Hypertension in a Pregnant Woman
A 35-year-old woman who is pregnant for the first time has had elevated blood pressure since she first presented for prenatal care at 28 weeks' gestation. Her blood pressure at that time was 148/94 mm Hg (unchanged in the lateral decubitus position). She is now at 32 weeks' gestation.
The patient has no personal or family history of hypertension. At her last checkup 2 years earlier, all findings were normal. She takes no medications and does not smoke, drink, or use illicit drugs. She denies headache, vision changes, chest pain, palpitations, abdominal pain, nausea, and vomiting. She has gained 15 lb since she became pregnant and has bilateral foot swelling but no other symptoms.
Blood pressure is 146/94 mm Hg bilaterally, and heart rate is 68 beats per minute. Results of an examination of the head, eyes, ears, nose, throat, and neck are normal. Cardiac examination reveals a grade 2/4 systolic ejection murmur without gallops. Lungs are clear and abdomen is gravid. There is 1+ pedal edema bilaterally but no skin lesions. Results of an obstetric examination are appropriate for 32 weeks' gestation.
Results of a metabolic panel are normal. A complete blood cell count reveals a hemoglobin level of 10.5 g/dL, hematocrit of 36%, and normal indices. Urinalysis shows 1+ proteinuria but otherwise normal results.
What is the most likely cause of this patient's blood pressure elevation?
A. Chronic hypertension.
B. Pregnancy-associated hypertension.
D. Normal pregnancy-related change in blood pressure.
Answer and discussion on next page
CORRECT ANSWER: C
A blood pressure of 148/94 mm Hg is abnormal at any time--and even more so during pregnancy. Thus, choice D is incorrect. Normally, blood pressure during pregnancy reaches its nadir in the second trimester.
The American College of Obstetricians and Gynecologists has defined pregnancy-associated, or gestational, hypertension as a systolic blood pressure of more than 140 mm Hg or a diastolic blood pressure of more than 90 mm Hg without proteinuria that occurs after 20 weeks of gestation and continues for longer than 12 weeks postpartum in a woman who was normotensive before she became pregnant.1 Although this patient has hypertension after more than 20 weeks' gestation, she also has proteinuria. Thus, choice B is not correct.
Chronic hypertension is seen in up to 5% of pregnancies and is associated with increased risk of intra- uterine growth retardation, preterm labor, preeclampsia, and perinatal mortality.2 This patient was normotensive 2 years ago; thus, chronic hypertension (choice A) is not likely the cause of her current blood pressure elevation.
This woman has preeclampsia, which is defined as "new-onset" hypertension and proteinuria after 20 weeks' gestation; it occurs in up to 8% of pregnancies in the United States.3 Risk factors for preeclampsia include nulliparity, advanced maternal age, a family history of preeclampsia, hypertension, chronic renal disease, diabetes, multiple gestation, and angiotensin gene T235.4
The pathogenesis of preeclampsia is thought to involve multiple factors, including:
- Impaired trophoblast invasion and differentiation.5
- Exposure to antigens, especially to new paternal antigens.6
- Increased sensitivity to angiotensin II.7
There is no agreed-on screening test for preeclampsia as an adjunct to monitoring blood pressure and checking for proteinuria. Uterine artery Doppler ultrasonography is sensitive, but an abnormal result has poor predictive value.8 A roll-over (supine-pressor) test may be somewhat useful. An increase in diastolic blood pressure of 10 to 15 mm Hg is positive but not very specific.
|THE TAKE-HOME MESSAGE:|
|"New-onset" hypertension, along with proteinuria, in a pregnant woman after 20 weeks' gestation indicates preeclampsia. Antihypertensive agents and magnesium sulfate may be used, but the definitive treatment is delivery.|
The definitive management of preeclampsia is delivery; however, preterm delivery is not always in the best interest of the infant. Magnesium sulfate reduces the incidence of eclampsia in women with mild to moderate preeclampsia; its major benefit is the prevention of seizures.9 Blood pressure management in women with mild hypertension (diastolic blood pressure less than 100 mm Hg; systolic, less than 160 mm Hg) has not been shown to reduce perinatal morbidity or mortality. Treatment of higher blood pressures is advantageous; the agents of choice include methyldopa, hydralazine, and labetalol.10 Sodium restriction and diuretics play no role in management.
In retrospective studies of pregnant women in developed countries in whom eclampsia occurred, approximately 50% had their first convulsion while in the hospital under "close medical supervision."11 Because of these results, a leading expert now advises against prolonged hospitalization of women with gestational hypertension and recommends outpatient management for women with mild gestational hypertension.11
Outcome of this case. The patient was monitored closely with twice-weekly blood pressure measurements. At 35 weeks' gestation, her blood pressure was 152/ 98 mm Hg; methyldopa was started, which lowered her blood pressure to about 132/90 mm Hg. She delivered a healthy boy at term without complications. Her blood pressure 1 month after delivery was normal.
1. Cunningham FG, Lindheimer MD. Hypertension in pregnancy. N Engl J Med. 1992;326:927-932.
2. Sibai BM. Chronic hypertension in pregnancy. Obstet Gynecol. 2002;100: 369-377.
3. American College of Obstetricians and Gynecologists. Diagnosis and Management of Preeclampsia and Eclampsia. ACOG practice bulletin 33. Washington, DC: American College of Obstetricians and Gynecologists; 2002.
4. National Institutes of Health, National Heart, Lung, and Blood Institutes, National High Blood Pressure Education Program Coordinating Committee. Working group report on high blood pressure in pregnancy. 2000. Accessed February 16, 2005.
5. Lain KY, Roberts JM. Contemporary concepts of the pathogenesis and management of preeclampsia. JAMA. 2002;287:3183-3186.
6. Einarsson JI, Sangi-Haghpeykar H, Gardner MO. Sperm exposure and development of preeclampsia. Am J Obstet Gynecol. 2003;188:1241-1243.
7. Granger JP, Alexander BT, Bennett WA, Khalil RA. Pathophysiology of pregnancy-induced hypertension. Am J Hypertens. 2001;14(6 pt 2):178S-185S.
8. Becker R, Vonk R, Vollert W, Entezami M. Doppler sonography of uterine arteries at 20-23 weeks: risk assessment of adverse pregnancy outcome by quantification of impedance and notch. J Perinat Med. 2002;30:388-394.
9. Livingston JC, Livingston LW, Ramsey R, et al. Magnesium sulfate in women with mild preeclampsia: a randomized controlled trial. Obstet Gynecol. 2003;101: 217-220.
10. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003;102:181-192.
11. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005;105:402-410.