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Elevated abdominal compartment pressure compresses the abdominal vasculature. The resulting decrease in perfusion leads to ischemia of visceral organs, cellular hypoxia, and anaerobic metabolism, secondary to decreased intracellular adenosine triphosphate (ATP).1 Decreased ATP leads to failure of the sodium-potassium pump, and increased intracellular sodium causes cells to swell and rupture, leading to further ischemia (including bowel ischemia) and decreased vascular volume. Anaerobic metabolism creates a rise in lactic acid secondary to the dramatic fall in ATP, resulting in metabolic acidosis.


Decreased bowel perfusion causes changes in the normal barrier function of the gastrointestinal mucosa, promoting bacterial translocation and placing the patient at additional risk for sepsis. Metabolic acidosis worsens as the patient's condition deteriorates.2




1. Vegar-Brozovic V, Stoic-Brezak J. Pathophysiology of abdominal compartment syndrome. Transplant Proceedings. 38(3):833-835, April 2006. [Context Link]


2. Walker J, Criddle LM. Pathophysiology and management of abdominal compartment syndrome. American Journal of Critical Care Nursing. 12(4):367-371, July 2003. [Context Link]