Hypothesis: preeclampsia is a venous disease secondary to an increased intra-abdominal pressure

It is hypothesized that in some women an excessively high intra-abdominal pressure (IAP) compresses the inferior vena cava, uterine veins, portal vein, hepatic veins, splenic vein and renal veins which lead to a decreased flow in these vascular beds, producing lower extremity edema, fetal-placental ischemia, a glomerulopathy with proteinuria and hypertension, hepatic ischemia and thrombocytopenia, increased uric acid, and hemolysis/elevated liver enzymes/low platelet known as the HELLP syndrome. There can be variability in the expression of these components. Placental-fetal ischemia could lead to expression of soluble fms-like tyrosine kinase1 (sFLT) and endoglin which have been shown to cause additional diffuse endovascular damage. A further increase in IAP pushes the diaphragm cephalad, increasing intrathoracic pressure leading to upper extremity edema, decreased internal jugular venous flow, cerebral vascular engorgement, raised intracranial pressure, and if unresolved, seizures. Placental/fetal ischemia and hepatic ischemic necrosis may lead to diffuse inflammation and a septic inflammatory response syndrome (SIRS) which may become a vicious cycle, perpetuating the ischemia. It is further hypothesized that application of an externally applied negative abdominal pressure device will lower IAP and possibly reverse the pathophysiology of preeclampsia. As the abnormal placental proteins develop weeks before clinical preeclampsia, early application of external negative abdominal pressure may prevent development of the syndrome.