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Chronic Hypertension In Pregnancy

Data from the National Health and Nutrition Examination Survey (1999–2008), indicates that the prevalence of hypertension in women aged 20–44 years is 7.7%, and an estimated 4.9% of women use anti-hypertensive pharmacologic therapy, with the two most common categories of medications being diuretics (47.9%) and angiotension-converting enzyme (ACE) inhibitors (44.0%). Prenatal counseling in women with chronic hypertension is an important component of their care. The goals of the visit should be to evaluate for end-organ damage, to adjust medications as necessary, to discuss appropriate lifestyle modifications, and to consider secondary causes of hypertension. Given the teratogenic potential of ACE inhibitors (see below), women should be counseled on the importance of birth control while on ACE inhibitors, and this class of medication should be changed prior to attempting to conceive.

There is continued controversy over whether women with mild-moderate chronic hypertension on anti-hypertensive therapy prior to pregnancy should stop these medications, be kept under close observation, and only reinstitute therapy for blood pressure elevations of 140–160/90–100 mm Hg, versus continuing their usual anti-hypertensive regimen. Currently, both approaches are used and there is insufficient evidence to recommend one approach over the other. Central to this controversy is the concern that anti-hypertensive therapy for mild-moderate hypertension may provide no maternal benefits, while, at the same time, harming the fetus (a) from the intrauterine exposure to anti-hypertensive medications with their possible adverse effects, and (b) as a result of unfavorable hemodynamics, whereby a decrease in the maternal blood pressure may impair uteroplacental perfusion, and, ultimately, fetal growth. The evidence for an association between fetoplacental growth and the use of oral anti-hypertensive medications is limited. In the absence of well-designed and adequately powered studies, a meta-analysis of 14 treatment trials is frequently cited. This meta-analysis concluded that a 10 mm Hg decrease in mean arterial blood pressure was associated with a 145 gram decrease in neonatal birth weight. However, only 16% of the variation in birth weight was accounted for by the change in blood pressure, as several other variables may have contributed independently to the fetal growth impairment. These negative effects of anti-hypertensive therapy on birth weight have not been demonstrated consistently and, in turn, the presence of hypertension itself, irrespective of blood pressure medication use, has been shown to result in lower birth weights. Those in favor of treatment support their view by citing evidence that treatment of chronic hypertension may prevent progression to severe hypertension and that chronic hypertension has been associated with increased feto-maternal risks, including perinatal mortality and placental abruption . In general, most experts agree with the use of anti-hypertensive therapy for a blood pressure ≥ 150/100 mm Hg. Evaluation for end-organ damage is important in that it helps to guide therapy decisions. In the presence of renal disease, proteinuria, left ventricular hypertrophy, hypertensive retinopathy, microvascular disease, stroke and age greater than 40, therapy should be initiated for a diastolic BP ≥ 90 mm Hg. It should be noted that therapeutic guidelines as to when to institute treatment and subsequent BP targets vary among different obstetrical and medical societies due to the lack of evidence supporting a single BP goal.

Secondary hypertension should be considered in women with difficult to control BP requiring three or more anti-hypertensive agents, including a diuretic, and/or indicative laboratory and clinical findings, such as hypokalemia or an abdominal bruit. A thorough history and physical exam should be performed by a nephrologist or hypertension specialist and should include a review of lifestyle factors, such as nicotine use, caffeine intake and recreational drug use, in particular cocaine and methamphetamines, which can mimic conditions such as pheochromocytoma. The primary differential for secondary causes of hypertension includes primary hyperaldosteronism, pheochromocytoma and renal artery stenosis (primarily due to fibromuscular dysplasia in this age group). Women with secondary hypertension are at a particularly high risk for adverse pregnancy outcomes. Pheochromocytoma, in particular, is associated with significant maternal and fetal mortality, mainly due to hypertensive crisis in the mother and intrauterine growth restriction in the fetus. The diagnosis may be missed, mainly due to the fact that patients may present with atypical features, such as gestational diabetes and difficult to control hypertension (Figure 1), and may be inappropriately diagnosed as having preeclampsia. Primary hyperaldosteronism is also difficult to diagnose during pregnancy, mainly due to the stimulation of the renin-angiotensin-aldosterone axis in normal pregnancy, resulting in false negatives when measuring the renin-aldosterone ratio.

Specific interventions to treat the underlying cause should be pursued, when possible, prior to pregnancy, whether it is surgery for pheochromocytoma or revascularization for renal artery stenosis, which may result in cure of the hypertension. In the case that the diagnosis is not made before pregnancy, there are no official guidelines as to the management of these conditions, and decisions must be made on a case-by-case basis. Renal artery revascularization has been successfully used during pregnancy, and surgical resection of pheochromocytoma has been performed in all trimesters, after the initiation of 10–14 days of alpha blockage prior to surgery.

Lastly, women with chronic hypertension should be aware of the risks associated with pregnancy. In a study of 763 women with chronic hypertension enrolled in a multi-center trial of low-dose aspirin for the prevention of preeclampsia, 25% developed superimposed preeclampsia. In addition, the women in this study who developed preeclampsia were at increased risk for placental abruption, versus those with chronic hypertension alone (3% vs. 1%, p=0.04). Among women with severe or high risk hypertension (BP>160/110), placental abruption may affect as many as 5–10% of women. One study by Sibai and colleagues looked at the maternal and fetal outcomes of 44 women with severe chronic hypertension in the first trimester of pregnancy and found that while there were no maternal deaths, morbidity, including hospitalizations and reduction in renal function, was high. Of the twenty women with deterioration in renal function during pregnancy, 19 had returned to their baseline renal function by their post-partum visit, although one patient continued to have significant renal impairment. Nearly one-half of these women developed superimposed preeclampsia, and the perinatal mortality was 25% (ten stillbirths and 1 neonatal death), predominantly in the group of women with preeclampsia, and all in infants less than 800 grams at delivery and less than 29 weeks of age. The risk of recurrence of preeclampsia in subsequent pregnancies after a pregnancy complicated by severe preeclampsia is 25%, but the relative risk is 2 times greater in those with a history of chronic hypertension.

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