Preeclampsia: Systemic Endothelial Damage Leading to Increased Activation of The Blood Coagulation Cascade

Preeclampsia is a severe pregnancy complication affecting between five and seven percent of pregnant woman worldwide. Typically, this condition presents after twenty weeks of pregnancy and as late as six weeks after the birth of a child. This disease is characterized in pregnant women without previous hypertension by a diagnosis of elevated blood pressure in excess of 140 mmHg systolic over 90 mmHg diastolic and a finding of protein in the urine in excess of 300 mg over a 24 hour period. Preeclampsia carries with it a significant risk of injury or death to both the mother and child. Common complications include stroke, placental abruption, seizures, low fetal birth weight and hemorrhage. Once preeclampsia is present in a pregnancy, there is no definitive cure other than to deliver the child. Despite a great deal of research and statistical analysis, the origin of preeclampsia remains elusive. It is posited that systemic endothelial damage causes the blood coagulation cascade to be increasingly activated and results in an excess of minute thromboses in the placenta mass and renal system. It is the dysfunction caused in the placenta and kidneys that ultimately manifests into the hallmarks of a preeclamptic pregnancy, namely hypertension and proteinuria. Further, as the link between preeclampsia and cardiovascular disease is becoming stronger it seems likely that the dysfunctions that cause preeclampsia will reassert themselves as cardiac outcomes later in the mother’s life. The intention of this paper is to examine the major avenues of research that have been put forth as moving towards an answer to the nature of this disease and assess what the factors or combinations of factors results in preeclamptic complications.