The factors leading to abdominal compartment syndrome (ACS) are multifactorial, and include ischemia/reperfusion injury from hemorrhagic shock/resuscitation, third spacing of fluid into the gut lumen, interstitium, and peritoneum secondary to hemodilution and altered microvascular fluid flow, and polymorphonuclear (PMN) cell priming leading to distant organ injury. Hemorrhagic shock generally has minimal effects on IAP; however, with high volume resuscitation, the interplay of increased capillary permeability secondary to ischemia/reperfusion injury and decreased oncotic pressures (secondary to hemodilution from resuscitation) can lead to a rapid increase in IAPs. While major effects are intra-abdominal, the interplay of these factors lead to distant organ injury, potentially through systemic neutrophil priming and activation. Additionally, post-decompression, a reperfusion syndrome may occur and function as a second hit. This is secondary to sudden release of flow-limiting elevated IAP, leading to recurrent gut reperfusion injury and release of pro-inflammatory mediators. Additionally, peritoneal fluid may serve as a propogator of neutrophil priming.