A. Chronic hypertension. Hypertension preceding pregnancy or first diagnosed before 20 weeks’ gestation

B. Chronic hypertension with superimposed preeclampsia. Worsening hypertension and new-onset proteinuria, in addition to possible concurrent thrombocytopenia, or transaminase derangements after the 20th week of pregnancy in a woman with known chronic hypertension. It can be further subdivided into with or without severe features.

C. Gestational hypertension. Hypertension without proteinuria and without symptoms or abnormal laboratory tests after 20 weeks’ gestation (Table 3.1)

D. Preeclampsia. Blood pressures >140 mm Hg systolic or 90 mm Hg diastolic with proteinuria after 20 weeks’ gestation. It can be further subdivided into with or without severe features.

E. Eclampsia. Generalized tonic-clonic seizure activity in a pregnant woman with no prior history of a seizure disorder

F. Hemolysis, elevated liver enzymes, and low platelets syndrome. Clinical findings consistent with hemolysis, elevated liver function tests, and thrombocytopenia

II. INCIDENCE AND EPIDEMIOLOGY. Hypertensive disorders in pregnancy are a major cause of maternal morbidity and mortality, accounting for 15% to 20% of maternal deaths worldwide. In the United States, hypertensive disorders are the second leading cause of maternal mortality after thrombotic/hemorrhagic complications. Beyond 20 weeks’ gestation, preeclampsia complicates 5% to 8% of pregnancies, and preeclampsia with severe features complicates <1% of pregnancies. Eclampsia itself is much less frequent, occurring in 0.1% of pregnancies. Several risk factors have been identified, as outlined in Table 3.2.

Preeclampsia has been called the “disease of theories,” and many etiologies have been proposed. What is clear, however, is that it is a condition of dysfunction within the maternal endothelium. Increased levels of the soluble receptors sFLT1 and endoglin within the maternal circulation for vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β), respectively, may be associated with preeclamptic pathology. Higher circulating levels of these soluble receptors reduce the bioavailable levels of VEGF, placental growth factor (PlGF), and TGF-β, resulting in endothelial dysfunction within the maternal circulatory system. This dysfunction can manifest as both increased arterial tone (hypertension) and increased capillary leak (edema/proteinuria/pulmonary congestion). It is unclear what insult prompts the initial increase in sFLT1 and endoglin in some women versus others. One suggestion has been that abnormal trophoblastic invasion of both the maternal decidual arteries with an accompanying abnormal maternal immune response is at the root of this condition. This abnormal placentation is believed to lead to a reduction in placental perfusion and relative placental ischemia. Both sFLT1 and endoglin are proangiogenic proteins and may represent a placental
compensatory response. Recent work has, however, called the implied causality of this hypothesis into question; in early pregnancy, when placental formation is most active, sFLT1 and P1GF levels have failed to reliably predict the occurrence of preeclampsia.

III. DIAGNOSIS. The classic presentation which defines preeclampsia is hypertension and proteinuria after 20 weeks’ gestation. Some patients will also have nondependent edema, but this is no longer a part of the diagnostic criteria for preeclampsia. The clinical spectrum of preeclampsia ranges from mild to severe. Most patients have a nonsevere form of the disease that develops late in the third trimester (Fig. 3.1).

1. Hypertension defined as a blood pressure elevation to 140 mm Hg systolic or 90 mm Hg diastolic over two measurements at least 4 hours apart.
Measurements should be taken in the sitting position at the level of the heart, and the proper cuff size needs to be ensured.

2. Proteinuria defined as at least 300 mg of protein in a 24-hour period or protein to creatinine ratio ≥0.3 mg/mg.

B. Criteria for the diagnosis of preeclampsia with severe features Of note, you do not need every criteria listed here to make a diagnosis.

1. Blood pressure >160 mm Hg systolic or 110 mm Hg diastolic with the diagnostic readings taken twice at least 4 hours apart or severe hypertension can be verified within minutes to aid in administering antihypertensive therapy.

2. Symptoms suggestive of end-organ dysfunction. New visual disturbances such as scotomata, diplopia, blindness, or persistent severe headache. Other symptoms such as severe persistent right upper quadrant pain or severe epigastric pain not responsive to medications and not attributed to another medical cause are suggestive of preeclampsia with severe features.

4. Renal insufficiency is defined as serum creatinine >1.1 mg/dL.