* This is the Professional Version. *
Hypertension in Pregnancy
(See also Overview of Hypertension .)
Hypertension (systolic BP ≥ 140 mm Hg, diastolic BP ≥ 90 mm Hg, or both) during pregnancy can be classified as one of the following:
Chronic: BP is high before pregnancy or before 20 wk gestation. Chronic hypertension complicates about 1 to 5% of all pregnancies.
Gestational: Hypertension develops after 20 wk gestation (typically after 37 wk) and remits by 6 wk postpartum; it occurs in about 5 to 10% of pregnancies, more commonly in multifetal pregnancy.
Both types of hypertension increase risk of preeclampsia, eclampsia (see Preeclampsia and Eclampsia ), and other causes of maternal mortality or morbidity, including hypertensive encephalopathy, stroke, renal failure, left ventricular failure, and the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Risk of fetal mortality or morbidity increases because of decreased uteroplacental blood flow, which can cause vasospasm, growth restriction, hypoxia, and abruptio placentae. Outcomes are worse if hypertension is severe (BP > 160/110 mm Hg) or accompanied by renal insufficiency (eg, creatinine clearance < 60 mL/min, serum creatinine > 2 mg/dL [> 180 μmol/L]).
BP is measured routinely at prenatal visits. If severe hypertension occurs for the first time in pregnant women who do not have a multifetal pregnancy or gestational trophoblastic disease, tests to rule out other causes of hypertension (eg, renal artery stenosis, coarctation of the aorta, Cushing syndrome, SLE, pheochromocytoma) should be considered (see Overview of Hypertension : Testing).
For mild hypertension, conservative measures followed by antihypertensives if needed
Methyldopa, β-blockers, or Ca channel blockers tried first
Avoidance of ACE inhibitors, angiotensin II receptor blockers (ARBs), and aldosterone antagonists
For moderate or severe hypertension, antihypertensive therapy, close monitoring, and, if condition worsens, possibly termination of pregnancy or delivery, depending on gestational age
Treatment of mild to moderate hypertension without renal insufficiency during pregnancy is controversial; the issues are whether treatment improves outcome and whether the risks of drug treatment outweigh risks of untreated disease. Because the uteroplacental circulation is maximally dilated and cannot autoregulate, decreasing maternal BP with drugs may abruptly decrease uteroplacental blood flow. Diuretics reduce effective maternal circulating blood volume; consistent reduction increases risk of fetal growth restriction. However, hypertension with renal insufficiency is treated even if hypertension is mild or moderate.
Recommendations for chronic and gestational hypertension are similar and depend on severity. However, chronic hypertension may be more severe. In gestational hypertension, the increases in BP often occur only late in gestation and may not require treatment.
For mild to moderate hypertension (systolic BP 140 to 159 mm Hg or diastolic BP 90 to 109 mm Hg) with labile BP, reduced physical activity may decrease BP and improve fetal growth, making perinatal risks similar to those for women without hypertension. However, if this conservative measure does not decrease BP, many experts recommend drug therapy. Women who were taking methyldopa, a β-blocker, a Ca channel blocker, or a combination before pregnancy may continue to take these drugs. However, ACE inhibitors and ARBs should be stopped once pregnancy is confirmed.
For severe hypertension (systolic BP ≥ 160 mm Hg or diastolic BP ≥ 110 mm Hg), drug therapy is indicated. Risk of complications—maternal (progression of end-organ dysfunction, preeclampsia) and fetal (prematurity, growth restriction, stillbirth)—is increased significantly. Several antihypertensives may be required.
For systolic BP > 180 mm Hg or diastolic BP > 110 mm Hg, immediate evaluation is required. Multiple drugs are often required. Also, hospitalization may be necessary for much of the latter part of pregnancy. If the woman’s condition worsens, pregnancy termination may be recommended.
All women with chronic hypertension during pregnancy should be taught to self-monitor BP, and they should be evaluated for target organ damage. Evaluation, done at baseline and periodically thereafter, includes
Maternal echocardiography should be considered if women have had hypertension for > 4 yr. Ultrasonography is done monthly to monitor fetal growth; antenatal testing begins at 32 wk or, if complications develop, sooner. Delivery should occur by 37 to 39 wk but may be induced earlier if preeclampsia or fetal growth restriction is detected or if fetal test results are nonreassuring.
First-line drugs for hypertension during pregnancy include
Initial methyldopa dose is 250 mg po bid, increased as needed to a total of 2 g/day unless excessive somnolence, depression, or symptomatic orthostatic hypotension occurs.
The most commonly used β-blocker is labetalol (a β-blocker with some α1-blocking effects), which can be used alone or with methyldopa when the maximum daily dose of methyldopa has been reached. Usual dose of labetalol is 100 mg bid to tid, increased as needed to a total maximum daily dose of 2400 mg. Adverse effects of β-blockers include increased risk of fetal growth restriction, decreased maternal energy levels, and maternal depression.
Extended-release nifedipine, a Ca-channel blocker, may be preferred because it is given once/day (initial dose of 30 mg; maximum daily dose of 120 mg); adverse effects include headaches and pretibial edema. Thiazide diuretics are only used to treat chronic hypertension during pregnancy if the potential benefit outweighs the potential risk to the fetus. Dose may be adjusted to minimize adverse effects such as hypokalemia.
Several classes of antihypertensives are usually avoided during pregnancy:
ACE inhibitors are contraindicated because risk of fetal urinary tract abnormalities is increased.
ARBs are contraindicated because they increase risk of fetal renal dysfunction, lung hypoplasia, skeletal malformations, and death.
Aldosterone antagonists (spironolactone and eplerenone) should be avoided because they may cause feminization of a male fetus.
Both chronic and gestational hypertension increase risk of preeclampsia, eclampsia, other causes of maternal mortality or morbidity (eg, hypertensive encephalopathy, stroke, renal failure, left ventricular failure, HELLP syndrome), and uteroplacental insufficiency.
Check for other causes of hypertension if severe hypertension occurs for the first time in a pregnant woman who does not have a multifetal pregnancy or gestational trophoblastic disease.
If drug therapy is necessary (eg, BP > 150/100 mm Hg), start with methyldopa, a β-blocker, or a Ca channel blocker.
Do not use ACE inhibitors, ARBs, or aldosterone antagonists.
Consider hospitalization or termination of pregnancy if BP is > 180/110 mm Hg.
* This is the Professional Version. *