Preeclampsia: 3 preemptive tactics

A large prospective study on the relation between duration of sperm exposure with a partner and the rate of preeclampsia showed that women who conceive after a cohabitation period of 0 to 4 months have a 10-fold rate of preeclampsia, compared to those who conceive after a cohabitation period of at least 12 months. A similar study confirmed these findings.

The protective effects of long-term sperm exposure could explain the high frequency of preeclampsia in teenage pregnancy. (These women tend to have limited sperm exposure with a partner, or multiple partners). Thus, it is important to teach these women about their risks and the need for regular prenatal care.

Multifetal gestation increases the rate as well as the severity of preeclampsia, and the rate increases with the number of fetuses. Lowering the number of embryos transferred will substantially reduce the risk of preeclampsia and adverse outcomes.

There is no therapy to prevent preeclampsia in these women; however, we should acknowledge the increased risk and develop antenatal-care programs that allow close observation and early detection of preeclampsia in these women.

Hydropic degeneration of placenta. It is well-established that pregnancies complicated by fetal hydrops or hydropic degeneration of the placenta (with or without a coexisting fetus) are at very high risk for preeclampsia. In these cases, preeclampsia usually develops in the second trimester and is usually severe, and therefore causes substantial maternal and perinatal morbidities. Development of preeclampsia in such pregnancies requires immediate hospitalization and consideration for prompt delivery.

Unexplained elevated serum markers in the second trimester. Maternal serum screening with alpha fetoprotein (AFP), human chorionic gonadotropin (HCG) and inhibin A is commonly used to identify those at risk for aneuploidy or neural tube defects.

Unexplained elevations in AFP, HCG or inhibin A have been associated with increased adverse pregnancy outcome such as fetal death, intrauterine growth restriction (IUGR), preterm delivery, and preeclampsia. However, the data on the association between abnormalities in these biomarkers and preeclampsia have been inconsistent. Nevertheless, retrospective studies suggest that elevation in these serum markers during the second trimester increases the risk of preeclampsia by at least twofold. The risk is probably higher in those who have abnormalities in more than 1 of these markers. Since unexplained abnormalities of these serum markers may reflect early placental pathology, it is suggested that these pregnancies may benefit from close obstetric surveillance.

Serum and urinary markers of abnormal angiogenesis and subsequent preeclampsia were strongly associate, in newly published studies reported by Levine and colleagues. For example, circulating soluble fms-like tyrosine kinase (sFLt1) is elevated in pregnant women prior to onset of preeclampsia, whereas urinary placental growth factor is reduced several weeks prior to clinical onset of preeclampsia. Both of these markers appear to hold some promise.

Unexplained proteinuria or hematuria. Generally, proteinuria is considered a late manifestation of preeclampsia. However, recent retrospective studies suggest that some women with preeclampsia, particularly those with HELLP syndrome, might not have hypertension (>140 mm Hg systolic or >90 mm Hg diastolic). In some women, persistent proteinuria (3+ on dipstick) or >300 mg/24 hour may be the first sign of preeclampsia or could be a marker of silent renal disease.

No prospective studies have evaluated the risk of preeclampsia in asymptomatic women with persistent proteinuria. I suggest, however, that women with this finding will benefit from intensified obstetric surveillance (more frequent prenatal visits) and/or biochemical evaluation (platelet count, liver enzymes), particularly if they have headaches, visual changes, epigastric or right upper quadrant pain, nausea or vomiting, or respiratory symptoms (chest pain or shortness of breath)—likewise, for pregnant women with persistent hematuria of unknown origin.

Unexplained fetal growth restriction. Impaired trophoblast invasion is a key features of pregnancies complicated by preeclampsia or unexplained IUGR. Preeclampsia can manifest either as a maternal syndrome (hypertension and proteinuria with or without symptoms) or a fetal abnormal growth syndrome.

In clinical practice, most cases of unexplained IUGR are probably delivered before the maternal syndrome develops. In some cases, unexplained IUGR may be the first manifestation of preeclampsia, particularly those with IUGR before 34 weeks’ gestation. The absolute risk of clinical preeclampsia in such women is unknown because of lack of prospective data. Nevertheless, a woman with idiopathic IUGR prior to 34 weeks’ gestation whose pregnancy is managed expectantly is at increased risk for future preeclampsia. These women should receive intensive maternal surveillance for preeclampsia, and a diagnosis of preeclampsia should be considered in those who develop maternal symptoms or abnormal blood tests.

Abnormal uterine artery Doppler velocimetry at 18 to 24 weeks’ gestation. Several observational studies reported an association between elevated uterine artery resistance as measured by Doppler (with or without presence of a notch) in the second trimester and subsequent preeclampsia and/or IUGR. The reported rates of preeclampsia among women with abnormal Doppler results range from 6% to 40%. The risk varies depending on the site measured, gestational age at time of measurement, normal indices used, abnormality on repeat measurement, and population studied.