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Hipertensión gestacional
AUTORES: Dra. Lissa M Melvin, Dr. Edmund F. Funai
EDITOR DE SECCIÓN: Aaron B Caughey, MD, MPH, PhD
EDITOR ADJUNTO: Dra. Vanessa A. Barss, FACOG

Todos los temas se actualizan a medida que hay nueva evidencia disponible y se completa nuestro proceso de revisión
por pares .

Revisión de literatura actualizada hasta: febrero de 2025.

Última actualización de este tema: 13 de febrero de 2025.

INTRODUCCIÓN

La hipertensión gestacional y la preeclampsia (incluida la hipertensión crónica con

preeclampsia superpuesta, eclampsia y síndrome HELLP [hemólisis, enzimas hepáticas
elevadas y plaquetas bajas]) son trastornos hipertensivos inducidos por el embarazo que se
resuelven después del parto. Debido a esto y otras similitudes (la hipertensión gestacional a
menudo progresa a preeclampsia), algunos no los consideran trastornos independientes.
Por otro lado, los estudios de factores de riesgo indican que, aunque sus factores de riesgo
son similares, existen diferencias en la magnitud de las asociaciones con cada trastorno. Por
ejemplo, la primiparidad, la gestación múltiple y la diabetes mellitus son factores de riesgo
más fuertes para la preeclampsia que para la hipertensión gestacional [ 1,2 ]. El pronóstico
también es diferente: la tasa de recurrencia para la hipertensión gestacional es varias veces
más alta que para la preeclampsia (> 20 por ciento frente a aproximadamente el 5 por ciento
para la preeclampsia a término) [ 3,4 ]. También existen diferencias fisiológicas e histológicas
entre los dos trastornos. Los volúmenes totales de sangre y plasma son significativamente
más altos en pacientes con hipertensión gestacional (3139 mL/m 2 y 2132 mL/m 2 ,
respectivamente) que en aquellos con preeclampsia (media 2660 mL/m 2 y 1790 mL/m 2 ,
respectivamente) [ 5 ], las mediciones Doppler de la hemodinámica arterial y venosa y la
función endotelial vascular son normales en pacientes con hipertensión gestacional y
anormales en aquellos con preeclampsia [ 6,7 ], y los niveles de micropartículas asociadas
con daño de células endoteliales son significativamente más bajos en pacientes con
hipertensión gestacional que en aquellos con preeclampsia [ 8 ]. Los signos histológicos de
isquemia placentaria son menos prominentes en la hipertensión gestacional que en la
preeclampsia [ 9 ].

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Este tema abordará la hipertensión gestacional. La preeclampsia, la preeclampsia

superpuesta, la eclampsia y el síndrome HELLP se analizan por separado:

● (Ver "Preeclampsia: Características clínicas y diagnóstico" .)

● (Ver "Preeclampsia: manejo antes del parto y momento del parto" .)
● (Ver “Hipertensión crónica en el embarazo: Atención prenatal y posparto”, sección
“Pacientes con preeclampsia superpuesta” .)
● (Ver "Eclampsia" .)
● (Ver "Síndrome HELLP (hemólisis, enzimas hepáticas elevadas y plaquetas bajas)" .

PREDOMINIO

En un estudio de cohorte prospectivo de base poblacional que comenzó al comienzo del

embarazo (duración gestacional media de 14 semanas), se desarrolló hipertensión
gestacional en el 2 al 17 por ciento de la cohorte y preeclampsia en el 2 al 5 por ciento [ 10 ].
Los participantes con obesidad tuvieron la prevalencia más alta de hipertensión gestacional.

FACTORES DE RIESGO

Los factores de riesgo son similares a los de la preeclampsia (véase "Preeclampsia:

Características clínicas y diagnóstico", sección "Factores de riesgo" ). Sin embargo, estudios
epidemiológicos indican diferencias en la magnitud de las asociaciones con cada trastorno [
1 ].

HALLAZGOS CLÍNICOS Y DIAGNÓSTICO

Se debe sospechar hipertensión gestacional en una paciente embarazada con todos los
siguientes [ 11 ]:

● Nueva aparición de hipertensión (presión sistólica ≥140 mmHg y/o presión diastólica ≥90
mmHg) a las ≥20 semanas de gestación.

La elevación de la presión arterial generalmente debe documentarse al menos en dos

ocasiones con un intervalo mínimo de cuatro horas. Sin embargo, no es necesario ni
recomendable esperar horas para confirmar y tratar elevaciones graves de la presión
arterial (presión sistólica ≥160 mmHg o presión diastólica ≥110 mmHg).

● Excreción normal de proteínas en la orina durante el embarazo : la excreción normal

de proteínas en el embarazo es <300 mg por recolección de orina de 24 horas (o esta
cantidad extrapolada a partir de una recolección cronometrada), o una relación proteína-

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creatinina <0,3, o una lectura de la tira reactiva de orina <2+ (si no hay otros métodos
cuantitativos disponibles).

● Ausencia de signos y síntomas de disfunción de órganos terminales asociados a

preeclampsia con características graves, que se describen en la tabla ( tabla 1 ).

El diagnóstico de hipertensión gestacional se confirma después del parto si la paciente no

presenta posteriormente proteinuria o nuevos signos de disfunción de órganos terminales
(que son criterios para la preeclampsia) y la hipertensión no persiste ≥12 semanas después
del parto (lo que sugiere hipertensión crónica).

EVALUACIÓN DIAGNÓSTICA

Objetivos — Los principales objetivos en la evaluación inicial de pacientes embarazadas

con hipertensión de reciente desarrollo son:

● Confirmar presión arterial elevada (descartar hipertensión de bata blanca)

● Distinguir la hipertensión gestacional de la preeclampsia, que puede tener un curso
diferente y un pronóstico a corto plazo.

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 "Ambulatory blood pressure monitoring: Indications and procedure".)

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
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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
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"Hypertensive disorders in pregnancy: Approach to differential diagnosis" and "Urine drug

testing".)

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

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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:

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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 "Fetal assessment: Overview of antepartum tests of fetal well-
being".)

● 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

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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

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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].

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
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]. An ACOG practice
bulletin, based largely on expert opinion, suggested 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].

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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-
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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 in adults" and "Atherosclerotic cardiovascular disease risk
assessment for primary prevention in adults".)

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
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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 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)")

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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.)

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- 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

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pregnancies. The evidence for this recommendation is available separately. (See

"Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

Use of UpToDate is subject to the Terms of Use.

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GRAPHICS

In a patient with preeclampsia, the presence of one or more of the following

indicates 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.

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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 that 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

Oral contraceptives to 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

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Cushing 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 pulse
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 Elevated serum calcium

hyperparathyroidism

ACE: angiotensin-converting enzyme; ARB: angiotensin II receptor blocker; NSAID: nonsteroidal

antiinflammatory drug; VEGF: vascular endothelial growth factor.

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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 alcohol 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.
[Link] (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 crafft@[Link].

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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.

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* 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.

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

These criteria apply to singleton nonanomalous fetuses.

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

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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 (ISSHP) definition also includes signs
of uteroplacental dysfunction (eg, fetal growth restriction, abnormal angiogenic markers, abnormal
umbilical artery Doppler, abruption, fetal demise). The ISSHP also considers a platelet count
<150,000/microL rather than <100,000/microL consistent with preeclampsia.

* 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. Clasificación, diagnóstico y recomendaciones de manejo de la Sociedad
Internacional para el Estudio de la Hipertensión en el Embarazo de 2021 para la práctica internacional. Pregnancy
Hypertens 2022; 27:148.

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Abordaje diagnóstico y manejo de la hipertensión después de las 20 semanas

de gestación

Para obtener información detallada sobre el diagnóstico y el tratamiento de la preeclampsia y la

hipertensión gestacional, consulte el contenido de UpToDate sobre ambos trastornos.

* El parto generalmente está indicado, independientemente de la edad gestacional, dado el alto

riesgo de morbilidad materna grave. Sin embargo, la conducta expectante en un centro de atención
terciaria o en consulta con un especialista en medicina maternofetal es una opción para pacientes
seleccionadas que se encuentran lejos del término (<34 semanas de gestación) en quienes la presión
arterial puede controlarse.

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