PREECLAMPSIA: PLACENTAL PATHOPHYSIOLOGY, PREDICTIVE BIOMARKERS, MATERNAL-FETAL OUTCOMES, AND EVIDENCE-BASED MANAGEMENT IN CONTEMPORARY OBSTETRICS AND GYNECOLOGY

Background: Preeclampsia is a multisystem hypertensive disorder of pregnancy affecting 2–8% of all pregnancies globally and remaining a leading cause of maternal and perinatal mortality and morbidity worldwide. Characterized by new-onset hypertension (systolic blood pressure ≥ 140 mmHg or diastolic ≥ 90 mmHg) after 20 weeks of gestation with evidence of systemic organ involvement—including proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or new-onset headache—preeclampsia is responsible for approximately 70,000 maternal deaths and 500,000 perinatal deaths annually. Its underlying pathophysiology centers on defective placental implantation and impaired trophoblast invasion, resulting in placental ischemia, antiangiogenic factor imbalance, and systemic endothelial dysfunction that produces the clinical syndrome. Objective: To provide a comprehensive, evidence-based review of the pathophysiology, first-trimester risk stratification, biomarker-based prediction, maternal-fetal complications, pharmacological prevention with low-dose aspirin, and acute and definitive management of preeclampsia within the framework of contemporary obstetric and gynecological practice, synthesizing evidence from eight primary peer-reviewed sources. Methods: A systematic review of eight primary sources was conducted, including prospective cohort studies, large randomized controlled trials, meta-analyses, and authoritative clinical practice guidelines published between 2001 and 2024. Results: Defective deep placentation—failure of extravillous trophoblast (EVT) remodeling of spiral arteries beyond the decidual segment—is the central pathogenic mechanism, producing a high-resistance, low-flow uteroplacental circulation. Placental hypoxia and oxidative stress increase soluble fms-like tyrosine kinase-1 (sFlt-1) secretion and reduce placental growth factor (PlGF), with sFlt-1/PlGF ratio > 38 predicting preeclampsia onset with 80% sensitivity and 95% specificity within 4 weeks. First-trimester combined screening (uterine artery Doppler pulsatility index, MAP, PAPP-A, PlGF) identifies 90% of early-onset preeclampsia at a 10% false-positive rate. Low-dose aspirin (150 mg/day from 11–14 weeks until 36 weeks) reduces preterm preeclampsia by 62% in high-risk women (ASPRE trial). Magnesium sulfate prevents eclamptic seizures in severe preeclampsia with a number needed to treat of 50. Conclusion: The paradigm shift from reactive management of established preeclampsia to proactive first-trimester risk stratification and aspirin prophylaxis has transformed the preventive potential of obstetric care. Integration of the Fetal Medicine Foundation (FMF) competing-risks algorithm into routine antenatal practice offers the most validated pathway for identifying high-risk pregnancies that benefit from early aspirin prophylaxis and intensified surveillance.