Preeclampsia and Related Conditions
Thomas F. McElrath
I. CATEGORIES OF PREGNANCY-ASSOCIATED HYPERTENSIVE DISORDERS
Chronic hypertension. Hypertension preceding pregnancy or first diagnosed before 20 weeks’ gestation.
Chronic hypertension with superimposed preeclampsia. Worsening hypertension and new-onset proteinuria, in addition to possible concurrent hyperuricemia, thrombocytopenia, or transaminase derangements after the 20th week of pregnancy in a woman with known chronic hypertension.
Pregnancy-induced hypertension. Hypertension without proteinuria after 20 weeks’ gestation.
Preeclampsia. Hypertension with proteinuria after 20 weeks’ gestation.
E. Eclampsia. Generalized tonic—clonic seizure activity in a woman with no prior history of a seizure disorder.
II. INCIDENCE AND EPIDEMIOLOGY.
Hypertensive disorders 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 severe preeclampsia 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 4.1.
III.
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-beta (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 (P1GF), 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.
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.
Table 4.1 Risk Factors for Hypertensive Disorders | |||||||||||||||||||||||||||||||||||||||||
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IV. DIAGNOSIS.
The classic triad that defines preeclampsia is hypertension, proteinuria, and nondependent edema. At this point, the diagnosis is made exclusively on clinical criteria. The clinical spectrum of preeclampsia ranges from mild to severe. Most patients have mild disease that develops late in the third trimester.
Criteria for the diagnosis of mild preeclampsia
Hypertension defined as a blood pressure elevation to 140 mm Hg systolic or 90 mm Hg diastolic over two measurements at least 6 hours apart. Measurements should be taken in the sitting position, and proper cuff size should be ensured.
Proteinuria defined as at least 300 mg of protein in a 24-hour period.
Nondependent edema (e.g., facial or upper extremity) is also noted in many but not all cases of preeclampsia.
Criteria for the diagnosis of severe preeclampsia
Blood pressure > 160 mm Hg systolic or 110 mm Hg diastolic with the diagnostic readings taken twice at least 6 hours apart.
Proteinuria >5 g per 24-hour collection.
Symptoms suggestive of end-organ dysfunction. Visual disturbances such as scotomata, diplopia or blindness, persistent severe headache, or epigastric pain.
Pulmonary edema.
Oliguria defined as <500 mL of urine per 24-hour collection.
Microangiopathic hemolysis.
Thrombocytopenia defined as a platelet count of < 100,000.
Hepatocellular dysfunction. Elevated transaminases.
Intrauterine growth restriction (IUGR) or oligohydramnios.
HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) represents an alternative presentation of preeclampsia associated with disseminated intravascular coagulation (DIC) and reflects systemic end-organ damage. HELLP syndrome often appears without hypertension or proteinuria and may, in fact, have a separate pathologic origin from that of preeclampsia.
V.
Complications of preeclampsia result in a maternal mortality rate
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