INTRODUCTION — In pregnant women, chronic hypertension (also called preexisting hypertension) can be defined as hypertension known to be present before conception or first recognized before 20 weeks of gestation. In women with a previous pregnancy complicated by gestational hypertension, hypertension that persists 12 or more weeks post-delivery is also considered chronic.

Women with chronic hypertension are at risk for a variety of adverse maternal and fetal/neonatal outcomes (table 1), some of which can be mitigated by appropriate pregnancy management.

This topic will discuss the risks and management of pregnancy complicated by chronic hypertension. Treatment of high blood pressure in pregnancy is reviewed separately. (See "Treatment of hypertension in pregnant and postpartum patients".)

DEFINITION/DIAGNOSTIC CRITERIA — Diagnostic definitions for the various hypertensive disorders related to pregnancy are described in the table (table 2) [1,2].

Blood pressure criteria for hypertension in pregnancy are systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or both. Severe hypertension is defined as systolic blood pressure ≥160 mmHg, diastolic blood pressure ≥110 mmHg, or both [3]. In pregnant women who first present for prenatal care in the second trimester without recent prepregnancy blood pressure measurements for comparison, the diagnosis of chronic hypertension can be missed due to the normal physiologic decrease in blood pressure between 12 and 19 weeks of gestation: systolic and diastolic blood pressures are approximately 5 to 10 mmHg below baseline at this time. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes", section on 'Blood pressure and vascular resistance'.)

Blood pressure criteria for hypertension had been the same in pregnant and nonpregnant individuals until 2017, when the American College of Cardiology (ACC) and the American Heart Association (AHA) modified the traditional criteria for diagnosing hypertension in nonpregnant adults to better identify and modify long-term cardiovascular risk [4]. Under the new criteria, in nonpregnant adults [5]:

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

●Stage 1 hypertension – Systolic blood pressure 130 to 139 mmHg or diastolic blood pressure 80 to 89 mmHg.

●Stage 2 hypertension – Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg.

These new criteria are estimated to at least double the number of reproductive-age women in the United States diagnosed with chronic hypertension [4,6,7], but the pregnancy implications remain unclear. Emerging evidence suggests that women with stage 1 hypertension may be at increased risk of preeclampsia, gestational diabetes, small for gestational age newborn, and indicated preterm birth compared with women with normal blood pressures (<120 mmHg systolic and <80 mmHg diastolic) at the first-trimester visit [7-9]. In retrospective studies of deliveries before publication of the revised criteria, applying the lower blood pressure thresholds would increase identification of pregnancies at risk for development of hypertensive disorders of pregnancy by 20 percent [7,10] and would increase identification of pregnancies at risk for adverse neonatal outcome (small for gestational age, preterm birth, neonatal intensive care unit admission) by 3.8 percent [7].

In this topic, the term "chronic hypertension" will be used to refer to women who meet current ACC/AHA criteria for stage 2 hypertension unless otherwise noted. Further evidence is needed to determine whether pregnancy management should differ for those with stage 1 versus stage 2 hypertension. The American College of Obstetricians and Gynecologists suggests a conservative management approach to women with stage 1 hypertension, such as closer maternal monitoring during pregnancy [2]

EPIDEMIOLOGY — Among pregnant women in the United States, the prevalence of chronic hypertension is estimated to be 0.6 to 1.5 percent [11,12]. The prevalence has increased severalfold in recent decades, largely related to both increasing maternal age and obesity [12]. The prevalence is twofold higher in Black pregnant women compared with White pregnant women [12]. (See "Overweight and obesity in adults: Health consequences", section on 'Hypertension' and "Overweight, obesity, and weight reduction in hypertension".)

RISKS OF CHRONIC HYPERTENSION IN PREGNANCY — Chronic hypertension and cardiovascular disease are among the leading causes of maternal and fetal/neonatal morbidity and mortality (table 1) [11,13]. Superimposed preeclampsia, which develops in 13 to 40 percent of pregnant women with chronic hypertension, is associated with higher rates of adverse outcomes [14,15]. (See 'Women with superimposed preeclampsia' below.)

The frequency of adverse outcomes is difficult to cite precisely because reports do not uniformly distinguish between pregnancies complicated by superimposed preeclampsia and those with uncomplicated chronic hypertension alone. Where possible, we will review outcomes of patients with chronic hypertension alone, acknowledging that most analyses combine these outcomes with those in patients with superimposed preeclampsia.

Maternal risks — Population-based studies, as well as systematic reviews and meta-analyses, consistently demonstrate an increased risk of adverse maternal outcomes associated with chronic hypertension in pregnancy [11,12,16-19]. The risk increases with the severity of hypertension and presence of end-organ damage [20-23]. Although the relative risks (RR) for these complications are significantly increased, the absolute risk for serious end-organ damage (eg, heart, kidney, brain) is low in the absence of preeclampsia or uncontrolled hypertension. Obesity may be a confounder since it is associated with hypertension, diabetes, insulin resistance, chronic inflammation, and endothelial dysfunction [24].

●Acute kidney failure – 5.9 per 1000 deliveries (odds ratio [OR] 14.6, 95% CI 12.1-17.7) [11].

●Pulmonary edema – 1.5 per 1000 deliveries (OR 9.3, 95% CI 6.7-12.9) [11].

●Superimposed preeclampsia – 13 to 40 percent [11,14,15,25] (RR 7.7, 95% CI 5.7-10.1) [26].

●In-hospital mortality – 0.4 per 1000 deliveries (OR 6.2, 95% CI 3.3-11.5) [11].

●Stroke/cerebrovascular complications – 2.7 per 1000 deliveries (OR 5.4, 95% CI 4.3-6.9) [11].

●Cesarean delivery – Estimated prevalence 41.4 percent (95% CI 35.5-47.7) [17] (OR 2.7, 95% CI 2.4-3) [16].

●Placental abruption (adjusted OR 2.3, 95% CI 1.5-3.5) [19], with the highest risk in patients with superimposed preeclampsia [14,19,27].

●Postpartum hemorrhage (OR 2.2, 95% CI 1.4-3.7) [16].

●Gestational diabetes – 8.1 percent (adjusted OR 1.6, 95% CI 1.3-2.1) [16], likely reflecting common risk factors, such as obesity, and similar pathogenic mechanisms, such as insulin resistance [17,18,28].

●Hospitalization – Mean inpatient length of stay for chronic hypertension without preeclampsia 5.4 days (standard deviation [SD] 7 days) [25] and 12.7 days (SD 9.3) for superimposed preeclampsia; odds of length of stay >6 days (OR 6.7, 95% CI 6.2-7.3) [11,28].

Fetal/neonatal risks — Rates of adverse perinatal outcomes are higher with longer duration and greater severity of maternal hypertension, presence of end-organ damage, and occurrence of superimposed preeclampsia.

●Perinatal mortality – Perinatal mortality is two to four times higher in pregnancies complicated by chronic hypertension compared with pregnancies in the general obstetric population, and the increase persists after adjusting for preeclampsia and birth weight [16,26,29,30]. The increase in perinatal mortality is likely attributable to increases in indicated preterm birth and fetal growth restriction (FGR).

●Preterm birth, low birth weight, neonatal intensive care unit admission – In a meta-analysis comparing pregnancy outcomes of women with chronic hypertension with population-based data (55 studies, nearly 800,000 pregnancies), women with chronic hypertension had a threefold increase in pooled incidence of the following outcomes [26]:

•Preterm delivery <37 weeks (33 and 12 percent, respectively, RR 2.7, 95% CI 1.9-3.6).

•Birth weight <2500 grams (22 and 8 percent, respectively, RR 2.7, 95% CI 1.9-3.8).

•Newborns admitted to the neonatal intensive care unit (19 and 6 percent, respectively, RR 3.2, 95% CI 2.2-4.4).

●Small for gestational age – In a prospective cohort study of pregnant women receiving care in the United Kingdom that compared outcomes of those with chronic hypertension (n = 1417) to those without (n = 108,515), women with chronic hypertension were twice as likely to deliver a small for gestational age (SGA) infant (19.2 versus 10.9 percent, adjusted OR 2.06, 95% CI 1.79-2.39) [16]. The increased risk of SGA with chronic hypertension was not attributable to preeclampsia; in stratified analysis of those without preeclampsia, the odds of delivering an SGA neonate remained elevated for women with chronic hypertension alone (OR 1.66, 95% CI 1.41-1.95). Other reports indicate even higher rates of SGA for women with chronic hypertension, exceeding 30 percent [31,32].

●Congenital malformations – In both untreated and treated chronic hypertensive women, chronic hypertension in pregnancy has also been associated with an increased risk for congenital malformations, with RR estimates of congenital cardiac malformations ranging from 1.4 to 1.5 for untreated hypertension and 1.6 to 2 for treated hypertension [33,34]. Smaller studies have suggested an increase in other anomalies, including esophageal atresia and hypospadias [35]. Further investigation is needed to understand the pathophysiology underlying these associations. These findings warrant obtaining a standard fetal anatomic survey at 18 to 20 weeks of gestation, but not routine fetal echocardiography, which should be ordered selectively for standard indications. (See "Congenital heart disease: Prenatal screening, diagnosis, and management".)

Long-term prognosis

●Maternal – Both chronic hypertension and preeclampsia are clearly associated with increased cardiovascular risk in later life [36-40]. (See "Overview of hypertension in adults", section on 'Complications of hypertension' and "Preeclampsia: Management and prognosis", section on 'Long-term maternal risks of pregnancy-associated hypertension' and "Overview of atherosclerotic cardiovascular risk factors in females", section on 'Hypertensive disorder of pregnancy'.)

●Offspring – The existing data on long-term offspring outcomes of pregnancies complicated by chronic hypertension are largely population-based and do not always account for preeclampsia, medication use, severity of disease, and gestational age at birth. With these limitations, long-term follow-up of offspring of pregnancies complicated by hypertensive disorders in the Helsinki Birth Cohort showed a modest association with self-reported cognitive decline and mental and mood disorders [41-43].

PRECONCEPTION CARE — Ideally, women with chronic hypertension are seen prior to conception to address the following issues, which are summarized in the table (table 3), in addition to routine preconception assessments (see "The preconception office visit"). Maternal-fetal medicine consultation should be considered for counseling and management both preconception and during pregnancy.

●Counseling – Counseling is provided about the pregnancy risks of chronic hypertension and the potential interventions to minimize these risks. Patients are informed about the anticipated course of pregnancy, need for heightened maternal and fetal surveillance, and likely need for more frequent obstetric visits and possibly hospitalization (eg, if superimposed preeclampsia develops) compared with a low-risk population. (See 'Risks of chronic hypertension in pregnancy' above and 'Women with superimposed preeclampsia' below.)

●Consideration of secondary causes of hypertension – While the majority of hypertensive, reproductive-age women with chronic hypertension have essential (idiopathic or primary) hypertension, consideration of secondary causes of hypertension is important (summarized in the table (table 4)), if not already evaluated, since these causes can require specific testing and therapy, ideally before pregnancy. A finding suggestive of secondary hypertension is resistant hypertension, particularly in younger women (<30 years) with no family history of hypertension. (See "Initial evaluation of the hypertensive adult" and "Evaluation of secondary hypertension".)

●Laboratory tests

•Creatinine

•Urine protein/creatinine ratio or 24-hour urine protein

If abnormal, additional information on issues in pregnant women with chronic kidney disease is discussed in detail separately. (See "Pregnancy in women with nondialysis chronic kidney disease".)

●Cardiac evaluation – Baseline cardiac evaluation is recommended in women with long-standing hypertension, based on age or poorly controlled hypertension for more than four years, given the increased risk of cardiac hypertrophy, dysfunction, and ischemic heart disease [2]. Because of the enhanced detection of left ventricular hypertrophy and cardiac dysfunction, we utilize transthoracic echocardiography for baseline cardiac evaluation. When echocardiography is not available, a twelve-lead electrocardiogram can be used as an alternative first-line test. (See "Initial evaluation of the hypertensive adult".)

Issues in pregnant women with acquired heart disease are discussed in detail separately. (See "Acquired heart disease and pregnancy".)

●Blood pressure management – For patients who have achieved stable blood pressure control with pharmacotherapy and are considering pregnancy or attempting to conceive, the risks and benefits of continuing a stable antihypertensive drug regimen versus changing the regimen to the few drugs preferred for use in pregnant patients (labetalol, nifedipine, methyldopa) must be considered. We suggest shared decision-making involving the obstetrician/maternal-fetal medicine specialist, primary care provider, and patient. However, angiotensin converting enzyme inhibitors and angiotensin receptor blockers should be discontinued before pregnancy since they have been associated with fetal malformations, including renal dysgenesis and calvarial hypoplasia, as well as fetal growth restriction and oligohydramnios [44-46]. (See "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy", section on 'Clinical approach to use of RAAS inhibitors in females of childbearing potential'.)

In patients who have not achieved stable blood pressure control, blood pressure should be optimized with similar considerations about choice of drug therapy as described above. (See "Treatment of hypertension in pregnant and postpartum patients".)

●Modifiable risk factors – Weight loss in overweight and obese patients, smoking cessation in smokers, increased exercise for sedentary individuals, and dietary changes (eg, sodium restriction, Dietary Approaches to Stop Hypertension [DASH] diet) when appropriate are encouraged as nonpharmacologic means of reducing blood pressure and potentially improving pregnancy outcome and overall health. (See "Overview of hypertension in adults", section on 'Nonpharmacologic therapy' and "Exercise during pregnancy and the postpartum period" and "Obesity in pregnancy: Complications and maternal management" and "Tobacco and nicotine use in pregnancy: Cessation strategies and treatment options".)

PRENATAL CARE AND DELIVERY

Women with chronic hypertension — The following discussion applies to the prenatal care and delivery of women with chronic hypertension. Monitoring for development of superimposed preeclampsia is a key component of the prenatal care of these women. If it develops, pregnancy management needs to be modified because preeclampsia is a progressive and potentially life-threatening disease. (See 'Women with superimposed preeclampsia' below.)

Baseline clinical evaluation, laboratory testing, and preeclampsia prophylaxis

●Clinical evaluation should include baseline blood pressure and heart rate and a general physical examination, including cardiopulmonary auscultation and evaluation for any signs of cardiac dysfunction (ie, cyanosis, hepatomegaly, jugular venous distention, pulmonary edema).

●In addition to routine prenatal laboratory testing, the following laboratory tests are recommended, if not obtained within the six months prior to conception:

•Creatinine

•Urine protein/creatinine ratio or 24-hour urine protein

We also obtain liver transaminases (aspartate aminotransferase and alanine aminotransferase) and a platelet count as a baseline, as this information is useful if the patient exhibits signs/symptoms of preeclampsia later in pregnancy. We obtain electrolytes in patients with renal dysfunction.

●If not assessed within one year prior to conception, transthoracic echocardiography or twelve-lead electrocardiogram are suggested for women with long-standing hypertension, based on age or poorly controlled hypertension for more than four years [2]. Cardiac dysfunction increases morbidity in pregnancy and delivery given the increase in cardiac output and cardiac stress. (See 'Preconception care' above.)

●Accurate gestational dating is particularly important given the increased risks for growth restriction and indicated preterm delivery in patients with chronic hypertension. Whether to perform an ultrasound examination in the first trimester or wait until the time of the 18- to 20-week fetal anatomic survey depends on the clinician's confidence in the menstrual dates. (See "Prenatal assessment of gestational age, date of delivery, and fetal weight".)

●Low-dose aspirin is recommended after 12 weeks of gestation for prevention of preeclampsia as these patients are at high risk of developing the disease [47]. Some have advocated doses of ≥100 mg daily based on a meta-analysis of eight trials [48]. However, there was significant heterogeneity, and none directly compared the higher doses with 81 mg. Based on the existing evidence and dose availability in the United States, we use 81 mg daily. (See "Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

●Initiation and discontinuation of antihypertensive therapy are discussed below. (See 'Blood pressure management' below.)

Diet and gestational weight gain — Women should be encouraged to meet gestational weight gain targets that are appropriate for their body mass index (table 5). In particular, excessive gestational weight gain should be avoided because increased adiposity is strongly associated with higher blood pressure. Excessive gestational weight gain can also lead to significant postpartum weight retention. (See "Gestational weight gain", section on 'Recommendations for gestational weight gain'.)

There is minimal information on the effects of initiating a low salt or Dietary Approaches to Stop Hypertension (DASH) diet before pregnancy or continuing it throughout pregnancy [49-51]. These are healthy dietary approaches and would be reasonable to continue during pregnancy.

Ongoing maternal monitoring — Obstetric provider visits should include evaluation of blood pressure and potential symptoms of superimposed preeclampsia. More frequent visits than standard schedules (ie, every 4 weeks until 28 to 30 weeks, every 2 weeks until 35 weeks, then weekly) for blood pressure monitoring may be needed in the setting of poorly controlled blood pressure or if ongoing medication titration is needed.

●Blood pressures should be measured with the appropriate sized cuff, proper positioning, and rest period; ideally, a blood pressure cuff that has been validated in pregnancy should be used [52,53]. Home blood pressure monitoring is reliable, useful to complement office visits, and may reduce office visits and the need for hospitalization [54,55], although there are limitations to available data [56]. We use this approach in our practice. In a meta-analysis, systolic blood pressure values measured at home were lower than office values by 4 mmHg (95% CI –6 to –3) and diastolic measurements were lower by 3 mmHg (95% CI –4 to –2) [56]. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Technique for accurate measurement of blood pressure'.)

While worsening blood pressure, possibly in the late second trimester and more commonly in the third trimester, could indicate the anticipated physiologic rise in blood pressure in the second half of pregnancy, superimposed preeclampsia must be excluded, based on gestational age at onset, symptoms and laboratory studies, risk factors, and course over time. We recommend a low threshold for in-hospital evaluation if superimposed preeclampsia is suspected. (See 'Clinical presentation and evaluation' below.)

●Patient education on the symptoms and signs of preeclampsia and clear instructions on when to contact providers are essential. Symptoms of persistent and/or severe headache, visual changes (scotomata, photophobia, blurred vision, or temporary blindness [rare]), right upper quadrant or epigastric pain, new onset of nausea or vomiting in the third trimester, new onset of shortness of breath, altered mental status, or vaginal bleeding warrant additional investigation. (See "Preeclampsia: Clinical features and diagnosis", section on 'Clinical presentation'.)

Blood pressure management — Recommendations for management of severe hypertension and nonsevere chronic hypertension in pregnancy are reviewed below, along with supporting evidence. The optimal treatment of chronic hypertension in pregnancy, particularly mildly elevated blood pressure, continues to be debated, with few clinical trials specifically addressing this issue. Many studies combine patients with chronic hypertension and gestational hypertension, which may represent different pathophysiologic mechanisms. Varied study designs and inconsistent comparisons have limited the quality of evidence. Varying recommendations from leading pregnancy societies based on interpretation of the existing evidence has added to the lack of clarity.

Although the American College of Cardiology and the American Heart Association have published recommendations for management of chronic hypertension in nonpregnant individuals, these guidelines are not fully generalizable to pregnant women due to fetal safety concerns and the physiologic changes of pregnancy and because the long-term goals of adult hypertension treatment over the course of a lifetime are different from those of the short-term time frame of pregnancy.

Severe hypertension — Regardless of etiology (chronic hypertension, gestational hypertension, preeclampsia), there is consensus among medical organizations that severe maternal hypertension (systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg) should be pharmacologically treated in a timely manner to reduce maternal cerebrovascular, cardiac, and renal events as well as death [2,57,58]. Evidence for this recommendation is extrapolated from studies on the management of preeclampsia and on management of severe hypertension in nonpregnant adults, with few studies conducted exclusively in pregnant women with chronic hypertension [4,5,59]. (See "Preeclampsia with severe features: Expectant management remote from term", section on 'Potential consequences of severe disease' and "Management of severe asymptomatic hypertension (hypertensive urgencies) in adults" and "Evaluation and treatment of hypertensive emergencies in adults".)

The general principle is to gradually lower blood pressure out of the severely elevated range and into the mildly elevated range, thereby avoiding sudden hypotension and reduced flow in the uterine arteries. The precise blood pressure targets are less clear.

The choice of medication is based on need for acute versus chronic treatment of blood pressures as well as safety. Medications used for acute lowering of blood pressure in pregnancy include intravenous labetalol, intravenous hydralazine, or oral nifedipine (table 6). In a meta-analysis of 35 randomized trials involving 3573 women comparing one antihypertensive agent against another, no agent was clearly superior [59]. Thus, the choice of antihypertensive agent should depend on availability, the clinician's experience and familiarity with a particular drug, and adverse effects.

Nonsevere hypertension

Our approach for initiating or continuing therapy

●Patients not on antihypertensive therapy and without end-organ disease – For women with nonsevere hypertension (systolic blood pressure ≥140 and <160 mmHg or diastolic blood pressure ≥90 and <110 mmHg) who are not on antihypertensive therapy and have no end-organ involvement, we generally initiate this therapy when blood pressures approach the severe range in order to prevent development of severe maternal hypertension while minimizing fetal exposure.

After initiation of therapy, target blood pressure continues to be an area of controversy. Our target blood pressure range is 120 to 150/80 to 95 mmHg; a target range of 130 to 150/80 to 100 mmHg is also common. We use the fewest medications at the lowest effective dose to achieve this goal. (See 'Choice of drug and dosing' below.)

●Patients on antihypertensive therapy and without end-organ disease – For women with nonsevere hypertension on antihypertensive therapy with no end-organ involvement, our decision making is individualized. For most women with well-controlled blood pressures on an antihypertensive medication regimen with a good safety profile, it is reasonable to continue medications to decrease the occurrence of severe hypertension. As discussed above, our target blood pressure range is 120 to 150/80 to 95 mmHg; a target range of 130 to 150/80 to 100 mmHg is also common. However, it is also reasonable to discontinue medications during the first trimester to minimize fetal exposure and restart them if blood pressures approach the severe range. With this approach, close blood pressure monitoring is imperative, and the blood pressure changes, such as the decline in the midtrimester and rise in the third trimester, must be considered. (See 'Choice of drug and dosing' below.)

●Patients with end-organ disease – For women with nonsevere hypertension and end-organ involvement, such as cardiac or renal disease, the threshold for initiating or continuing antihypertensive therapy is lower: systolic blood pressure ≥150 mmHg or diastolic blood pressure ≥100 mmHg. (See 'Choice of drug and dosing' below.)

After initiation of therapy, it may be desirable to maintain blood pressure at 120 to 140/80 to 90 mmHg, though whether lowering blood pressure to a "normal" level (ie, <120/80 mmHg) would confer maternal benefit is unresolved [21]. The American Diabetes Association suggests treating pregnant women with diabetes and hypertension, with the blood pressure target of 110 to 135/85 mmHg to reduce the risk for accelerated maternal hypertension and minimize impaired fetal growth [60]. (See "Treatment of hypertension in patients with diabetes mellitus".)

Choice of drug and dosing — In women with nonsevere hypertension, our preference is to start treatment with either labetalol, a long-acting calcium channel blocker (eg, extended-release nifedipine), or methyldopa (table 7). If maximum doses of one drug are ineffective to achieve the goal blood pressure range as discussed above, then a second or third drug can be added. It is important to closely monitor women in whom blood pressure is not responding well to antihypertensive therapy since this may be a sign of preeclampsia. (See 'Clinical presentation and evaluation' below.)

Evidence of potential benefits of treatment — The body of data indicates that treatment of chronic hypertension in pregnancy reduces the occurrence of severe hypertension. Treatment does not appear to significantly reduce other adverse pregnancy outcomes; however, these data are less consistent.

●In a 2022 network meta-analysis of 72 randomized trials including nearly 7000 participants addressing which antihypertensives are superior to placebo/no therapy or another antihypertensive for controlling nonsevere pregnancy hypertension, major findings were [61]:

•Commonly used antihypertensive drugs reduced the occurrence of severe hypertension by 30 to 70 percent compared with placebo/no treatment

•Labetalol decreased proteinuria/preeclampsia (odds ratio [OR] 0.73, 95% CI 0.54–0.99) and fetal/newborn death (OR 0.54, 95% CI 0.30–0.98) compared with placebo/no therapy

•Labetalol decreased proteinuria/preeclampsia compared with methyldopa (OR 0.66, 95% CI 0.44–0.99) and calcium channel blockers (OR 0.63, 95% CI 0.41–0.96).

No other differences were identified. The possible benefit of labetalol over other antihypertensive drugs should be interpreted with caution given the wide confidence intervals.

Although some have opined that reducing the chances of developing severe hypertension is not in itself an important outcome because progression to severe hypertension is an event that can be identified and treated before complications occur, experts have cautioned against making this assumption. They point out that the failure to identify and treat severe maternal hypertension has been recognized in reviews of maternal deaths as the single most important failure in the care of women with pregnancy hypertension [62].

Evidence of potential harms of treatment — Other data suggest potential harms from blood pressure reduction.

●In a network meta-analysis of the comparative efficacy and safety of oral antihypertensive agents in pregnant women with chronic hypertension (14 randomized trials and 8 cohort studies), atenolol was associated with an increased risk for small for gestational age infants (OR 26, 95% CI 2.6-259.3) [63].

●In a meta-regression including over 2300 pregnant women (some with chronic hypertension and most with late-onset hypertension), a 10 mmHg reduction in mean arterial pressure was associated with a 176 gram decrease in infant birth weight [64].

●Subsequently, the international multicenter randomized Control of Hypertension in Pregnancy Study (CHIPS) was designed specifically to test the effects of less tight control (target diastolic blood pressure 100 mmHg) versus tight control (target diastolic blood pressure 85 mmHg) on pregnancy complications [62,65]. Importantly, 75 percent of the 987 women included in the trial had chronic hypertension. Women with severe hypertension were included as long as systolic blood pressure was below 160 mmHg with treatment. Major findings were:

•In a subgroup analysis of women with chronic hypertension, less tight blood pressure control appeared to result in a lower incidence of SGA (adjusted OR 0.66, 95% CI 0.44-1.00); however, in the overall study, the less tight and tight groups had a similar incidence of SGA (16 versus 20 percent for birth weight <10^th centile, OR 0.78, 95% CI 0.56-1.08).

•The achieved blood pressures in the less tight and tight groups were 139/90 and 133/85 mmHg, respectively, and, similar to previous studies, severe hypertension (≥160/110 mmHg) developed significantly more often in the less tight control group (40.6 versus 27.5 percent).

•Both groups had similar rates of the primary outcome (perinatal loss or high-level neonatal care for >48 hours: 31 percent in both) and secondary outcome (serious maternal complications: 3.7 versus 2 percent, OR 1.74, 95% CI 0.79-3.84).

Although this was a well-designed randomized trial, key concerns have been raised with respect to extrapolating the results of CHIPS to women with mild and moderate chronic hypertension. The sample size was inadequate to evaluate key perinatal outcomes such as SGA and indicated preterm birth. In addition, only a small percentage of women with mild-moderate hypertension were enrolled prior to 20 weeks, and over one-half of the women stayed on antihypertensive therapy at randomization, so there was inadequate comparison between antihypertensive therapy and no therapy.

Recommendations of selected medical organizations — Based on their interpretation of existing data (particularly the CHIPS trial) and the reduction in maternal morbidity associated with severe hypertension, key medical organizations have provided varying recommendations regarding blood pressure management for pregnant women with chronic hypertension.

●American College of Obstetricians and Gynecologists (ACOG) – ACOG recommends not initiating medication therapy for mild chronic hypertension in pregnancy (>140/90 mmHg and <160/110 mmHg) given the limited evidence for a clear benefit and safety of treatment [2]. In addition, ACOG recommends considering discontinuing medication in women with mild hypertension who become pregnant and recommending lifestyle modifications (diet, exercise).

Pharmacologic therapy is recommended for pregnant women with severe hypertension (systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥105 to 110 mmHg) since the short-term benefits for women and fetuses are well-defined. A lower threshold for initiation of medications (≥150/100 mmHg) is recommended for women with end-organ involvement, such as cardiac or renal disease.

For most women, the blood pressure target is systolic blood pressure ≥120 and <160 mmHg and diastolic blood pressure ≥80 and <110 mmHg. ACOG has not made specific recommendations for women with end-organ involvement.

●National Institute for Health and Care Excellence (NICE) – NICE guidelines recommend offering treatment for systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, with goal blood pressures of <135/85 mmHg [58].

●International Society for the Study of Hypertension in Pregnancy (ISSHP) – The ISSHP recommends pharmacologic therapy to keep blood pressures in the range of 110 to 140 mmHg/80 to 85 mmHg during pregnancy [57].

Screening for fetal growth restriction — Our general approach to screening for fetal growth restriction (FGR) in women with chronic hypertension is to perform serial ultrasound examinations to monitor fetal growth every three to four weeks. We initiate sonographic screening for FGR at 28 to 32 weeks but will perform an earlier examination if there is a clinical suspicion of FGR (eg, size << dates).

Despite the consistent association between chronic hypertension and SGA in meta-analyses, the optimal timing and frequency of screening for FGR have not been determined. Furthermore, while it is generally accepted that detection of FGR and intervention (close monitoring, early delivery) will improve perinatal outcomes, several observational studies have failed to show a reduction in perinatal mortality [66-68]. (See "Fetal growth restriction: Screening and diagnosis" and "Fetal growth restriction: Evaluation and management".)

Tests to monitor fetal well-being — We take the following approach to fetal surveillance in pregnant women with chronic hypertension, while acknowledging the high degree of uncertainty regarding preferred strategies for optimizing perinatal outcomes:

●We suggest daily assessment of fetal kick counts starting at 28 weeks of gestation; <10 fetal movements in two hours should prompt further assessment of fetal well-being. Maternal assessment of fetal movement, or fetal kick counts, is an inexpensive and easily implemented method to assess fetal well-being and, when normal, generally reassuring to mothers; however, its value for reducing perinatal mortality is unproven. (See "Decreased fetal movement: Diagnosis, evaluation, and management".)

●As chronic hypertension has been consistently demonstrated to confer an increased risk for stillbirth (see 'Fetal/neonatal risks' above) and most studies have not distinguished between severe or mild hypertensive disease, we perform routine fetal surveillance on all pregnancies complicated by chronic hypertension. We initiate twice weekly fetal surveillance at 32 weeks of gestation because routine surveillance is unlikely to improve perinatal outcomes when implemented earlier in gestation [69]. Twice weekly rather than weekly fetal testing is performed routinely based on limited evidence suggesting a reduction in fetal deaths with frequent testing [70]. Testing may be started earlier and performed more frequently in patients thought to be at high risk of early stillbirth. ACOG recommends antenatal fetal surveillance for pregnant individuals with chronic hypertension who need medication or who have fetal growth restriction, superimposed preeclampsia, or underlying medical conditions that may affect fetal outcome, as these pregnancies are at increased risk for fetal demise [71,72]. For patients with hypertension that is well-controlled with medication, they suggest weekly testing beginning at 32 weeks; initiation and frequency of testing are individualized for patients with poorly controlled hypertension.

Comparison of serial nonstress tests, biophysical profiles (BPPs), or modified BPPs reveals no significant difference in perinatal mortality rates associated with any specific modality of fetal surveillance [73]. The choice among these tests should be based on provider preference and other local factors.

●In pregnancies with FGR, management based on umbilical artery Doppler ultrasound findings is recommended as it has been demonstrated to reduce perinatal mortality [74-76]. (See "Fetal growth restriction: Evaluation and management" and "Fetal growth restriction: Evaluation and management", section on 'Umbilical artery'.)

Delivery

Timing

●We recommend delivery at 39+0 to 39+6 weeks of gestation for women with well-controlled chronic hypertension alone and no indications for earlier delivery (eg, uncontrolled hypertension, superimposed preeclampsia, previous stillbirth, abruption in the current or past pregnancy, FGR).

An analysis of perinatal outcome data from over 170,000 women with chronic hypertension (both with and without superimposed preeclampsia) concluded that delivery at 38+0 to 39+6 weeks appeared to provide the optimal trade-off between the risk of adverse fetal and adverse neonatal outcomes [77]. We prefer to wait until 39 weeks because of the clearly demonstrated risks associated with iatrogenic delivery before 39+0 weeks [78,79] and the increased likelihood of more favorable perinatal outcomes in women with chronic hypertension alone.

ACOG suggested the following approach for delivery of women with chronic hypertension [2]:

•≥38+0 to 39+6 weeks of gestation for women not requiring medication

•≥37+0 to 39+0 weeks for women with hypertension controlled with medication

•34+0 to 36+6 weeks for women with severe hypertension that is difficult to control

The ranges allow for clinician judgment on a case-by-case basis, with consideration of factors such as steady-state levels of and trends in blood pressure, fetal growth and amniotic fluid volume, and cervical status. The Society of Obstetricians and Gynaecologists of Canada also states that women with uncomplicated preexisting hypertension who are otherwise well should be considered for delivery at 38+0 to 39+6 weeks of gestation [80].

For women with superimposed preeclampsia or other pregnancy complications, the timing of delivery should be decided on a case-by-case basis based on the type and severity of these complications. (See 'Women with superimposed preeclampsia' below and "Placental abruption: Management and long-term prognosis" and "Stillbirth: Incidence, risk factors, etiology, and prevention" and "Fetal growth restriction: Evaluation and management", section on 'Timing of delivery'.)

Intrapartum care

●Intrapartum management of women with chronic hypertension should be driven by the same principles guiding intrapartum management in the general obstetric population. Cesarean delivery should be reserved for standard obstetric indications. (See "Management of normal labor and delivery".)

●Intrapartum magnesium sulfate therapy for seizure prophylaxis is not indicated in the absence of superimposed preeclampsia as the risk of seizure is less than 0.1 percent [81]. In women with chronic kidney disease on magnesium sulfate for fetal/neonatal neuroprotection, close maternal monitoring is essential for prevention and early recognition of magnesium toxicity. (See 'Management' below and "Preeclampsia: Management and prognosis", section on 'Signs of magnesium toxicity'.)

●The goal of intrapartum blood pressure management is to prevent maternal cerebrovascular or coronary events while minimizing rapid fluctuations in blood pressure that could influence uterine perfusion [59]. Antihypertensive medication regimens started prior to labor should be continued intrapartum. Rapid-acting medications should be used for blood pressures ≥160 mmHg systolic or ≥110 mmHg diastolic that persist for 15 minutes or more, with intravenous labetalol or hydralazine the preferred first-line agents (table 6) [3]. ACOG endorses use of immediate-release oral nifedipine as a first-line option for emergency treatment of acute, severe hypertension in pregnancy, particularly when intravenous access is not in place.

●Volume status (fluid intake and output) should be recorded, with the goal of maintaining euvolemia. Maintenance of euvolemia during labor is particularly important in women with a long-standing history of hypertension and left ventricular hypertrophy and/or diastolic dysfunction, as they are predisposed to pulmonary edema with volume overload, whereas volume depletion can lead to tachycardia and reduced filling times, exacerbating any preexisting diastolic dysfunction.

Women with superimposed preeclampsia

Definition/diagnostic criteria — Preeclampsia is considered superimposed when it occurs in a woman with preexisting chronic hypertension. In women with chronic hypertension, distinguishing superimposed preeclampsia from third-trimester physiologic increases in blood pressure and proteinuria can be challenging.

Superimposed preeclampsia is likely when any of the following are present:

●A sudden increase in blood pressure that was previously well-controlled or a need for a rapid escalation of antihypertensive medications to control blood pressure.

●The new onset of proteinuria or a sudden increase in proteinuria in a woman with known prepregnancy or early pregnancy proteinuria. A sudden increase in proteinuria is not precisely defined by various societies or in the existing literature. Based on limited evidence, we typically diagnose superimposed preeclampsia when the level of proteinuria increases 100 percent from baseline in women with preexisting renal disease or proteinuria [82].

The presence of any of the following severe features of preeclampsia supports the diagnosis of superimposed preeclampsia with severe features:

●Severely elevated blood pressure despite increasing antihypertensive therapy.

●Thrombocytopenia (platelet count <100,000/microliter).

●Elevated transaminases (two times the upper limit of the normal concentration for a particular laboratory) or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses, or both.

●New-onset or worsening renal insufficiency.

●Pulmonary edema.

●Persistent cerebral or visual disturbances.

In the absence of severe features, there may be ambiguity in the diagnosis of superimposed preeclampsia. Given the risk of disease progression and adverse outcomes, increased vigilance is recommended whenever the diagnosis is suspected.

Incidence and risk factors — Superimposed preeclampsia develops in 13 to 40 percent of pregnant women with chronic hypertension. The risk for developing superimposed preeclampsia is higher in patients with long-standing, severe, or secondary hypertension; obesity; Black race; history of preeclampsia; and smoking [25].

Clinical presentation and evaluation — The clinical presentation of superimposed preeclampsia is similar to that in women without chronic hypertension, and their evaluation should be the same. (See "Preeclampsia: Clinical features and diagnosis", section on 'Clinical presentation' and "Preeclampsia: Clinical features and diagnosis", section on 'Patient evaluation'.)

Results of laboratory testing should be compared with baseline information obtained early in pregnancy. As discussed above, new-onset proteinuria or a sudden large increase in protein excretion along with one or more features of severe disease strongly supports the diagnosis. However, in women with long-standing kidney disease or kidney disease of unknown duration, changes in creatinine level and proteinuria should be cautiously interpreted before a definitive diagnosis of superimposed preeclampsia is made. (See "Hypertensive disorders in pregnancy: Approach to differential diagnosis".)

Management — Upon diagnosis of superimposed preeclampsia, management of women with chronic hypertension is generally similar to that of other women with preeclampsia. (See "Preeclampsia: Management and prognosis".)

Some considerations for women with superimposed preeclampsia include:

●Women with superimposed preeclampsia should initially be monitored in the inpatient setting. If there are no severe features, outpatient monitoring may be considered if the woman remains stable, has no severe features of preeclampsia, and is able to comply with self-monitoring and frequent visits. While outpatient care after a period of inpatient monitoring may be a reasonable option for women with superimposed preeclampsia without severe features, those with severe features should be in the hospital until delivery.

●As with preeclampsia, administration of betamethasone for preterm gestations and antihypertensive therapy to treat severe range blood pressures are important considerations. (See "Preeclampsia: Management and prognosis", section on 'Components of expectant management'.)

●Timing and indications for delivery with superimposed preeclampsia are based on gestational age, disease severity, progression of disease, and results of ongoing assessment of maternal and fetal well-being. With any attempts to prolong pregnancy, the potential neonatal benefits must be weighed against the risk of maternal harm. (See "Preeclampsia: Management and prognosis".)

Small retrospective studies of women with preterm superimposed preeclampsia with severe features report that outcomes are similar to those observed with expectant management of preterm preeclampsia with severe features [83,84]. Although these studies are small and limited by their study design, they suggest that a similar approach to management is reasonable. (See "Preeclampsia with severe features: Expectant management remote from term".)

●The frequency of eclampsia in women with superimposed preeclampsia is not well-defined but is up to 2.4 percent based on observational and retrospective studies [25,83]. We administer magnesium sulfate peripartum for seizure prophylaxis to women who have superimposed preeclampsia with severe features. Other UpToDate authors administer seizure prophylaxis to all women with preeclampsia. In women with chronic kidney disease on magnesium sulfate for prevention of seizures or fetal/neonatal neuroprotection, close maternal monitoring is essential for prevention and early recognition of magnesium toxicity. (See "Preeclampsia: Management and prognosis", section on 'Seizure prophylaxis' and "Preeclampsia: Management and prognosis", section on 'Signs of magnesium toxicity'.)

●Intrapartum and postpartum, volume status and fluid management are of particular importance as increased third-spacing from preeclampsia may predispose to pulmonary edema. (See "Preeclampsia: Management and prognosis", section on 'Fluids'.)

Recurrence risk — Reports regarding the recurrence risk of superimposed preeclampsia are variable. In one study that was based on a secondary analysis of a larger antioxidant trial, women with chronic hypertension and prior preeclampsia had a 1.95-fold increase in risk of superimposed preeclampsia [25]. By contrast, a secondary analysis of a United States-based antioxidant trial found that the risk of superimposed preeclampsia was similar in women with chronic hypertension and prior preeclampsia and those with no prior preeclampsia [85]. Placental abruption, perinatal death, and SGA infant were also similar between groups, but there was a trend toward a higher rate of preterm delivery <37 weeks in patients with prior preeclampsia (36.9 versus 27.1 percent). Counseling regarding future pregnancy risk should be based on these data and those available for chronic hypertension in pregnancy overall.

POSTPARTUM CARE

Analgesia — The decision to use nonsteroidal anti-inflammatory drugs (NSAIDs) for analgesia should be individualized as these drugs are known to cause elevations in blood pressure in nonpregnant individuals with hypertension. (See "NSAIDs and acetaminophen: Effects on blood pressure and hypertension".)

Overall, the body of data supports the safe use of NSAIDs in postpartum patients with blood pressure issues [86] and their use in patients with hypertension is supported by the American College of Obstetricians and Gynecologists [87]. If blood pressure is elevated in the postpartum period, we use acetaminophen as our first-line medication for pain management. NSAIDs should be used preferentially over opioid analgesics, when possible. However, we avoid post-delivery NSAID use in women with preexisting renal disease and/or elevated serum creatinine levels. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Management'.)

Blood pressure management — Blood pressure control is an ongoing issue during the postpartum period, even in women with chronic hypertension who did not require antihypertensive therapy during pregnancy. Blood pressure often declines immediately after delivery and continues to decline for a few days before increasing three to five days after delivery when the woman may already be at home [88]. The immediate decline is generally attributed to blood loss and the effects of analgesia, while the subsequent increase is likely due to mobilization of extravascular fluid with a rise in intravascular volume, as well as factors such as pain.

Early postpartum visits for a blood pressure check (within 3 to 10 days after delivery [2]) or home blood pressure monitoring, particularly in the first two weeks post-delivery, is recommended. Home blood pressure monitoring strategies are likely to be helpful given the often suboptimal compliance with postpartum visits [89]. The risk for developing severe hypertension postpartum was illustrated in a retrospective cohort study of 235 women with chronic hypertension in which 13 percent developed severe hypertension postpartum [90]. At discharge, these women had mean systolic and diastolic blood pressures of 141 and 78 mmHg, respectively, and 87 percent were discharged on antihypertensive medications.

Choice of medications for blood pressure control is the same as during pregnancy, or the patient's prepregnancy antihypertensive regimen can be resumed after delivery, with consideration of safety in breastfeeding. Dose adjustments of antepartum regimens may be needed to reflect the decrease in volume of distribution and glomerular filtration rate that occurs after delivery [91]. If volume overload is suspected or diagnosed, then diuresis should be considered.

Family planning — Contraception and appropriate timing of future pregnancies should be discussed. Estrogen-containing contraceptive agents are generally avoided in women with stage 2 hypertension or higher (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg) even if well-controlled because the theoretic or proven risks generally exceed the benefits, and good alternatives are available. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Eligibility criteria (WHO and CDC)'.)

Referral for primary care — Women with known chronic hypertension should resume care with their primary care provider postpartum. Women with chronic hypertension first diagnosed during pregnancy or in the postpartum period based on persistently elevated blood pressure 12 weeks after delivery should be referred to a primary care provider for ongoing management of hypertension, which may persist or resolve. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Long-term occurrence of chronic hypertension in patients with hypertension presenting in pregnancy'.)

The pregnancy/postpartum time frame is an opportunity to educate women regarding the long-term risks of hypertension and the importance of ongoing care, which may help to ensure follow-up with a primary care provider for long-term management of chronic hypertension and cardiovascular risks. (See "Overview of hypertension in adults".)

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".)

SUMMARY AND RECOMMENDATIONS

●Diagnosis – Blood pressure criteria for hypertension in pregnancy are systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or both. Severe hypertension is defined as systolic blood pressure ≥160 mmHg, diastolic blood pressure ≥110 mmHg, or both. Diagnostic definitions/criteria for the various hypertensive disorders related to pregnancy are described in the table (table 2). (See 'Definition/diagnostic criteria' above.)

The diagnosis of superimposed preeclampsia is challenging in the absence of severe features of preeclampsia. Given the risk of disease progression and adverse outcomes, increased vigilance is recommended whenever the diagnosis is suspected. Management is the same as that in other women with preeclampsia. (See 'Women with superimposed preeclampsia' above.)

●Overview of management

•Preconception – Ideally, women with chronic hypertension are assessed prior to conception to address the issues described in the table (table 3), in addition to routine preconception assessments. Maternal-fetal medicine consultation should be considered for counseling and management both preconception and during pregnancy. (See 'Preconception care' above.)

•Early pregnancy evaluations – Baseline laboratory and cardiac evaluation is repeated at the first prenatal visit (table 3), if not recently performed. In addition, accurate gestational dating is important since these pregnancies are at increased risk for developing fetal growth restriction (FGR) and undergoing obstetrically indicated preterm delivery. (See 'Baseline clinical evaluation, laboratory testing, and preeclampsia prophylaxis' above.)

•Low dose aspirin prophylaxis – Low-dose aspirin is recommended after 12 weeks of gestation for prevention of preeclampsia as these patients are at high risk of developing the disease. (See "Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

•Monitoring for FGR – We monitor for FGR beginning at 28 to 32 weeks and initiate twice weekly nonstress tests or biophysical profiles at 32 weeks.

•Timing of delivery – We suggest delivery at 39+0 to 39+6 weeks of gestation for women with well-controlled chronic hypertension alone and no standard indications for earlier delivery. (See 'Timing' above.)

•Use of intrapartum magnesium sulfate – Intrapartum magnesium sulfate therapy for seizure prophylaxis is not indicated in the absence of superimposed preeclampsia. Antihypertensive medication regimens started prior to labor should be continued intrapartum, and severe hypertension should be treated promptly (table 6). (See 'Intrapartum care' above.)

•Postpartum monitoring – Postpartum visits for a blood pressure check within 3 to 10 days after delivery or home blood pressure monitoring is recommended as severe hypertension can develop after hospital discharge. (See 'Blood pressure management' above.)

●Treatment of hypertension

•Severe hypertension – Severe maternal hypertension (systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg) should be pharmacologically treated in a timely manner to reduce the risk for stroke. Options for drug therapy are shown in the table (table 6). (See 'Severe hypertension' above.)

•Nonsevere hypertension – Our approach to women with nonsevere chronic hypertension depends on whether there is end-organ involvement. Oral antihypertensive therapy dosing is shown in the table (table 7). (See 'Nonsevere hypertension' above.)

No end-organ involvement:

-For women with nonsevere hypertension (systolic blood pressure ≥140 and <160 mmHg or diastolic blood pressure ≥90 and <110 mmHg) not on antihypertensive therapy and with no end-organ involvement, we generally initiate this therapy when blood pressures approach the severe range in order to prevent development of severe maternal hypertension while minimizing fetal exposure. After initiation of therapy, our target blood pressure range is 120 to 150/80 to 95 mmHg.

-For women with nonsevere hypertension on antihypertensive therapy with no end-organ involvement, our decision-making is individualized. It is reasonable to discontinue medications during the first trimester and restart them if blood pressures approach the severe range.

End-organ involvement:

-For women with nonsevere hypertension and end-organ involvement, our threshold for initiating or continuing antihypertensive therapy is lower: systolic blood pressure ≥150 mmHg or diastolic blood pressure ≥100 mmHg. After initiation of therapy, our target blood pressure is 120 to 140/80 to 90 mmHg.

●Pregnancy outcome – Chronic hypertension is associated with substantial maternal and fetal/neonatal morbidity and mortality (table 1). Superimposed preeclampsia increases the risk of adverse outcomes. (See 'Risks of chronic hypertension in pregnancy' above.)