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.