Chronic hypertension is defined as blood pressure 140/90 mmHg or greater on two occasions before pregnancy, prior to 20 weeks of gestation, or persisting 12 weeks postpartum. Severe hypertension is defined as diastolic blood pressure ≥110 mm Hg. Hypertensive women tend to have a greater decline in blood pressure during early pregnancy than normotensive women.8
Secondary hypertension is an important consideration in women of reproductive age. A brief screen for secondary causes includes bilateral arm pressures and femoral pulse assessment, renal bruit assessment, inquiry into snoring, gasping, and daytime somnolence, as well as measurement of serum thyrotropin, potassium, calcium, creatinine, and urinalysis. This kind of evaluation will assess for coarctation of the aorta, renal artery stenosis, obstructive sleep apnea, hyper- or hypothyroidism, hyperaldosteronism, hyperparathyroidism, and underlying renal disease.9,10 Patient reports of episodic headache, palpitations, and diaphoresis should prompt investigation for pheochromocytoma.
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Newly identified hypertension or accelerating hypertension after 20 weeks warrants close evaluation for preeclampsia.
Hyperaldosteronism, pheochromocytoma, or hyperthyroidism might be quiescent during pregnancy but flare in the postpartum period.
Women with severe chronic hypertension or target organ damage have higher rates of superimposed preeclampsia. In these individuals, preeclampsia is more likely to present early (before 34 weeks gestation) or with severe disease.1
Preeclampsia is defined as hypertension and proteinuria (greater than 300 mg/day) at or beyond 20 weeks gestation in a previously normotensive woman. Preeclampsia rates vary from 5% to 10% of nulliparous women, to much higher rates in women with medical comorbidities or fetal factors (e.g., multiple gestations, molar pregnancies, hydrops, or triploidy). Preeclampsia’s pathogenesis is attributed to abnormal placental implantation with abnormal maternal immune adaptation, altered angiogenic factors with increased systemic vascular resistance and endothelial dysfunction leading to the clinically apparent maternal syndrome.11
Severe preeclampsia criteria include any of the following: eclampsia, HELLP syndrome (platelets less than 100,000/mm³, transaminases more than twice the upper limit of normal, and/or epigastric pain), SBP ≥160 mmHg, DBP ≥110 mmHg, proteinuria ≥5 grams per day, oliguria, pulmonary edema, placental abruption, or fetal manifestations such as intrauterine growth restriction (≤10th percentile of expected fetal weight based on gestational age), decreased amniotic fluid index, or fetal demise.2,5,12
Maternal symptoms might include headache, visual disturbances, epigastric or right upper quadrant (RUQ) pain, rapid weight gain, and severe edema. Some women remain asymptomatic. Preeclampsia can rapidly progress from “less severe” to severe. Maternal symptoms and abnormal lab findings are more predictive of adverse pregnancy outcomes than the degree of hypertension and/or proteinuria.1
It is always in the mother’s interest to deliver when preeclampsia is diagnosed, because preeclampsia will not resolve until after delivery, with hypertension and lab abnormalities sometimes persisting for months postpartum. Preeclampsia might be diagnosed before fetal viability (approximately 24 weeks gestation), although the vast majority of cases occur near term.
Risks of premature delivery must be balanced with the risks of progressively severe manifestations for the mother and fetus. Guidelines for expectant management of early (<34 weeks) preeclampsia are based on available evidence and expert opinion.13 Magnesium sulfate has been shown to be the most effective agent to minimize the likelihood of seizure in preeclamptic women.14 With an initial bolus of 4 g to 6 g IV followed by infusion of 1-2 g/hour, magnesium sulfate is usually continued for 24 to 48 hours after delivery.
Preeclampsia can first appear postpartum, most likely in the first days to weeks. A growing body of literature links preeclampsia, particularly early and/or recurrent, to subsequent increased risk for cardiovascular disease and end-stage renal disease.15
Preeclampsia superimposed on chronic hypertension is defined as the new onset or markedly increasing proteinuria or accelerating hypertension in the latter half of pregnancy. Maternal symptoms, transaminase elevation, thrombocytopenia, or fetal manifestations further support this diagnosis.