Preeclampsia: Recent Advances in Predicting, Preventing, and Managing the Maternal and Fetal Life-Threatening Condition

Abstract

Preeclampsia accounts for one of the most common documented gestational complications, with a prevalence of approximately 2 to 15% of all pregnancies. Defined as gestational hypertension after 20 weeks of pregnancy and coexisting proteinuria or generalized edema, and certain forms of organ damage, it is life-threatening for both the mother and the fetus, in terms of increasing the rate of mortality and morbidity. Preeclamptic pregnancies are strongly associated with significantly higher medical costs. The maternal costs are related to the extra utility of the healthcare system, more resources used during hospitalization, and likely more surgical spending due to an elevated rate of cesarean deliveries. The infant costs also contribute to a large percentage of the expenses as the babies are prone to preterm deliveries and relevant or causative adverse events. Preeclampsia imposes a considerable financial burden on our societies. It is important for healthcare providers and policy-makers to recognize this phenomenon and allocate enough economic budgets and medical and social resources accordingly. The true cellular and molecular mechanisms underlying preeclampsia remain largely unexplained, which is assumed to be a two-stage process of impaired uteroplacental perfusion with or without prior defective trophoblast invasion (stage 1), followed by general endothelial dysfunction and vascular inflammation that lead to systemic organ damages (stage 2). Risk factors for preeclampsia including race, advanced maternal age, obesity, nulliparity, multi-fetal pregnancy, and co-existing medical disorders, can serve as warnings or markers that call for enhanced surveillance of maternal and fetal well-being. Doppler ultrasonography and biomarkers including the mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI), and serum pregnancy-associated plasma protein A (PAPP-A) can be used for the prediction of preeclampsia. For women perceived as high-risk individuals for developing preeclampsia, the administration of low-dose aspirin on a daily basis since early pregnancy has proven to be the most effective way to prevent preeclampsia. For preeclamptic females, relevant information, counseling, and suggestions should be provided to facilitate timely intervention or specialty referral. In pregnancies complicated with preeclampsia, closer monitoring and antepartum surveillance including the Doppler ultrasound blood flow study, biophysical profile, non-stress test, and oxytocin challenge test can be arranged. If the results are unfavorable, early intervention and aggressive therapy should be considered. Affected females should have access to higher levels of obstetric units and neonatal institutes. Before, during, and after delivery, monitoring and preparation should be intensified for affected gravidas to avoid serious complications of preeclampsia. In severe cases, delivery of the fetus and the placenta is the ultimate solution to treat preeclampsia. The current review is a summary of recent advances regarding the knowledge of preeclampsia. However, the detailed etiology, pathophysiology, and effect of preeclampsia seem complicated, and further research to address the primary etiology and pathophysiology underlying the clinical manifestations and outcomes is warranted.

The clinical value of combining shear wave elastography, VOCAL technique, and T2* MRI of early gestation placenta to predict pre‐eclampsia

“…Although PE is a severe complication of pregnancy, its exact mechanism is not yet fully understood. 9 Some studies [10][11][12] Prior studies [22][23][24] have also shown that calculating modulus values, VI, FI, VFI indices, and perfusion scores may not be fully objective. When placental tissue is heterogeneous or non-directional, measurement errors can occur.…”

“…Although PE is a severe complication of pregnancy, its exact mechanism is not yet fully understood 9 . Some studies 10–12 have hypothesized that, in normal pregnancy, placental formation occurs via the invasion of trophoblast cells into maternal spiral arteries, establishing low resistance and high flow maternal‐uterine‐placental circulation. In PE, the invasion of trophoblast cells into maternal spiral arteries is impaired, thus creating a hypoxic environment that can lead to abnormal differentiation of trophoblast cells.…”

Anesthetic recommendations for maternal and fetal safety in nonobstetric surgery: a balancing act

“…Early in pregnancy, the nearly 50% increase in maternal cardiac output is ascribed primarily to increased stroke volume, whereas later increases are primarily due to elevated heart rate [10]. Although reduced systemic vascular resistance results in decreased systolic, diastolic, and mean arterial pressures during pregnancy, patients usually maintain normal blood pressures in the absence of underlying pathology [11 ▪ ]. Maternal systolic pressure <90–95 mmHg is associated with decreased uteroplacental circulation threatening fetal development [12].…”

“…Physiologic respiratory alkalosis notwithstanding, maternal hypocapnia and hypercapnia must be avoided as both can interfere with placental oxygen delivery [52]. Since uteroplacental circulation lacks autoregulation, maternal hypotension can also lead to fetal acidosis [11 ▪ ,51].…”

Systematic Design and Evaluation of Aptamers for Specific Detection of VEGF and PLGF Biomarkers of Preeclampsia

“…Preeclampsia is a complex pregnancy disorder for maternal and neonatal health and can be lifethreatening if not diagnosed early. It is marked by hypertension and potential organ damage, especially to the liver and kidneys, and is tied to diverse pathophysiological processes [1][2][3][4]. Oral and IV medications to lower blood pressure can be administered to the women to treat the disease until the baby is mature enough to be delivered.…”