Gestational hypertension

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 Basics patient education pieces are written in plain language, at the 5^th to 6^th 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 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

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

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

SUMMARY AND RECOMMENDATIONS

●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

•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'.)