Abdominal Compartment Syndrome

Updated: Jan 30, 2023
  • Author: Richard Paula, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
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Practice Essentials

Although compartment syndrome is well recognized to occur in the extremities, it also occurs in the abdomen and, some believe, in the intracranial cavity. Compartment syndrome occurs when a fixed compartment, defined by myofascial elements or bone, becomes subject to increased pressure, leading to ischemia and organ dysfunction. The exact clinical conditions that define abdominal compartment syndrome (ACS) are controversial; however, organ dysfunction caused by intra-abdominal hypertension (IAH) is considered to be abdominal compartment syndrome. Intra-abdominal hypertension is defined as sustainedIAP above 12 mm Hg, and  ACS results from repeated elevation of pressure above 20 mm Hg with associated organ dysfunction. [1, 2, 3, 4, 5]

Organ dysfunction may be respiratory insufficiency secondary to compromised tidal volumes, decreased urine output caused by falling renal perfusion, or any organ dysfunction caused by increased abdominal compartment pressure. Surgical decompression remains the mainstay treatment of ACS. [6] However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS. [7, 1, 2, 8, 9, 10, 3, 11]

The frequency of abdominal compartment syndrome in trauma ICU admissions is anywhere from 5 to 15% and 1% of general trauma admissions. Abdominal compartment syndrome has been documented in all age groups. The intra-abdominal pressure (IAP) that leads to morbidity (>20 mm Hg) appears to be similar in the pediatric population. [12, 13]  The incidence of IAH/ACS in the pediatric population is 12.7 to 20%. [14, 15, 16]

In a retrospective study, by Bozer et al, of 2887 children (< 18 yr) in 49 children’s hospitals wth ACS, overall mortality was 48.87%, with mortality in patients aged zero to 30 days being 58.61%. [17]

Abdominal compartment syndrome was recognized clinically in the 19th century when Marey and Burt observed its association with declines in respiratory function. In the early 20th century, Emerson's animal experiments demonstrated mortality associated with abdominal compartment syndrome. Initially, cardiorespiratory compromise was thought to be the cause; however, renal failure was hypothesized by Wendt and was later studied by Thorington and Schmidt. Kron and Iberti developed a simple method of accurately measuring intra-abdominal pressure. This has led to a better understanding of the relationship between IAH and abdominal compartment syndrome. [18, 19, 20, 21, 22, 23]

WSACS guidelines

The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations [2, 16, 24] :

  • Intra-abdominal pressure (IAP) is approximately 5-7 mm Hg in critically ill adults.
  • Intra-abdominal hypertension is defined by a sustained or repeated pathological elevation in IAP of ≥12 mm Hg.
  • ACS is defined as a sustained IAP >20 mm Hg associated with organ dysfunction/failure.
  • IAH is graded as follows: Grade I: IAP 12-15 mm Hg;  Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg.
  • Patients should be screened for IAH/ACS risk factors upon ICU admission and in the presence of new or progressive organ failure.
  • APP should be maintained above 50-60 mm Hg in patients with IAH/ACS [Abdominal perfusion pressure (APP) = mean arterial pressure (MAP) – IAP].
  • Fluid resuscitation volume should be carefully monitored to avoid overresuscitation in patients at risk for IAH/ACS.
  • Hypertonic crystalloid and colloid-based resuscitation should be considered in patients with IAH to decrease the progression to secondary ACS.
  • Surgical decompression should be performed in patients with ACS that is refractory to other treatment options.
  • Presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH/ACS.
  • Recommend that studies of IAH or ACS adopt the transbladder technique as a standard IAP measurement technique
  • Suggest brief trials of neuromuscular blockade as temporizing measure in treatment of IAH.

Three categories

As the diagnosis of abdominal compartment syndrome became easier to establish, it was observed to occur as a consequence of a variety of primary clinical events. Abdominal compartment syndrome can be divided into the following 3 categories:

  • Primary or acute abdominal compartment syndrome occurs when intra-abdominal pathology is directly and proximally responsible for the compartment syndrome

  • Secondary abdominal compartment syndrome occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation [25]

  • Chronic abdominal compartment syndrome occurs in the presence of cirrhosis and ascites or related disease states, often in the later stages of the disease

In the ED and ICU

In the emergency department and intensive care unit, abdominal compartment syndrome is recognized with growing frequency as the cause of morbidity such as metabolic acidosis, decreased urine output, and decreased cardiac output. The cause of these events might easily be mistaken for other pathologic events such as hypovolemia if the clinician is not alert to the morbidity associated with abdominal compartment syndrome.

Therapy should include fluid resuscitation and transfusion if needed. Pharmacologic therapy is less effective than mechanical drainage. Paracentesis may be a superior alternative to decompressive laparotomy in this patient population.



Organ dysfunction with abdominal compartment syndrome is a product of the effects of IAH on multiple organ systems. Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremity.

Problems begin at the organ level with direct compression; hollow systems such as the intestinal tract and portal-caval system collapse under high pressure. Immediate effects such as thrombosis or bowel wall edema are followed by translocation of bacterial products, leading to additional fluid accumulation, which further increases intra-abdominal pressure.

At the cellular level, oxygen delivery is impaired, leading to ischemia and anaerobic metabolism. Vasoactive substances such as histamine and serotonin increase endothelial permeability; further capillary leakage impairs red cell transport; and ischemia worsens.

Simon et al demonstrated a significantly lowered threshold for injury from IAH in pigs after hemorrhage and fluid resuscitation. [26] Oxygen delivery may play an important role.

Although the abdominal cavity (ie, the peritoneal and, to a lesser extent, retroperitoneal cavities) is much more distensible than an extremity, it reaches an endpoint at which the pressure rises dramatically. This is less apparent in chronic cases because the fascia and skin slowly stretch and thus tolerate greater fluid accumulation.

As pressure rises, abdominal compartment syndrome impairs not only visceral organs but also the cardiovascular and the pulmonary systems; it may also cause a decrease in cerebral perfusion pressure. Therefore, abdominal compartment syndrome should be recognized as a possible cause of decompensation in any critically injured patient.



Abdominal compartment syndrome occurs when the IAP is too high, similar to compartment syndrome in an extremity. The 3 types of abdominal compartment syndrome (primary, secondary, and chronic) have different and sometimes overlapping causes.

Primary ACS

Causes of primary (ie, acute) abdominal compartment syndrome include the following:

In one review and meta-analysis of studies of patients who developed ACS after repair of ruptured abdominal aortic aneurysms, mortality was found to be 47%. Treatment included open decompression in 86 patients; percutaneous drainage in 18 (catheter only in 5; combined with tissue plasminogen activator infusion in 13); and conservative measures in 5. [29]

Secondary ACS

Secondary abdominal compartment syndrome may occur in patients without an intra-abdominal injury, when fluid accumulates in volumes sufficient to cause IAH. Causes include the following:

  • Large-volume resuscitation: The literature shows significantly increased risk with infusions greater than 3 L

  • Large areas of full-thickness burns [30] : Hobson et al demonstrated abdominal compartment syndrome within 24 hours in burn patients who had received an average of 237 mL/kg over a 12-hour period [31]

  • Penetrating or blunt trauma without identifiable injury

  • Postoperative

  • Packing and primary fascial closure, which increases incidence

  • Sepsis

A retrospective study reported on risk factors directly associated with mortality in patients with both intra-abdominal hypertension and ACS. Polytransfusion was a strong predictor of mortality, along with a reported history of diabetes and the total amount of blood products used. [32]

Secondary ACS in patients with lower extremity vascular injuries from penetrating injury or blunt trauma was associated with a 60% mortality in one study. [33]


Causes of chronic abdominal compartment syndrome include the following:

  • Peritoneal dialysis

  • Morbid obesity

  • Cirrhosis

  • Meigs syndrome

  • Intra-abdominal mass



If left untreated, abdominal compartment syndrome is almost uniformly fatal. [7, 34, 35] Eddy and colleagues noted a mortality of 68% for patients with documented abdominal compartment syndrome. [36] Most of the population was male (70%), and most had experienced blunt trauma (80%). In the subsequent literature, mortality rates have ranged from 25 to 75%.

The high mortality associated with abdominal compartment syndrome, even with treatment, reflects the fact that the condition affects multiple organ systems. Furthermore, abdominal compartment syndrome is often a sequela to severe injuries that independently carry a high morbidity and high mortality. Malbrain et al demonstrated that, by itself, elevation of abdominal pressure correlates with increased mortality before the actual development of abdominal compartment syndrome. [37]

In a meta-analysis by Karkos et al, mortality was 47% in patients in whom ACS developed after repair of a ruptured abdominal aortic aneurysm. [29]

A retrospective study reported on risk factors directly associated with mortality in patients with both intra-abdominal hypertension and ACS. Polytransfusion was a strong predictor of mortality, along with a reported history of diabetes and the total amount of blood products used. [32]

A 5-year retrospective study at 3 level 1 trauma centers in Chicago identified the following prognostic factors in trauma patients with ACS [38] :

  • The 30-day mortality was strongly associated with an initial intra-abdominal pressure >20 mm Hg and moderately associated with blunt injury mechanism.
  • Lactic acid level >5 mmol/L on admission was moderately associated with increased blood transfusion requirements and with acute renal failure during hospitalization.
  • Developing ACS within 48 hr of admission was moderately associated with increased length of stay in the ICU, more ventilator days, and longer hospital stay.
  • Initial operative intervention lasting more than 2 hr was moderately associated with risk of developing multiorgan failure.
  • Hemoglobin level < 10 g/dL on admission, ongoing mechanical ventilation, and ICU stay >7 days were moderately associated with a disposition to long-term support facility.