According to the World Society of Abdominal Compartment Syndrome, normal IAP in healthy persons is less than 5 to 7 mm Hg. The upper limit of nonpathological IAP is 12mmHg, and sustained increased pressure greater than 12 mm Hg is defined as intra-abdominal hypertension. Similar to the situation in cerebral perfusion pressure, a relationship exists between mean arterial
pressure and IAP that is related to abdominal perfusion pressure.69 Increased IAP compromises venous return, cardiac output, and systemic oxygen delivery. As IAP increases, oliguria and renal injury occur despite continued fluid replacement. Unfortunately, once intraabdominal hypertension has occurred, relieving this pressure (ie, abdominal compartment syndrome) does not stop the renal injury. The goal is to detect the onset of renal injury by using new biomarkers. Currently, relief of abdominal compartment
syndrome by laparotomy is the standard of care to prevent further renal injury. The primary strategy to prevent AKI is to minimize
the risk of kidney injury by monitoring IAP before the onset of abdominal compartment syndrome.