The two faces of preeclampsia

During normal pregnancy, blood volume increases by nearly two liters. Distinctively, the absence and also the extreme extent regarding the volume expansion are likely accompanied with serious conditions. Undoubtedly, preeclampsia, defined as the appearance of hypertension and proteinuria during the second half of pregnancy, is not a homogenous disease. The early onset which begins prior to the 34th week, is characteristically a hypovolemia-associated form and depicts the placental origination, in which endothelial damage leads to hypertension and organ damage due to vasoconstriction and microthrombosis. Fetal blood supply progressively worsens due to placental insufficiency. The outcome of this condition often leads to fetal death, eclampsia, or placental abruption. Management is confined to a diligent prolongation of pregnancy to accomplish improved neonatal pulmonary function. The late onset form, associated with high cardiac output, is a maternal disease, in which obesity is a risk factor since it predisposes individuals to enhanced water retention, hypertension, and a weakened endothelial dysfunction. Initially, low extremity edema often times progresses to a generalized form and frequently results in hypertension. In several cases proteinuria appears. This condition entirely meets the preedampsia criteria. Fetal weight is normal or frequently over the average. It is very likely, the increasing parenchymal stasis will lead to ascites, eclampsia, or placental abruption. During the management of this hypervolemia-associated preedampsia, the administration of diuretic furosemide treatment seemingly offers promise.