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  • Blood pressure of 140 mm Hg or higher systolic or 90 mm Hg or higher diastolic after 20 weeks of gestation.

  • Proteinuria of 0.3 g or more in 24 hours.

  • When hypertension is present with severe features of preeclampsia, seizure prophylaxis could be beneficial.

Preeclampsia with severe features

  • Blood pressure of 160 mm Hg or higher systolic or 110 mm Hg or higher diastolic.

  • Progressive kidney injury.

  • Thrombocytopenia.

  • Hemolysis, elevated liver enzymes, low platelets (HELLP).

  • Pulmonary edema.

  • Vision changes or headache.


  • Seizures in a patient with evidence of preeclampsia.


Preeclampsia is defined as the presence of newly elevated blood pressure and proteinuria during pregnancy. Eclampsia is diagnosed when seizures develop in a patient with evidence of preeclampsia. Historically, the presence of three elements was required for the diagnosis of preeclampsia: hypertension, proteinuria, and edema. Edema was difficult to objectively quantify and is no longer a required element. In addition, proteinuria may not always be present.

Preeclampsia-eclampsia can occur any time after 20 weeks of gestation and up to 6 weeks’ postpartum. It is a disease unique to pregnancy, with the only cure being delivery of the fetus and placenta. Preeclampsia develops in approximately 7% of pregnant women in the United States; of those, eclampsia will develop in 5% (0.04% of pregnant women). Primiparas are most frequently affected; however, the incidence of preeclampsia-eclampsia is increased with multi-fetal pregnancies, chronic hypertension, diabetes mellitus, kidney disease, collagen-vascular and autoimmune disorders, and gestational trophoblastic disease. Uncontrolled eclampsia is a significant cause of maternal death. The cause of preeclampsia-eclampsia is not known, but it is likely a multifactorial, two-stage process. The first stage is thought to be a disturbance in placental implantation involving the spiral arteries very early in gestation. The abnormal placental perfusion that results leads to the formation of noxious free radicals. The second stage is characterized by excessive inflammation causing endothelial damage, vasospasm, and finally clinical signs and symptoms. An immunologic component to preeclampsia-eclampsia has been proposed, citing the increased incidence in primigravidas. This entire process is likely enhanced by environmental factors, genetic predisposition, and preexisting maternal disease.


Clinically, the severity of preeclampsia-eclampsia can be measured with reference to the six major sites in which it exerts its effects: the central nervous system, the kidneys, the liver, the hematologic system, the vascular system, and the fetal-placental unit. By evaluating each of these areas for the presence of mild to severe preeclampsia, the degree of involvement can be assessed, and an appropriate management plan can be formulated that balances the severity of disease and gestational age (Table 19–3).

Table 19–3.Indicators of mild to moderate versus severe preeclampsia-eclampsia.

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