Compartment syndrome occurs when the pressure within a closed anatomic space (a compartment) becomes so elevated that capillary perfusion is compromised and tissue ischemia develops. Compartment syndromes are classically thought of as complications associated with orthopedic trauma, occurring when muscular compartments of extremities develop elevated pressures requiring decompressive fasciotomies. However, any closed anatomic space, including the abdominal cavity, is at risk of developing a compartment syndrome. Abdominal compartment syndrome is a clinical disease spectrum that results from elevated intra-abdominal pressure (IAP) due to tissue edema or free fluid collecting in the abdominal cavity. Elevated pressure in the abdomen is referred to as intra-abdominal hypertension (IAH) while the end stage organ failure that occurs due to the pathophysiologic derangements that occur as a result of increasing intra-abdominal pressure is referred to as the abdominal compartment syndrome (ACS). This clinical spectrum dramatically impacts patient outcome: The end result of undetected and untreated intra-abdominal hypertension is multisystem organ failure and patient death.

The primary pathophysiologic event leading to intra-abdominal hypertension and the abdominal compartment syndrome (IAH/ACS) is interstitial edema in the bowel and mesentery due to capillary endothelial damage (see Figure). This capillary endothelial damage occurs due to ischemia from the original physiologic insult (sepsis, hemorrhage, etc) and due to secondary damage from the pro-inflammatory cytokines released in response to this insult. Many liters of intersitial fluid can accumulate within the intra-abdominal compartment via this mechanism. As fluid accumulates the abdominal wall and fascia are slowly stretched until they becomes less compliant, causing the pressure within the abdominal cavity to rise. Elevation of IAP has serious impact on organ perfusion throughout the body.

An especially susceptible organ to tissue ischemia/reperfusion injury, capillary leak and edema is the bowel. Since the abdominal wall limits the total volume of intra-abdominal space, as bowel expands the pressure within the abdomen also increases. This causes occlusion of capillary blood flow and ultimately ends in compromise of venous return and arterial flow. The resulting ischemia triggers a vicious cycle of further inflammation, capillary leak, bowel edema and increasing intra-abdominal pressure. Normal intra-abdominal pressure is 0-5 mm Hg. Physiologic compromise begins when the pressure rises above 8-10 mm Hg. Once the pressures increase beyond about 20 mm Hg irreversible tissue injury occurs, ultimately resulting in ACS and multiple organ failure. Early recognition of rising abdominal pressure is critically important because it allows prompt intervention which will prevent ACS from developing, leading to a much better prognosis for the patient.

Traditionally, ACS was considered a traumatic surgical disease. However, ACS is a problem in many critically ill patients who have suffered no trauma, especially those suffering systemic inflammatory response syndromes (SIRS). Table 1 lists a number of clinical conditions associated with ACS development. While this list is a helpful reminder of conditions that can be complicated by ACS, recognizing a clinical pattern is more useful. Any patient with either an inflammatory response causing capillary leak and requiring volume resuscitation (of 5 liters or more) or vasopressor support is at risk for developing bowel edema, intra-abdominal hypertension and ACS. A second group is patients who have suffered direct peritoneal or retroperitoneal injury from trauma, surgery or inflammation (pancreatitis, bowel obstruction, mesenteric ischemia). Intra-abdominal pressure monitoring should be strongly considered in all patients with this clinical presentation.

Overview of the pathophysiology leading to intra-abdominal hypertension