Abdominal compartment syndrome

Classification of etiology

Abdominal compartment syndrome is classified into three groups: primary, secondary, and recurrent. Primary ACS results from causes originating inside the abdominal cavity, such as peritoneal edema from diffuse peritonitis, abdominal trauma, reperfusion injury after bowel ischemia, retroperitoneal edema from acute pancreatitis, ileus, bowel obstruction, intra-abdominal masses, abdominal packing, or closure under tension. Secondary ACS arises from conditions outside the abdomen, often linked to massive fluid resuscitation, retroperitoneal hematoma from trauma or aortic rupture, and ascites. Recurrent (tertiary) ACS occurs when elevated intra-abdominal pressure returns after initial treatment of primary or secondary ACS.

Pathophysiology

ACS develops when fluid (edema, blood, or free fluid) accumulates in the peritoneal and retroperitoneal space beyond the abdominal wall's compliance threshold, preventing further stretch. Once the wall cannot expand, additional fluid causes rapid pressure rises. Initially, pressure above 12 mmHg defines intra-abdominal hypertension (IAH), which impairs organ function without causing failure. ACS is sustained IAP above 20 mmHg with new or progressive organ failure.

Pressure thresholds are relative: small children develop compartment syndromes at lower pressures, while young healthy individuals may tolerate 20 mmHg. The underlying driver is capillary permeability from systemic inflammatory response syndrome (SIRS), which leaks fluid into interstitial spaces, particularly the gut wall, mesentery, and retroperitoneum. As pressure rises, organs collapse, affecting cardiovascular and pulmonary systems; without surgical decompression and a silo, mortality is high.

Diagnosis

Diagnosis requires intra-abdominal pressure above 20 mmHg with evidence of organ failure, typically developing over several hours and lasting six or more hours. The gold standard for measurement is via the urinary bladder; the trend in bladder pressure may be more informative than a single value. Elevated pressure compresses renal veins, causing oliguria unresponsive to fluid resuscitation. Diagnosis combines clinical findings with bladder pressure measurement.

Multiorgan failure can involve cardiac, pulmonary, renal, neurological, gastrointestinal, abdominal wall, and ophthalmic systems. The gut is most sensitive to IAH, showing end-organ damage before other systems. Risk factors for IAH and ACS include large-volume crystalloid resuscitation, which clinicians should target for prevention.

Treatment

Surgical decompression of the abdomen is the treatment of choice, typically improving organ function. The procedure involves opening the abdominal wall and fascia to create space for viscera. After decompression, temporary abdominal closure techniques (e.g., Bogota bag, artificial bur, vacuum devices using negative pressure wound therapy) are employed to prevent secondary intra-abdominal hypertension.

Did You Know?

• ACS is more common in surgical intensive care units than medical intensive care units due to risk factors such as burns, abdominal trauma, and large volume transfusions.
• Most ACS cases are predicted to arise from primary causes, attributed to diligent evaluation of large volume resuscitation efforts.
• Risk factors for ACS include hypothermia (30°C) and burns over 50% total body surface area or with inhalation injury.