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Wednesday, December 1, 2021



Preeclampsia (once called toxemia of pregnancy) is a pregnancy-specific syndrome occurring after 20 weeks’ gestation. It involves reduced organ perfusion, vasospasm, and endothelial activation and is characterized by hypertension, proteinuria, and other symptoms. Pregnancy can induce hypertension or aggravate existing hypertension. Edema and proteinuria (one or both) are characteristic pregnancy-induced changes. If pre-eclampsia is untreated, convulsions (eclampsia) may occur. Chronic hypertension may be worsened by being superimposed on pregnancy-induced changes. Severe cases may include hemolysis, elevated liver enzymes, and low platelet counts, labeled HELLP syndrome, which occurs in up to 20% of severe preeclampsia. Preeclampsia occurs in 5% to 8% of all births (250,000 cases per year) and results in 150 maternal deaths and 3000 fetal deaths per year. (Overall, hypertensive disease of some type occurs in approximately 12% to 22% of pregnancies, and it is directly responsible for 17.6% of maternal deaths in the United States.)


In the great majority of cases, the clinical manifestations of preeclampsia occur after the 20th week of gestation and disappear following delivery. Preeclampsia before 20 weeks’ gestation may occur with gestational trophoblastic neoplasia and antiphospholipid antibody syndrome. Another uncommon presentation for pre-eclampsia is in the postpartum period, when it has been reported to occur up to 7 days after delivery.

The earliest clinical signs of preeclampsia are often sudden and excessive weight gain, accompanied by a blood pressure higher than 140/90 mmHg and by proteinuria. Such weight gain reflects the retention of water and electrolytes. Eventually, pitting edema, particularly in the legs and face, develops. However, before the stage of pitting edema is reached, the interstitial space may accumulate large quantities of fluid. The normal average weight gain during pregnancy does not exceed 2½ to 3 lb per month, and a greater weight gain should be suspected as abnormal water retention. Edema may precede hypertension, but for the clinical diagnosis of preeclampsia, the increased blood pressure is essential. In this respect the elevation of the diastolic blood pressure is more significant than that of the systolic, because it is the former which reflects the status of the peripheral resistance.

The criteria needed to diagnose a patient with pre-eclampsia include the results of 24-hour urinary protein measurement that demonstrate >300 mg of protein in 24 hours. In addition, these patients have blood pressure measures above 140/90 mm Hg. These patients also have characteristic renal glomerular lesions (capillary endotheliosis) and increased vascular reactivity. They often manifest elevated liver enzymes, and thrombocytopenia. In the past, hypertension indicative of preeclampsia has been defined as an elevation of more than 30 mm Hg systolic or more than 15 mm Hg diastolic above the patient’s baseline pressure; however, this has not proven to be a good predictor of outcome and is no longer part of the criteria for preeclampsia, though these patients do require close monitoring. Pre-eclamptic patients may undergo convulsions with only moderate blood pressure elevation and only a slight degree of edema.

Conscientious, regular prenatal care is important in order to detect signs of preeclampsia as early as possible. The onset of preeclampsia may be insidious or abrupt. The patient may feel well and not be aware of abnormal weight gain, proteinuria, or rising blood pressure. There may be a sudden progression into the convulsive phase, necessitating the termination of the pregnancy, thereby resulting in prematurity of the infant, which is the most frequent cause of perinatal mortality in preeclampsia. It is thought that severe preeclampsia predisposes to chronic hypertensive vascular disease, and the incidence of severe preeclampsia in subsequent pregnancies is increased.

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