Pre-eclampsia renamed and reframed: Intra-abdominal hypertension in pregnancy

Abstract

This hypothesis proposes pre-eclampsia is caused by intra-abdominal hypertension in pregnancy. Sustained or increasing intra-abdominal pressure ⩾12mmHg causes impaired venous return to the heart, systemic vascular resistance, ischemia reperfusion injury, intestinal permeability, translocation of lipopolysaccharide endotoxin to the liver, cytotoxic immune response, systemic inflammatory response, pressure transmission to thoracic and intra-cranial compartments, and multi-organ dysfunction. This hypothesis is predicated on Pascal's law, evidence founded in the intra-abdominal hypertension literature, and the adapted equation ΔIAP-P=ΔIAVF/Cab, where ΔIAP-P=change in intra-abdominal pressure in pregnancy, ΔIAVF=change in intra-abdominal vector force (volume and force direction) and Cab=abdominal compliance. Factors causing increased intra-abdominal pressure in pregnancy include: progressive uterine expansion, obstetrical factors that increase intra-uterine volume excessively or acutely, maternal anthropometric measurements that affect intra-abdominal pressure thresholds, maternal postures that increase abdominal force direction, abdominal compliance that is decreased, diminished with advancing gestation, or has reached maximum expansion, habitation at high altitude, and rapid drops in barometric pressure. We postulate that the threshold for lipopolysaccharide translocation depends on the magnitude of intra-abdominal pressure, the intestinal microbiome complex, and the degree of intestinal permeability. We advance that delivery cures pre-eclampsia through the mechanism of abdominal decompression.