Abstract
Preeclampsia (PET) is a multisystem inflammatory disorder that represents a leading cause of feto-maternal morbidity and mortality, complicating 2–5% of all pregnancies. PET incurs an increased risk of venous thromboembolism, which is one of the leading causes of death in pregnancy and in the postpartum period. This prothrombotic phenotype is attributable to the maternal phase of PET, which is characterized by a systemic inflammatory response and coagulation activation. Research continues to be undertaken in terms of preventative measures, however, currently revolves around pharmacological low dose aspirin initiated in the first trimester of pregnancy for those with risk factors. Treatment involves antenatal corticosteroids for fetal lung development in preterm birth, parenteral magnesium sulfate for fetal neuroprotection and maternal seizure prophylaxis, and timely birth of the fetus and placenta being the only definitive treatment of PET. Patients with a venous thromboembolism (VTE) risk deemed to be >1–3% are treated with pharmacological thromboprophylaxis in the form of low molecular weight heparin. Completing each woman’s VTE risk assessment is crucial, particularly in the setting of PET, as there is also a proven associated competing hemorrhagic risk.
Highlights
Preeclampsia (PET) complicates 2–5% of all pregnancies and represents a leading cause of feto-maternal morbidity and mortality worldwide [1–3]
Complications of PET include intrauterine growth restriction (IUGR), fetal death (1–2% of cases), preterm birth, hepatic and renal dysfunction, thrombosis, coagulopathy, eclampsia and maternal death [8–10]
It is postulated that this hypercoagulable state develops to limit the risk of major bleeding associated with labor and birth [61, 62]. This pregnancy-associated hypercoagulability may reduce the risk of major peripartum bleeding, the shift toward a procoagulant phenotype confers an increased risk of venous thromboembolism (VTE). This baseline pregnancy-associated elevated thromboembolic risk is increased in the presence of additional VTE risk factors
Summary
Preeclampsia (PET) complicates 2–5% of all pregnancies and represents a leading cause of feto-maternal morbidity and mortality worldwide [1–3]. Complications of PET include intrauterine growth restriction (IUGR), fetal death (1–2% of cases), preterm birth, hepatic and renal dysfunction, thrombosis, coagulopathy, eclampsia (a severe manifestation of PET characterized by severe hypertension and generalized seizures) and maternal death (up to 70,000 deaths annually worldwide) [8–10]. PET is characterized by alterations in pro and anticoagulant pathways [18], beyond the physiological hypercoagulable state that occurs in pregnancy [19, 20]. This hypercoagulable state may increase venous thromboembolism (VTE) risk [1], a major contributor to maternal morbidity and mortality [21–24]. VTE is a risk factor and a consequence of PET [13]
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