the clinician believes that an individual patient is at increased risk for delivery within seven days
and before 34 weeks of gestation (eg, coexistent pregnancy complications, development of
preeclampsia), then corticosteroids should be administered. (See 'Antenatal corticosteroids'
above.)

● For uncomplicated pregnancies with only occasional blood pressures ≥140/90 mmHg and
<160/110 mmHg, we suggest delivery at 38 to 39 weeks (Grade 2C). (See 'Timing of delivery'
above.)

● For pregnancies with frequent blood pressures ≥140/90 mmHg and <160/110 mmHg,
comorbidities, or other risk factors for adverse outcome, we suggest delivery at 37 weeks of
gestation (Grade 2C). (See 'Timing of delivery' above.)

● Gestational hypertension is severe when systolic blood pressure is ≥160 mmHg and/or diastolic
blood pressure is ≥110 mmHg. Gestational hypertension is considered severe preeclampsia
when blood pressures are at this level and/or when other signs/symptoms of preeclampsia with
severe features are present (table 1) (see 'Definition/diagnosis' above). Management is the same
as in other patients with preeclampsia with severe features. (See "Preeclampsia: Management
and prognosis", section on 'Preeclampsia with features of severe disease'.)

● Hypertension recurs in approximately 22 percent of subsequent pregnancies and is associated

with development of hypertension later in life. (See 'Maternal prognosis' above.)

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GRAPHICS

Features of severe disease in a woman with a pregnancy-related hypertensive

disorder

Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg, or both (on
two separate occasions)

Symptoms of central nervous system dysfunction:

New-onset cerebral or visual disturbance, such as:
Photopsia, scotomata, cortical blindness, retinal vasospasm
Severe headache (ie, incapacitating, "the worst headache I've ever had") or headache that persists and
progresses despite analgesic therapy

Hepatic abnormality:
Severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by an
alternative diagnosis or serum transaminase concentration ≥2 times the upper limit of the normal range, or both

Thrombocytopenia:
<100,000 platelets/microL

Renal abnormality:
Progressive renal insufficiency (serum creatinine >1.1 mg/dL [97.2 micromol/L] or doubling of serum creatinine
concentration in the absence of other renal disease)

Adapted from ACOG Practice Bulletin No. 202: Gestational Hypertension and Preeclampsia. Obstet Gynecol 2019; 133:e1.

Graphic 111086 Version 2.0

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Criteria for the diagnosis of preeclampsia

Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on at least 2 occasions at least
4 hours apart after 20 weeks of gestation in a previously normotensive patient AND the new onset of 1 or
more of the following*:

Proteinuria ≥0.3 g in a 24-hour urine specimen or protein/creatinine ratio ≥0.3 (mg/mg) (30 mg/mmol) in a
random urine specimen or dipstick ≥2+ if a quantitative measurement is unavailable

Platelet count <100,000/microL

Serum creatinine >1.1 mg/dL (97.2 micromol/L) or doubling of the creatinine concentration in the absence of
other renal disease

Liver transaminases at least twice the upper limit of the normal concentrations for the local laboratory

Pulmonary edema

Cerebral or visual symptoms (eg, new-onset and persistent headaches not accounted for by alternative diagnoses
and not responding to usual doses of analgesics ¶; blurred vision, flashing lights or sparks, scotomata)

In a woman with chronic/preexisting hypertension, criteria for superimposed preeclampsia are new onset of
proteinuria, significant end-organ dysfunction, or both after 20 weeks of gestation. For women with
chronic/preexisting hypertension who have proteinuria prior to or in early pregnancy, superimposed preeclampsia is
defined by worsening or resistant hypertension (especially acutely) in the last half of pregnancy or development of
signs/symptoms of the severe end of the disease spectrum.

* If systolic blood pressure is ≥160 mmHg or diastolic blood pressure is ≥110 mmHg, confirmation within minutes is
sufficient.
¶ Response to analgesia does not exclude the possibility of preeclampsia.

Adapted from: American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin No. 202: Gestational
Hypertension and Preeclampsia. Obstet Gynecol 2019; 133:e1-e25.

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Contributor Disclosures
Lissa Magloire, MD Nothing to disclose Edmund F Funai, MD Nothing to disclose Charles J Lockwood, MD,
MHCM Nothing to disclose Vanessa A Barss, MD, FACOG Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.

Conflict of interest policy

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