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Gestational hypertension
AUTHORS: Lissa M Melvin, 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: Apr 2024.

This topic last updated: Apr 10, 2024.

INTRODUCTION

Gestational hypertension and preeclampsia (including chronic hypertension with superimposed

preeclampsia, eclampsia, and HELLP syndrome [hemolysis, elevated liver enzymes, and low platelets])
are hypertensive disorders induced by pregnancy that resolve postpartum. Because of this and other
similarities (gestational hypertension often progresses to preeclampsia), some do not consider them
independent disorders. On the other hand, studies of risk factors note that although their risk factors
are similar, there are differences in the magnitude of associations with each disorder. For example,
primiparity, multiple gestation, and diabetes mellitus are stronger risk factors for preeclampsia than for
gestational hypertension [1,2]. 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) [3,4]. Physiologic and histologic differences also exist between the
two disorders. Total blood and plasma volumes are significantly higher in patients with gestational
hypertension (3139 mL/m2 and 2132 mL/m2, respectively) than in those with preeclampsia (mean 2660
mL/m2 and 1790 mL/m2, respectively) [5], Doppler measures of arterial and venous hemodynamics and
vascular endothelial function are normal in patients with gestational hypertension and abnormal in
those with preeclampsia [6,7], and levels of microparticles associated with endothelial cell damage are
significantly lower in patients with gestational hypertension than in those with preeclampsia [8].
Histologic signs of placental ischemia are less prominent in gestational hypertension than in
preeclampsia [9].

This topic will discuss gestational hypertension. Preeclampsia, superimposed preeclampsia, eclampsia,
and HELLP syndrome are reviewed separately:

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

● (See "Preeclampsia: Antepartum management and timing of delivery".)
● (See "Chronic hypertension in pregnancy: Prenatal and postpartum care", section on 'Patients with
superimposed preeclampsia'.)
● (See "Eclampsia".)
● (See "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)
PREVALENCE

In a population-based prospective cohort study beginning in early pregnancy (median gestational

duration 14 weeks), gestational hypertension developed in 2 to 17 percent of the cohort and
preeclampsia developed in 2 to 5 percent [10]. Participants with obesity had the highest prevalence of
gestational hypertension.

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 with each disorder [1].

CLINICAL FINDINGS AND DIAGNOSIS

Gestational hypertension should be suspected in a pregnant patient with all of the following [11]:

● New onset of hypertension (systolic pressure ≥140 mmHg and/or diastolic pressure ≥90 mmHg)
at ≥20 weeks of gestation.

The blood pressure elevation generally should be documented on at least two occasions at least
four hours apart. However, it is neither necessary nor desirable to wait hours before confirming
and treating severe blood pressure elevations (systolic pressure ≥160 mmHg and/or diastolic
pressure ≥110 mmHg).

● Normal urine protein excretion for pregnancy – Normal protein excretion in pregnancy is <300
mg per 24-hour urine collection (or this amount extrapolated from a timed collection), or protein-
to-creatinine ratio <0.3, or urine dipstick reading <2+ (if other quantitative methods are not
available).

● Absence of the signs and symptoms of end-organ dysfunction associated with preeclampsia
with severe features, which are described in the table ( table 1).

The diagnosis of gestational hypertension is confirmed postpartum if the patient does not
subsequently develop proteinuria or new signs of end-organ dysfunction (which are criteria for
preeclampsia), and the hypertension does not persist ≥12 weeks postpartum (which suggests chronic
hypertension).

DIAGNOSTIC EVALUATION

Goals — The main goals in the initial evaluation of pregnant patients with newly developed
hypertension are to:

● Confirm elevated blood pressure (exclude white coat hypertension)

 ● Distinguish gestational hypertension from preeclampsia, which can have a different course and
short-term prognosis

Confirm hypertension — Systolic pressure ≥140 mmHg and/or diastolic pressure ≥90 mmHg on at
least two occasions at least four hours apart confirms hypertension. As discussed above, it is neither
necessary nor desirable to wait hours before confirming and treating severe blood pressure elevation
(systolic pressure ≥160 mmHg and/or diastolic pressure ≥110 mmHg). (See 'Clinical findings and
diagnosis' above and 'Management: blood pressures ≥160/110 mmHg' below.)

Accurate blood pressure assessment requires proper technique (see "Treatment of hypertension in
pregnant and postpartum patients", section on 'Technique for accurate measurement of blood
pressure') and excluding white coat hypertension (also called isolated clinic or office hypertension). The
latter can be excluded by repeating the blood pressure measurement when the patient is relaxed.
Results of home blood pressure monitoring can be useful to establish the patient's blood pressure
profile [12]. Approximately 30 percent of pregnant participants in a trial of self-blood pressure
monitoring had discordancy between the home and office readings, most of which were attributed to
white coat hypertension [13,14]. (See "Out-of-office blood pressure measurement: Ambulatory and self-
measured blood pressure monitoring".)

Ask about symptoms — Gestational hypertension is asymptomatic. Preeclampsia without severe

features is also asymptomatic, whereas patients with severe features may have new-onset cerebral or
visual symptoms (eg, photopsia, scotomata, cortical blindness, retinal vasospasm); severe headache or
a headache that persists and progresses despite analgesic therapy with acetaminophen and not
accounted for by alternative diagnoses; severe persistent right upper quadrant or epigastric pain
unresponsive to medication and not accounted for by an alternative diagnosis; and/or dyspnea due to
pulmonary edema. (See "Preeclampsia: Clinical features and diagnosis".)

Measure protein excretion, platelet count, and chemistries — Absence of proteinuria is a key
criterion that distinguishes gestational hypertension from preeclampsia. In gestational hypertension,
protein excretion should be <300 mg in a 24-hour urine collection, or the protein-to-creatinine ratio
should be <0.3 in a random urine specimen, or the urine dipstick should be <2+ if other quantitative
methods are not available. A negative to trace urine dipstick does not definitively exclude significant
proteinuria since false-negative results occur with low specific gravity (<1.010), high salt concentration,
highly acidic urine, or with nonalbuminic proteinuria. A positive urine dipstick value, especially if only
+1, also requires confirmation since false positives occur. (See "Proteinuria in pregnancy: Diagnosis,
differential diagnosis, and management of nephrotic syndrome".)

Even after a normal 24-hour urine collection or protein-to-creatinine ratio, it can be difficult to exclude
preeclampsia conclusively because 10 percent of pregnant patients with other clinical and/or histologic
manifestations of preeclampsia have no proteinuria and 20 percent of those with eclampsia do not
have significant proteinuria prior to seizing [15].

Laboratory evaluation (platelet count, creatinine, alanine transaminase, aspartate transaminase) helps
to determine whether end-organ damage has occurred (findings are listed in the table ( table 1)),
which can happen with preeclampsia but not with gestational hypertension. (See "Preeclampsia: Clinical
features and diagnosis".)
Rule out other causes of hypertension — Previously unrecognized chronic hypertension is a
possibility when prepregnancy blood pressures are not available for comparison with blood pressures
during pregnancy. Some pregnant people may have undiagnosed prepregnancy hypertension. When
such individuals present for prenatal care, they may have normal blood pressures because of normal
early pregnancy physiology. Development of isolated hypertension later in pregnancy may reflect
return to their baseline blood pressure level rather than gestational hypertension. Similarly, if they
present late in gestation for prenatal care and have isolated hypertension, it is difficult to determine
whether this reflects chronic hypertension or gestational hypertension.

Secondary causes of hypertension are listed and described in the table ( table 2) and discussed
separately (see "Evaluation of secondary hypertension"). In addition, acute hypertension can be caused
by use of drugs that can produce a hyperadrenergic state, such as cocaine, amphetamine(s), and
phencyclidine. A standardized interview to screen for misuse of substances can be performed; some
examples are provided in the table ( table 3). The Society for Maternal-Fetal Medicine suggests
considering drug testing in patients with acute clinical complications such as unexplained severe
hypertension [16]. (See "Hypertensive disorders in pregnancy: Approach to differential diagnosis" and
"Testing for drugs of abuse (DOAs)".)

RISK OF PROGRESSION TO PREECLAMPSIA

Ten to 50 percent of patients diagnosed with gestational hypertension go on to develop preeclampsia

in the next one to five weeks [17,18]. It is unclear whether gestational hypertension and preeclampsia
are independent diseases with a similar phenotype (hypertension) or if gestational hypertension is an
early mild stage of preeclampsia.

Predictive factors — Patients who progress to preeclampsia have characteristics different from those
who continue to have nonproteinuric nonsevere hypertension. Clinical characteristics at presentation of
gestational hypertension that predict an increased risk for progression to preeclampsia include
gestational age <34 weeks at diagnosis (sensitivity 85 percent, specificity 60 percent) or mean systolic
blood pressure >135 mmHg on 24-hour blood pressure monitoring (sensitivity 61 percent, specificity 76
percent) [19]. Placental growth factor (PlGF)-based tests are sometimes used to rule in or rule out
preeclampsia in patients suspected of the disorder. (See "Preeclampsia: Clinical features and diagnosis",
section on 'Role of measurement of angiogenic markers'.)

MANAGEMENT: BLOOD PRESSURES ≥160/110 MMHG

Patients who develop severe gestational hypertension have rates of pregnancy complications
comparable to those of patients with preeclampsia with severe features; thus, the two groups are
managed similarly [11].

Severe hypertension should be confirmed with a repeat measurement within five minutes and, if
confirmed, should be treated expeditiously in the hospital ( algorithm 1). Delivery is generally
indicated, regardless of gestational age, given the high risk of serious maternal morbidity. However,
expectant management in a tertiary care setting or in consultation with a maternal-fetal medicine
specialist is an option for selected patients remote from term (<34 weeks of gestation) in whom blood
pressure can be controlled. Management of these patients is reviewed separately. (See "Preeclampsia:
Antepartum management and timing of delivery", section on 'Preeclampsia with features of severe
disease'.)

MANAGEMENT: BLOOD PRESSURES <160/110 MMHG

Site of care — Patients with gestational hypertension without severe blood pressure elevation can be
managed safely as outpatients if they are able to comply with weekly or twice weekly office visits
[12,20].

Patient education and counseling — Patient education and counseling are important components of
management since these patients are at increased risk of developing preeclampsia. We instruct them
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 compromise, such as
decreased fetal movement and vaginal bleeding, and signs of preterm labor.

Level of physical activity — Patients 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 compared with usual activity, but reduces the risk of developing severe hypertension (odds
ratio 0.47, 95% CI 0.26-0.83) [21,22]. The decision to advise reduced physical activity should be
individualized, taking into consideration the patient's blood pressures, comorbidities, and psychosocial
factors.

We advise against strength training and pure isometric exercise, such as weightlifting, 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 patients' blood pressure responses to their usual aerobic exercise activities, we
advise against aerobic exercise.

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

Maternal blood pressure and laboratory monitoring

● We obtain in-office blood pressure measurements once or twice weekly when the patient comes
in for a prenatal visit. Ideally, this is supplemented with home blood pressure monitoring to
determine the patient's average and peak blood pressures serially during usual activity, and
exclude the effects of white coat hypertension [12].

● We assess the following laboratory tests weekly:

• Urine protein-to-creatinine ratio

• Platelet count
• Serum creatinine
• Alanine transaminase, aspartate transaminase
 Proteinuria, thrombocytopenia, renal insufficiency, or elevated transaminases change the
diagnosis to preeclampsia, which affects management and prognosis. (See "Preeclampsia:
Antepartum management and timing of delivery" and "Preeclampsia: Intrapartum and
postpartum management and long-term prognosis".)

Role of antihypertensive therapy — We hospitalize and prescribe antihypertensive drugs for patients
with severe hypertension, frequent blood pressures approaching the severe range, or with preexisting
end-organ dysfunction (eg, kidney or heart disease) that may be worsened by hypertension. In rare
complex patients with labile pressures that are occasionally approaching the severe range, we offer
antihypertensive therapy with the goal of maintaining blood pressures in the range of 130 to 140/85 to
90 mmHg. Choice of drug(s), dosing, and target pressure are described in detail separately. (See
"Treatment of hypertension in pregnant and postpartum patients", section on 'When to initiate
antihypertensive therapy in pregnancy'.)

The American College of Obstetricians and Gynecologists (ACOG) suggests pharmacotherapy of

gestational hypertension when systolic pressures are ≥160 mmHg or diastolic pressures are ≥110
mmHg, or both [11]. By comparison, the National Institute for Health and Care Excellence suggests
offering pharmacotherapy to patients with gestational hypertension if their blood pressure remains
above 140/90 mmHg [23].

Fetal monitoring — The need for, type, and frequency of fetal assessment in patients with nonsevere
gestational hypertension is controversial [24]. 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 obstetric practice in the United States.

● NST, BPP – We monitor fetal well-being by a weekly biophysical profile (BPP) or nonstress test
(NST) plus assessment of amniotic fluid volume, increasing the frequency to twice weekly in
patients with comorbidities. We also ask them to monitor fetal movement daily and call if it
decreases. (See "Overview of antepartum fetal assessment".)

● Estimated fetal weight – We also obtain a sonographic estimation of fetal weight. If the initial
examination is normal, we repeat the ultrasound examination every three to four weeks as
hypertension of any etiology may be associated with placental insufficiency, which can lead to
impaired fetal growth [25,26]. If growth restriction with or without oligohydramnios is present,
management is the same as in any pregnancy with this finding and reviewed separately. (See
"Fetal growth restriction: Pregnancy management and outcome".)

● Role of Doppler – We reserve use Doppler velocimetry for monitoring fetuses with growth
restriction, but some non-US guidelines include various Doppler parameters for diagnosis of
growth restriction as well ( table 4). (See "Fetal growth restriction: Pregnancy management and
outcome" and "Fetal growth restriction: Screening and diagnosis".)

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 a course of antenatal corticosteroids (ACS) should be administered.
ACS is not routinely administered to patients with nonsevere gestational hypertension because preterm
birth <34 weeks is uncommon. A review of pregnancy outcomes in patients with nonsevere gestational
hypertension found that delivery before 34 weeks occurred in only 1 to 5 percent of cases [24].

Use of ACS at late-preterm gestational ages is more controversial. (See "Antenatal corticosteroid
therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

No role for 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 patients with gestational hypertension.

Meta-analyses have found that beginning low-dose aspirin in the second trimester to pregnant people
at average or high risk of developing preeclampsia is associated with a modest reduction in
preeclampsia and its sequelae (growth restriction, preterm birth) [27]. Most participants in these trials
began low-dose aspirin before 20 weeks of gestation and the trials had a wide variety of inclusion and
exclusion criteria, with some including and others excluding individuals with gestational hypertension.
A detailed discussion regarding use of low-dose aspirin for preeclampsia prophylaxis is available
separately. (See "Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

Timing of delivery — We plan for a term rather than preterm delivery, in general agreement with
guidelines from multiple major societies [28]. We individualize timing at term based on the blood
pressure level, comorbidities, and other risk factors for adverse pregnancy outcome. Our approach
tries to balance the fetal benefits of expectant management (ie, further growth and maturation) with
the maternal and fetal risks of expectant management (eg, progression to preeclampsia or severe
gestational hypertension and possible sequelae, including stillbirth or asphyxia), which may be avoided
by early delivery.

● For patients with gestational hypertension who have only a few blood pressures ≥140/90 mmHg
but <160/110 mmHg and otherwise uncomplicated pregnancies (no comorbidities or other risk
factors for adverse outcome), we plan delivery for 38+0 to 39+0 weeks, or at diagnosis if
diagnosed later. We believe maternal morbidity is unlikely to increase from only occasional
episodes of nonsevere blood pressure elevation, whereas the extra one to two weeks of expectant
management is likely to reduce neonatal morbidity. Our approach is supported by findings of a
retrospective cohort study in patients with gestational hypertension from the Consortium on Safe
Labor in which induction between 38 and 39 weeks of gestation achieved the optimal balance of
low maternal and low neonatal morbidity/mortality [29].

● For patients with gestational hypertension who have frequent blood pressures ≥140/90 mmHg
but <160/110 mmHg, comorbidities, or other risk factors for adverse outcome, we plan delivery
for 37+0 weeks or at diagnosis if diagnosed later. Delivery at 37 weeks rather than later in this
more complicated patient population is supported by the HYPITAT-I trial, which randomly assigned
patients at 36+0 to 41+0 weeks with gestational hypertension or mild preeclampsia to immediate
delivery or expectant management and found immediate induction reduced the composite risk of
poor maternal outcome (new-onset severe preeclampsia, HELLP syndrome, eclampsia, pulmonary
edema, placental abruption: 31 versus 44 percent, relative risk 0.71, 95% CI 0.59-0.86), without
significantly increasing neonatal morbidity at or near term [30]. HYPITAT-II, which was performed
in patients at 34+0 to 36+6 weeks of gestation, also found immediate delivery reduced maternal
 morbidity, but noted that the maternal benefit of preterm delivery was small in contrast to the
significant increase in neonatal morbidity with delivery before 37 weeks [31].

Our approach is similar to that of a consensus opinion of a workshop held by the Eunice Kennedy
Shriver National Institute of Child Health and Human Development and the Society for Maternal-Fetal
Medicine that suggested delivery at 37+0 to 38+6 weeks for all patients with any degree of gestational
hypertension because of the risk of progression to preeclampsia [32]. It differs from an ACOG practice
bulletin, based largely on expert opinion, that suggests delivery rather than expectant management for
all patients with uncomplicated gestational hypertension at ≥37+0 weeks [11].

Route of birth — Most patients give birth vaginally. Cesarean birth is performed for standard obstetric
indications.

Intrapartum management — Intrapartum care is routine, with the following points:

● Monitor for development of severe hypertension or preeclampsia – During labor, we monitor

patients for development of proteinuria, worsening hypertension, and symptoms of severe
disease since preeclampsia can manifest intrapartum. Intrapartum management of preeclampsia
is reviewed separately. (See "Preeclampsia: Intrapartum and postpartum management and long-
term prognosis".)

● Magnesium sulfate – We do not administer magnesium sulfate seizure prophylaxis unless the
patient develops severe hypertension or preeclampsia with severe features ( table 1) [11].

Magnesium sulphate is administered for fetal neuroprotection in pregnancies less than 32 weeks.
(See "Neuroprotective effects of in utero exposure to magnesium sulfate".)

● Anesthesia – Intrapartum anesthesia for patients with gestational hypertension and

preeclampsia without severe features is managed as it would be for patients without these
disorders, recognizing that severity may increase at any time. (See "Anesthesia for the patient with
preeclampsia".)

Postpartum care — Postpartum care is routine. Patients with excessive uterine bleeding due to atony
should not receive methylergonovine as it exacerbates hypertension. (See "Postpartum hemorrhage:
Medical and minimally invasive management", section on 'Manage atony'.)

For most patients, acetaminophen and/or nonsteroidal anti-inflammatory agents provide safe and
effective analgesia. (See "Treatment of hypertension in pregnant and postpartum patients", section on
'Analgesia'.)

Blood pressure should be followed closely after discharge since blood pressure peaks three to six days
postpartum when most patients are at home. Patients should be advised to seek medical attention if
they develop severe headaches or if blood pressure increases to severe levels. ACOG suggests daily
blood pressure evaluation for 72 hours postpartum and again around 7 to 10 days postpartum, or
earlier in patients with symptoms [33,34]. Another approach is to ensure measurement at least once
during postpartum days 3 to 5 [35]. Adjunctive home blood pressure monitoring is useful for daily
monitoring. Blood pressure returns to the prepregnancy baseline in most patients within two to six
weeks. (See 'Resolution of gestational hypertension' below.)
MATERNAL PROGNOSIS

Resolution of gestational hypertension — Approximately 50 percent of patients will have blood

pressures <140/90 mmHg without antihypertensive medication by two weeks postpartum, 80 percent
by six weeks [36], and all by 12 weeks (unless they had unrecognized preexisting chronic hypertension).

Recurrence risk — In a meta-analysis of individual patient data from almost 24,000 patients with
gestational hypertension who became pregnant again, 22 percent developed hypertension in a
subsequent pregnancy: gestational hypertension 15 percent, preeclampsia 7 percent [37].

Given these data, other data that individuals with a strong risk factor or several moderate risk factors
for preeclampsia benefit from low-dose aspirin therapy during pregnancy, and the minimal risk of
harm, we offer patients with a history of gestational hypertension low-dose aspirin in future
pregnancies. The evidence for this recommendation is available separately. (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) [38-46].

● A prospective study of over 15,000 patients with a first singleton birth observed that those with
gestational hypertension in three consecutive pregnancies had significantly higher blood pressure
later in life than patients who remained normotensive (systolic pressure 27 mmHg higher,
diastolic pressure 12 mmHg higher) [40]. 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
patients with a history of hypertension in pregnancy.

● In another study, patients 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 patients 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 (SGA) infants and/or preterm birth [45].

Gestational hypertension and preeclampsia appear to have similar long-term cardiovascular risks,
including chronic hypertension. Many long-term outcome studies evaluate outcomes among females
with a history of "pregnancy-induced 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: Intrapartum and postpartum management and long-term prognosis",
section on 'Long-term maternal risks of pregnancy-associated hypertension'.)

Clinical monitoring, risk factor evaluation, and early intervention might benefit patients with a history
of hypertension of any etiology in pregnancy. (See "Overview of primary prevention of cardiovascular
disease" and "Atherosclerotic cardiovascular disease risk assessment for primary prevention in adults:
Our approach".)
PERINATAL OUTCOME

● Nonsevere hypertension – Pregnancy outcomes of patients with nonsevere gestational

hypertension are generally favorable [18,24,48-52]. Most studies report that the mean birth
weight and rates of growth restriction, preterm birth, abruption, and perinatal death are similar to
those in the general obstetric population. However, one population-based cohort study reported
that the risk of delivering a small for gestational age (SGA) 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 [53].

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

at increased risk of maternal and perinatal morbidity [2,18,24,48-51]. These pregnancies have
rates of preterm birth, SGA, and placental abruption significantly higher than the rates in the
general obstetric population, and similar rates to those reported for patients with severe features
of preeclampsia.

In a study that compared selected outcomes in patients with severe preeclampsia (n = 45), severe
gestational hypertension (n = 24), and mild gestational hypertension or normotension (n = 467),
the preterm birth rates <35 weeks were 36, 25, and 8 percent, respectively, and SGA rates were 11,
21, and 7 percent, respectively [49]. 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
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they answer the four or five key questions a patient might have about a given condition. These articles
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articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth
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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

● Clinical manifestations and diagnosis – Gestational hypertension should be suspected in a
pregnant patient with all of the following:

• New-onset hypertension (systolic pressure ≥140 mmHg and/or diastolic pressure ≥90 mmHg)
at ≥20 weeks of gestation

• Normal urine protein excretion for pregnancy (<300 mg per 24-hour urine collection, or
protein-to-creatinine ratio <0.3, or urine dipstick reading <2+)

• Absent signs and symptoms of end-organ dysfunction associated with preeclampsia with
severe features ( table 1)

The diagnosis is confirmed postpartum if the patient does not subsequently develop criteria for
preeclampsia and the hypertension does not persist ≥12 weeks postpartum (which suggests
chronic hypertension). (See 'Clinical findings and diagnosis' above.)

● Diagnostic evaluation – The main goal is to confirm elevated blood pressure (exclude white coat
hypertension) and distinguish gestational hypertension from preeclampsia by documenting
absence of the symptoms and laboratory abnormalities listed in the table ( table 5). (See
'Diagnostic evaluation' above.)

● Management – Our approach is shown in the algorithm ( algorithm 2) and described below.

• Systolic pressure ≥160 mmHg and/or diastolic pressure ≥110 mmHg – Management is the
same as that for preeclampsia with severe features. Severe hypertension should be treated
urgently ( algorithm 1). (See "Preeclampsia: Antepartum management and timing of
delivery", section on 'Preeclampsia with features of severe disease'.)

• Systolic pressure <160 mmHg and diastolic pressure <110 mmHg

- Ten to 50 percent of these patients will go on to develop preeclampsia in the next one to
five weeks, thus they require close outpatient monitoring and counseling about signs of
symptoms of the disease. (See 'Risk of progression to preeclampsia' above and 'Patient
education and counseling' above and 'Site of care' above and 'Level of physical activity'
above.)

- We measure blood pressure once or twice weekly and measure urine protein, platelet
count, and liver transaminases weekly. (See 'Maternal blood pressure and laboratory
monitoring' above.)

- We monitor fetal well-being weekly with a biophysical profile (BPP) or nonstress test (NST)
plus assessment of amniotic fluid volume, increasing the frequency to twice weekly in
patients with comorbidities. We also obtain an initial sonographic estimation of fetal
weight. If this examination is normal, we repeat the ultrasound examination every three to
four weeks. (See 'Fetal monitoring' above.)

- Antenatal corticosteroids (ACS) are administered for standard indications. (See "Antenatal
corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from
preterm delivery".)
 ● Timing of delivery

• Systolic pressure ≥160 mmHg and/or diastolic pressure ≥110 mmHg – Management is the
same as that for preeclampsia with severe features. Expeditious delivery is generally indicated,
regardless of gestational age, given the high risk of serious maternal morbidity. However,
expectant management in a tertiary care setting or in consultation with a maternal-fetal
medicine specialist is an option for selected patients <34 weeks of gestation in whom blood
pressure can be controlled. Management of preeclampsia with severe features is reviewed
separately. (See "Preeclampsia: Antepartum management and timing of delivery", section on
'Preeclampsia with features of severe disease'.)

• Frequent blood pressures ≥140/90 mmHg but <160/110 mmHg, comorbidities, or other
risk factors for adverse outcome – We suggest delivery at 37+0 weeks of gestation, or at
diagnosis if diagnosed later (Grade 2B). (See 'Timing of delivery' above.)

• Uncomplicated pregnancies (no comorbidities or other risk factors for adverse outcome)
with most blood pressures <140/90 mmHg but intermittent values of ≥140/90 mmHg but
<160/110 mmHg – We suggest delivery at 38+0 to 39+0 weeks, or at diagnosis if diagnosed
later (Grade 2C). (See 'Timing of delivery' above.)

● Outcome – Pregnancy outcomes of patients with nonsevere gestational hypertension are

generally favorable. Severe gestational hypertension is associated with increased risks of maternal
and perinatal morbidity (preterm birth, small for gestational age [SGA] neonate, placental
abruption). Later in life, these mothers are at increased risk of developing chronic hypertension
and related disorders (eg, cardiovascular disease, hyperlipidemia, chronic kidney disease, diabetes
mellitus). (See 'Perinatal outcome' above and 'Long-term prognosis' above.)

● Recurrence risk – Hypertension recurs in approximately 22 percent of subsequent pregnancies

(gestational hypertension 15 percent, preeclampsia 7 percent) (see 'Recurrence risk' above).
Therefore, we treat patients with low-dose aspirin in future pregnancies. The evidence for this
recommendation is available separately. (See "Preeclampsia: Prevention", section on 'Low-dose
aspirin'.)

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REFERENCES

1. Ros HS, Cnattingius S, Lipworth L. Comparison of risk factors for preeclampsia and gestational
hypertension in a population-based cohort study. Am J Epidemiol 1998; 147:1062.

2. Villar J, Carroli G, Wojdyla D, et al. Preeclampsia, gestational hypertension and intrauterine growth
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Pregnancy Hypertens 2023; 31:25.
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Future Cardiovascular Disease. Hypertension 2017; 70:798.
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Cardiovascular Disease Among 617 589 Norwegian Women. J Am Heart Assoc 2018; 7.

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49. Buchbinder A, Sibai BM, Caritis S, et al. Adverse perinatal outcomes are significantly higher in
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for Gestational Age Infant and Stillbirth. Hypertension 2016; 67:640.
Topic 6805 Version 74.0
GRAPHICS

In a patient with preeclampsia, the presence of one or more of the following indicate
a diagnosis of "preeclampsia with severe features"

Severe blood pressure elevation:

Systolic blood pressure ≥160 mmHg and/or diastolic blood pressure ≥110 mmHg on 2 occasions at least 4
hours apart while the patient is on bedrest; however, antihypertensive therapy generally should be initiated
upon confirmation of severe hypertension, in which case criteria for severe blood pressure elevation can be
satisfied without waiting until 4 hours have elapsed

Symptoms of central nervous system dysfunction:

New-onset cerebral or visual disturbance, such as:

Photopsia, scotomata, cortical blindness, retinal vasospasm
and/or
Severe headache (ie, incapacitating, "the worst headache I've ever had") or headache that persists and
progresses despite analgesic therapy with acetaminophen and not accounted for by alternative diagnoses

Hepatic abnormality:

Impaired liver function not accounted for by another diagnosis and characterized by serum transaminase
concentration >2 times the upper limit of the normal range
and/or
Severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for
by an alternative diagnosis

Thrombocytopenia:

Platelet count <100,000 platelets/microL

Kidney function impairment:

Serum creatinine >1.1 mg/dL [97.2 micromol/L]

and/or
Doubling of the serum creatinine concentration in the absence of other kidney disease

Pulmonary edema

Reference:
1. American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia.
Obstet Gynecol 2020; 135:e237.

Graphic 76975 Version 29.0

Clinical features of several causes of secondary hypertension

Disorder Suggestive clinical features

General Severe or resistant hypertension

An acute rise in blood pressure over a previously stable value
Proven age of onset before puberty
Age less than 30 years with no family history of hypertension and no obesity

Renovascular disease Unexplained creatinine elevation and/or acute and persistent elevation in
serum creatinine of at least 50% after administration of ACE inhibitor, ARB,
or renin inhibitor
Moderate to severe hypertension in a patient with diffuse atherosclerosis, a
unilateral small kidney, or asymmetry in kidney size of more than 1.5 cm tha
cannot be explained by another reason
Moderate to severe hypertension in patients with recurrent episodes of flash
pulmonary edema
Onset of hypertension with blood pressure >160/100 mmHg after age 55
years
Systolic or diastolic abdominal bruit (not very sensitive)

Primary kidney disease Elevated serum creatinine concentration

Abnormal urinalysis

Drug-induced hypertension: New elevation or progression in blood pressure temporally related to

Oral contraceptives exposure
Anabolic steroids
NSAIDs
Chemotherapeutic agents
(eg, tyrosine kinase
inhibitors/VEGF blockade)
Stimulants (eg, cocaine,
methylphenidate)
Calcineurin inhibitors (eg,
cyclosporine)
Antidepressants (eg,
venlafaxine)

Pheochromocytoma Paroxysmal elevations in blood pressure

Triad of headache (usually pounding), palpitations, and sweating

Primary aldosteronism Unexplained hypokalemia with urinary potassium wasting; however, more
than one-half of patients are normokalemic

Cushing's syndrome Cushingoid facies, central obesity, proximal muscle weakness, and
ecchymoses
May have a history of glucocorticoid use

Sleep apnea syndrome Common in patients with resistant hypertension, particularly if overweight
or obese
Loud snoring or witnessed apneic episodes
Daytime somnolence, fatigue, and morning confusion
 Coarctation of the aorta Hypertension in the arms with diminished or delayed femoral pulses and low
or unobtainable blood pressures in the legs
Left brachial pulse is diminished and equal to the femoral pulse if origin of
the left subclavian artery is distal to the coarct

Hypothyroidism Symptoms of hypothyroidism

Elevated serum thyroid stimulating hormone

Primary hyperparathyroidism Elevated serum calcium

ACE: angiotensin-converting enzyme; ARB: angiotensin II receptor blocker; NSAID: nonsteroidal antiinflammatory
drug; VEGF: vascular endothelial growth factor.

Graphic 56130 Version 13.0

Clinical screening tools for substance use disorders during pregnancy

4 Ps [1]
Parents: Did any of your parents have a problem with alcohol or other drug use?

Partner: Does your partner have a problem with alcohol or drug use?

Past: In the past, have you had difficulties in your life because of alcohol or other drugs, including prescription
medications?

Present: In the past month, have you drunk any alcohol or used other drugs?

Scoring: Any "yes" should trigger further questions.

NIDA Quick Screen [2]

Screen your patients

Step 1. Use the NIDA Quick Screen to ask the patient about past-year drug use

Step 2. Ask the patient about lifetime drug use

Step 3. Determine risk level

Step 4. Depending on risk level: Advise, Assess, Assist, and Arrange

CRAFFT – Substance Abuse Screen for Adolescents and Young Adults [3]

C Have you ever ridden in a CAR driven by someone (including yourself) who was high or had been using alcoho
or drugs?

R Do you ever use alcohol or drugs to RELAX, feel better about yourself, or fit in?

A Do you ever use alcohol or drugs while you are by yourself or ALONE?

F Do you ever FORGET things you did while using alcohol or drugs?

F Do your FAMILY or friends ever tell you that you should cut down on your drinking or drug use?

T Have you ever gotten in TROUBLE while you were using alcohol or drugs?

Scoring: Two or more positive items indicate the need for further assessment.

Confidentiality statement: NOTICE TO CLINIC STAFF AND MEDICAL RECORDS: The information on this page is
protected by special federal confidentiality rules (42 CFR Part 2), which prohibit disclosure of this information
unless authorized by specific written consent. A general authorization for release of medical information is NOT
sufficient. [3]

Reproduced from:
1. Ewing H. A practical guide to intervention in health and social services with pregnant and postpartum addicts and alcoholics:
theoretical framework, brief screening tool, key interview questions, and strategies for referral to recovery resources. Martinez (CA):
The Born Free Project, Contra Costa County Department of Health Services; 1990.
2. Screening for Drug Use in General Medical Settings: Quick Reference Guide, Version 2. National Institute on Drug Abuse.
https://nida.nih.gov/sites/default/files/pdf/screening_qr.pdf (Accessed on October 31, 2023).
3. Center for Adolescent Behavioral Health Research, Children's Hospital Boston. The CRAFFT screening interview. Boston (MA): CABHRe;
2009. © John R. Knight, MD, Boston Children's Hospital, 2018. All rights reserved. Reproduced with permission. For more information,
contact [email protected].

Graphic 128222 Version 3.0

Management of inpatient pregnant people with acute severe hypertension due to
preeclampsia (systolic blood pressure ≥160 mmHg and/or diastolic blood pressure
≥110 mmHg)*

Mean arterial pressure should not be reduced by more than 25% over two hours, systolic blood pressure should
not be reduced below 130 mmHg, and diastolic blood pressure should not be reduced below 80 mmHg. Blood
pressures in the range of 130 to 150/80 to 100 mmHg are ideal. During treatment, heart rate and blood pressure
should be monitored closely. If delivery will not occur for days to weeks, maintenance therapy can be initiated, if
required, with oral antihypertensive drugs. Refer to UpToDate content for additional information on treatment of
hypertension in pregnancy.

IV: intravenous; bpm: beats per minute; BP: blood pressure; mmHg: millimeters of mercury.

* Severe hypertension should be confirmed with a second BP reading within 15 minutes to facilitate initiation of
antihypertensive therapy.

¶ The American College of Obstetricians and Gynecologists (ACOG) considers use of intravenous hydralazine,
intravenous labetalol, and oral nifedipine similarly effective and safe. Dosing is slightly different from the doses in
the algorithm. ACOG guidance does not describe use of nicardipine or reserve immediate-release nifedipine for
patients without intravenous access.

Graphic 134292 Version 3.0

US and ISUOG diagnostic criteria for fetal growth restriction

ISUOG
SMFM-ACOG-AIUM
Early (<32 weeks) Late (≥32 weeks)

AC or EFW <10 th centile for GA AC or EFW <3rd centile for GA or UA- AC or EFW <3rd centile for GA
AEDF
or
or
Any two of the following:
AC or EFW <10 th centile a. AC or EFW <10 th centile for GA
b. AC/EFW crossing centiles >2
Combined with one of the following: quartiles on growth centiles
a. UtA PI >95 th centile c. CPR <5 th centile or UA-PI >95 th
b. UA-PI >95 th centile centile

These criteria apply to singleton nonanomalous fetuses.

US: United States; SMFM: Society for Maternal-Fetal Medicine; ACOG: American College of Obstetricians and
Gynecologists; AIUM: American Institute of Ultrasound in Medicine; ISUOG: International Society of Obstetricians
and Gynecologists; AC: abdominal circumference; EFW: estimated fetal weight; GA: gestational age; UtA: uterine
artery; UA: umbilical artery; AEDF: absent end-diastolic flow (estimated by Doppler ultrasonography); PI: pulsatility
index; CPR: cerebroplacental ratio.

Graphic 139438 Version 2.0

Diagnostic criteria for preeclampsia

Systolic blood pressure ≥140 mmHg and/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 (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 kidney disease

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

Pulmonary edema

New-onset and persistent headache not accounted for by alternative diagnoses and not responding to usual
doses of analgesics ¶

Visual symptoms (eg, blurred vision, flashing lights or sparks, scotomata)

Preeclampsia is considered superimposed when it occurs in a patient with chronic hypertension. Superimposed
preeclampsia is characterized by worsening or resistant hypertension (especially acutely), the new onset of
proteinuria or a sudden increase in proteinuria, and/or significant new end-organ dysfunction in a patient with
chronic hypertension. It typically occurs after 20 weeks of gestation or postpartum.

Definitions/diagnostic criteria for preeclampsia are generally similar worldwide except the International Society
for the Study of Hypertension in Pregnancy definition also includes signs of uteroplacental dysfunction (eg, fetal
growth restriction, abnormal angiogenic markers, abnormal umbilical artery Doppler, abruption, fetal demise).

* If systolic blood pressure is ≥160 mmHg and/or diastolic blood pressure is ≥110 mmHg, confirmation within
minutes is sufficient.

¶ Response to analgesia does not exclude the possibility of preeclampsia.

Adapted from:
1. American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin No. 222: Gestational Hypertension and Preeclampsia.
Obstet Gynecol 2020; 135:e237.
2. Magee LA, Brown MA, Hall DR, et al. The 2021 International Society for the Study of Hypertension in Pregnancy classification,
diagnosis & management recommendations for international practice. Pregnancy Hypertens 2022; 27:148.

Graphic 79977 Version 39.0

Approach to diagnosis and management of hypertension after 20 weeks of gestation

For detailed information about diagnosis and management of preeclampsia and gestational hypertension, refer
to the UpToDate content on both of these disorders.

* Delivery is generally indicated, regardless of gestational age, given the high risk of serious maternal morbidity.
However, expectant management in a tertiary care setting or in consultation with a maternal-fetal medicine
specialist is an option for selected patients remote from term (<34 weeks of gestation) in whom blood pressure
can be controlled.

Graphic 144462 Version 1.0

Contributor Disclosures
Lissa M Melvin, MD No relevant financial relationship(s) with ineligible companies to disclose. Edmund F Funai,
MD No relevant financial relationship(s) with ineligible companies to disclose. Charles J Lockwood, MD, MHCM No
relevant financial relationship(s) with ineligible companies to disclose. Vanessa A Barss, MD, FACOG No relevant
financial relationship(s) with ineligible companies 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