Figure 1

Increased survival from traumatic injury can be attributed in part to aggressive resuscitation including early resuscitation with crystalloid and blood products and the almost universal adoption of damage control surgical procedures (i.e., abdominal packing). The interplay of these factors alter hydrostatic and oncotic pressure differentials contributing to the formation of hydrostatic intestinal edema. Specifically, the decrease in plasma oncotic pressures (secondary to hemodilution from resuscitation) combined with the increase in capillary hydrostatic pressures (secondary to abdominal (peri-hepatic) packing induced increases in mesenteric venous pressures) leads to net efflux of fluid into the interstitium. Contributing factors also include increased capillary permeability from IR mediated gut injury in the context of hemorrhagic shock/resuscitation and elevated central venous pressure during resuscitation which prevents lymphatic mediated efflux of fluid out of the interstitium (secondary to an elevated central venous pressure to lymphatic flow gradient. In addition, edema leading to increases in IAP can act in a feed forward manner; increases in central venous pressure (CVP) seen with increased IAPs also prevents lymphatic efflux of fluid out of the interstitium. The decrease in cardiac output, in addition to leading to further ischemic injury, can also lead to increased administration of fluids, worsening exacerbating hemodilution. Additionally, venous hypertension is a documented consequence of increasing IAPs, leading to further exacerbation of intestinal edema.