eMedicine Specialties > Obstetrics and Gynecology > Medical Problems in Pregnancy

Hypertension and Pregnancy

Author: Paul Gibson, MD,, Associate Professor, Departments of Medicine and Obstetrics and Gynecology, Divisions of General Internal Medicine and Maternal-Fetal Medicine, University of Calgary
Coauthor(s): Michael P Carson, MD, Clinical Associate Professor, Department of Medicine, Clinical Assistant Professor, Department of Obstetrics/Gynecology and Reproductive Sciences, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Director of Research/Outcomes, Department of Medicine, Jersey Shore University Medical Center
Contributor Information and Disclosures

Updated: Jul 30, 2009

Introduction

Background

Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into 4 categories, as recommended by the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy: 1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia superimposed on chronic hypertension, and 4) gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).¹ This terminology is preferred over the older but widely used term pregnancy-induced hypertension (PIH) because it is more precise.

The Society of Obstetricians and Gynecologists of Canada (SOGC) recently released revised guidelines that simplified the classification of hypertension in pregnancy into 2 categories, preexisting or gestational, with the option to add "with preeclampsia" to either category if additional maternal or fetal symptoms, signs, or test results support this.²

Chronic hypertension is defined as blood pressure exceeding 140/90 mm Hg before pregnancy or before 20 weeks' gestation. When hypertension is first identified during a woman's pregnancy and she is at less than 20 weeks' gestation, blood pressure elevations usually represent chronic hypertension. In contrast, new onset of elevated blood pressure readings after 20 weeks' gestation mandates the consideration and exclusion of preeclampsia. Preeclampsia occurs in up to 5% of all pregnancies, in 10% of first pregnancies, and in 20-25% of women with a history of chronic hypertension. Hypertensive disorders in pregnancy may cause maternal and fetal morbidity, and they remain a leading source of maternal mortality.

Pathophysiology

Chronic hypertension

Chronic hypertension is a primary disorder in 90-95% of cases. Secondary causes are briefly discussed in Causes.

Preeclampsia

Although the exact pathophysiologic mechanism is not clearly understood, preeclampsia is primarily a disorder of placental dysfunction leading to a syndrome of endothelial dysfunction with associated vasospasm. In most cases, pathology demonstrates evidence of placental insufficiency with associated abnormalities such as diffuse placental thrombosis, an inflammatory placental decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium. This supports abnormal placental development or placental damage from diffuse microthrombosis as being central to the development of this disorder.

Evidence also indicates that an altered maternal immune response to fetal/placental tissue may contribute to the development of preeclampsia.

The widespread endothelial dysfunction may manifest as a maternal syndrome, fetal syndrome, or both. The pregnant woman may manifest dysfunction of multiple organ systems, including the central nervous, hepatic, pulmonary, renal, and hematological systems. Endothelial damage leads to pathologic capillary leak that can present in the mother as rapid weight gain, nondependent edema (face or hands), pulmonary edema, hemoconcentration, or a combination thereof. The diseased placenta can also affect the fetus via decreased utero-placental blood flow. This decrease in perfusion can manifest clinically as nonreassuring fetal heart rate testing, low scores on a biophysical profile, oligohydramnios, or as fetal growth restriction.

The hypertension occurring in preeclampsia is due primarily to vasospasm, with arterial constriction and relatively reduced intravascular volume compared to normal pregnancy. The vasculature of normal pregnant women typically demonstrates decreased responsiveness to vasoactive peptides such as angiotensin-II and epinephrine. In contrast, women who develop preeclampsia typically show a hyperresponsiveness to these hormones, an alteration that may be seen even before the hypertension and other manifestations of preeclampsia become apparent. In addition, blood pressures in preeclampsia are labile, and the normal circadian blood pressure rhythms may be blunted or reversed. One study found increased arterial stiffness in women with preeclampsia, as well as in those with gestational hypertension, compared with normotensive controls; treatment with alpha methyldopa significantly improved the vascular stiffness in preeclampsia but did not normalize it.³

Gestational hypertension

Gestational hypertension refers to hypertension with onset in the latter part of pregnancy (>20 weeks' gestation) without any other features of preeclampsia, and followed by normalization of the blood pressure postpartum. Of women who initially present with apparent gestational hypertension, about one third develop the syndrome of preeclampsia. As such, these patients should be observed carefully for this progression. The pathophysiology of gestational hypertension is unknown, but in the absence of features of preeclampsia, the maternal and fetal outcomes are usually normal. Gestational hypertension may, however, be a harbinger of chronic hypertension later in life.

Frequency

United States

Chronic hypertension occurs in up to 22% of women of childbearing age, with the prevalence varying according to age, race, and body mass index. Population-based data indicate that approximately 1% of pregnancies are complicated by chronic hypertension, 5-6% by gestational hypertension (without proteinuria), and 1-2% by preeclampsia.

Mortality/Morbidity

• Hypertensive disorders in pregnancy are among the leading causes of maternal mortality, along with thromboembolism, hemorrhage and nonobstetric injuries. Between 1991 and 1999, pregnancy-induced hypertension caused 15.7% of maternal deaths in the United States.⁴
• While maternal diastolic blood pressure (DBP) greater than 110 mm Hg is associated with an increased risk for placental abruption and fetal growth restriction, superimposed preeclamptic disorders cause most of the morbidity due to chronic hypertension during pregnancy. Severe maternal complications include eclamptic seizures, intracerebral hemorrhage, pulmonary edema due to capillary leak or myocardial dysfunction, acute renal failure due to vasospasm, proteinuria greater than 4-5 g/d, hepatic swelling with or without liver dysfunction, and disseminated intravascular coagulation and/or consumptive coagulopathy (rare). Consumptive coagulopathy usually is associated with placental abruption and is uncommon as a primary manifestation of preeclampsia.
• Fetal complications include abruptio placentae, intrauterine growth restriction, premature delivery, and intrauterine fetal death.
• Hypertension before pregnancy or during early pregnancy is associated with a twofold increased risk of gestational diabetes mellitus.⁵

Race

Black women have higher rates of preeclampsia complicating their pregnancies compared with other racial groups, mainly because they have a greater prevalence of underlying chronic hypertension. Among women aged 30-39 years, chronic hypertension is present in 22.3% of African Americans, 4.6% of non-Hispanic white persons, and 6.2% of Mexican Americans. Hispanic women generally have blood pressure levels that are the same as or lower than those of non-Hispanic white women.

Age

Preeclampsia is more common at the extremes of maternal age (<18 y or >35 y). The increased prevalence of chronic hypertension and other comorbid medical illnesses in women older than 35 years may explain the increased frequency of preeclampsia among older gravidas.

Clinical

History

Determining whether elevated blood pressure identified during pregnancy is due to chronic hypertension or to preeclampsia is sometimes a challenge, especially if no recorded blood pressures from the first half of the gestation are available. Clinical characteristics obtained via history, physical examination, and certain laboratory investigations may be used to help clarify the diagnosis.

• Gestational age
  • Hypertension prior to 20 weeks' gestation is almost always due to chronic hypertension; preeclampsia is rare prior to the third trimester.
  • New-onset or worsening hypertension after 20 weeks' gestation should lead to a careful evaluation for manifestations of preeclampsia.
  • The diagnosis of severe hypertension or preeclampsia in the first or early second trimester necessitates exclusion of gestational trophoblastic disease and/or molar pregnancy.
  • Women diagnosed with severe or early preeclampsia (in the second trimester or early third trimester) have a higher prevalence of thrombophilias. Studies are ongoing to evaluate whether administering anticoagulants in subsequent pregnancies decreases the risk of recurrent preeclampsia.
• Maternal personal risk factors for preeclampsia
  • First pregnancy
  • New partner/paternity
  • Age younger than 18 years or older than 35 years
  • History of preeclampsia
  • Family history of preeclampsia in a first-degree relative
  • Black race
  • Obesity (BMI ³ 30)
  • Interpregnancy interval less than 2 years or more than 10 years
• Maternal medical risk factors for preeclampsia
  • Chronic hypertension, especially when secondary to such disorders as hypercortisolism, hyperaldosteronism, pheochromocytoma, or renal artery stenosis
  • Preexisting diabetes (type 1 or type 2), especially with microvascular disease
  • Renal disease
  • Systemic lupus erythematosus
  • Obesity
  • Thrombophilia
  • History of migraine⁶
  • Use of selective serotonin uptake inhibitor antidepressants beyond the first trimester⁷
• Placental/fetal risk factors for preeclampsia
  • Multiple gestations
  • Hydrops fetalis
  • Gestational trophoblastic disease
  • Triploidy
• Symptoms of preeclampsia
  • Visual disturbances typical of preeclampsia are scintillations and scotomata. These disturbances are presumed to be due to cerebral vasospasm.
  • Headache is of new onset and may be described as frontal, throbbing, or similar to a migraine headache.
  • Epigastric pain is due to hepatic swelling and inflammation, with stretch of the liver capsule. Pain may be of sudden onset, is typically constant, and may be moderate to severe in intensity.
  • While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. Edema is no longer included among the criteria for diagnosis of preeclampsia.
  • Rapid weight gain is a result of edema due to capillary leak as well as renal sodium and fluid retention.

Physical

• Physical findings in preeclampsia
  • Blood pressure
    • Blood pressure should be measured in the sitting position, with the cuff at the level of the heart. Inferior vena caval compression by the gravid uterus while the patient is supine can alter readings substantially, leading to an underestimation of the blood pressure. Blood pressures measured in the left lateral position similarly may yield falsely low values if the blood pressure is measured in the higher arm, unless the cuff is carefully maintained at the level of the heart.
    • Women should be allowed to sit quietly for 5-10 minutes before each blood pressure measurement.
    • Korotkoff sounds I (the first sound) and V (the disappearance of sound) should be used to denote the systolic blood pressure (SBP) and DBP, respectively. In about 5% of women, an exaggerated gap exists between the fourth (muffling) and fifth (disappearance) Korotkoff sounds, with the fifth sound approaching zero. In this setting, both the fourth and fifth sounds should be recorded (eg, 120/80/40 with sound I = 120, sound IV = 80, sound V = 40) as the fourth sound will more closely approximate the true DBP.
    • Maternal SBP greater than 160 mm Hg or DBP greater than 110 mm Hg denotes severe disease; depending on the gestational age and maternal status, delivery should be considered for sustained BPs in this range.
    • Many automated blood pressure cuffs provide reasonable estimates of true blood pressure during normal pregnancy (especially those validated for pregnancy) but tend to underestimate blood pressure in preeclamptic women. Only a few automated BP cuffs have been validated in preeclampsia. Manual blood pressure measurement with a mercury sphygmomanometer remains the criterion standard in this setting.
    • Home and ambulatory BP measurements are increasingly being used in the pregnant population. Assuming the BP device is accurate (validated relative to an office measurement) they may provide valuable additional data regarding hypertension severity and control during pregnancy.
  • Retinal vasospasm is a severe manifestation of maternal disease; consider delivery.
  • Retinal edema is known as serous retinal detachment. This can manifest as severely impaired vision if the macula is involved. It generally reflects severe preeclampsia and should lead to prompt consideration of delivery. The condition typically resolves upon completion of pregnancy and resolution of the hypertension and fluid retention.
  • Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch. Consider delivery.
  • Brisk, or hyperactive, reflexes are common during pregnancy. Clonus is a sign of neuromuscular irritability that usually reflects severe preeclampsia.
  • In most normal pregnancies, the woman has some lower extremity edema by the third trimester. In contrast, a sudden worsening in dependent edema, edema in nondependent areas (such as the face and hands), or rapid weight gain suggest a pathologic process and warrant further evaluation for preeclampsia.
• Signs suggesting a secondary medical cause of chronic hypertension
  • Centripetal obesity, "buffalo hump," and/or wide purple abdominal striae suggest glucocorticoid excess.
  • A systolic bruit heard over the abdomen or in the flanks suggests renal artery stenosis.
  • Radiofemoral delay or diminished pulses in lower versus upper extremities suggests coarctation of the aorta.
  • Clinical signs may demonstrate hyperthyroidism, hypothyroidism, or growth hormone excess.
• Signs of end-organ damage from chronic hypertension
  • S₄ on cardiac auscultation is not a normal finding in pregnancy. It suggests left ventricular hypertrophy or diastolic dysfunction due to preeclampsia-induced vasospasm.
  • In pregnancy, and particularly in the presence of preeclampsia, any sustained cardiac gallop may be a pathological finding and warrants further evaluation with echocardiography. However, a well-conducted phonocardiographic study of pregnant women found a soft, intermittent S₃ to be common in normal pregnancy.
  • Retinal changes of chronic hypertension may be noted.
  • Carotid bruits may reflect atherosclerotic disease due to longstanding hypertension.

Causes

• Chronic hypertension
  • Chronic hypertension may be either essential (90%) or secondary to some identifiable underlying disorder, such as renal parenchymal disease (eg, polycystic kidneys, glomerular or interstitial disease), renal vascular disease (eg, renal artery stenosis, fibromuscular dysplasia), endocrine disorders (eg, adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma, hyperthyroidism or hypothyroidism, growth hormone excess, hyperparathyroidism), coarctation of the aorta, or oral contraceptive use.
  • About 20-25% of women with chronic hypertension develop preeclampsia during pregnancy.
• Preeclampsia
  • The exact cause is not known, but placental dysfunction seems to be integral to the development of the syndrome in most women.
  • The widespread endothelial dysfunction often manifests with primarily maternal effects and has the potential to cause dysfunction of multiple organ systems, including the brain and the hepatic, pulmonary, renal, and hematological systems. The endothelial damage leads to pathologic capillary leak that can manifest in the mother as rapid weight gain, edema of the face or hands, pulmonary edema, and/or hemoconcentration resulting in hemoglobin greater than 12 g/dL or creatinine greater than 0.8 mg/dL. Renal biopsy may show glomerular endotheliosis that is associated with proteinuria greater than 300 mg in 24 hours.
  • Histologically, the placenta often demonstrates in situ thrombosis and decidual vasculopathy. This can affect the fetus via decreased utero-placental blood flow. The decrease in flow can manifest clinically as nonreassuring fetal heart rate testing, low score on a biophysical profile, oligohydramnios, and fetal growth restriction.

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