Hypertension during pregnancy, of which preeclampsia and eclampsia predominate, constitutes a significant health problem both because of its high incidence (4%-11% of pregnancies in developed countries) and due to the maternal and fetal health outcomes it creates.1 Hypertensive disorders are the second leading cause of maternal mortality.1 They cause 15% of all maternal deaths and constitute considerable morbidity both during and after pregnancy.2 Fetal outcomes include premature delivery, small-for-gestational-age (SGA) infants, and fetal mortality.
The long-term cardiovascular risks for mothers who suffer from the triad of hypertension during pregnancy, SGA infants, and pre-term delivery are approximately eight times higher than for individuals without these complications during pregnancy.
Hypertension observed during pregnancy is defined according to one of the following classifications:
- Chronic hypertension, present prior to pregnancy;
- Preeclampsia/eclampsia: development of hypertension, proteinuria, and edema during pregnancy;
- Preeclampsia superimposed on preexisting renal disease; and
- Gestational hypertension: either transient mild hypertension during the third trimester or mild hypertension detected during the third trimester that does not resolve by 12 weeks postpartum.
Of these hypertensive entities, this article focuses on the most common and potentially serious one: preeclampsia/eclampsia. Preeclampsia is characterized by blood pressure over 140/90 mm Hg—measured on two separate occasions, and proteinuria greater than 300 mg/24 hours, occurring after 20 weeks gestation. Severe preeclampsia includes the same criteria, as well as proteinuria greater than 5,000 mg/24 hours; blood pressure higher than 160/110 mm Hg; or end-organ damage such as headaches, visual changes, renal dysfunction, hepatic dysfunction, or thrombocytopenia.
Historically, the term eclampsia has been reserved to describe the symptoms of preeclampsia combined with the occurrence of seizure activity. HELLP syndrome is a severe variant of preeclampsia that affects up to 1% of pregnancies and includes the constellation of hemolysis, elevated liver enzyme levels, and a low platelet count.
Given the potential risks for these disorders during pregnancy, it seems logical to target primarily those individuals at risk and attempt to prevent the disorder. Traditionally, the higher risk populations include patients experiencing primagravida pregnancies, those with a history of hypertension or renal disease, women who have had prior episodes of preeclampsia, and multiparous individuals with different paternal partners. Other less helpful or more expensive screening procedures include evaluation for inherited thrombophilias.
Several trials have attempted to prevent the development of preeclampsia using calcium supplementation or aspirin therapy, but current evidence demonstrates no benefit from these interventions except in selected populations.3,4 For the past several decades, the treatment for hypertension during pregnancy has consisted of either delivery of the fetus or bed rest combined with therapies involving alpha-methyl-DOPA, hydralazine, and intravenous magnesium sulfate, depending on the level of the patient’s blood pressure and proteinuria, as well as the stage of the pregnancy.
Because of the potential risks to the health of the infant (as well as that of the mother) generic interventional trials extrapolated from other hypertensive populations that may offer equivalent or more effective therapies have not been readily accomplished. In spite of this lack of clinical and outcomes studies, the following generalizations regarding care are currently advocated:
1. Continue anti-hypertensive therapy for chronic hypertension with a goal of maintaining blood pressure below 140/90 mm Hg. Though the risks of SGA infants and preeclampsia were not affected by therapy, the incidence of premature delivery was reduced. Nearly all anti-hypertensive drugs have been used in treating chronic hypertension in pregnancy, but angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are contraindicated because of teratogenecity. Diuretics and hydralazine may also have adverse outcomes on fetal and/or maternal health, respectively.