GI‎ > ‎

Abdominal Compartment Syndrome


  • Organ dysfunction due to increased abdominal pressure which compromises perfusion to vital organs
  • Can be thought of similarly as Cerebral Perfusion Pressure in that while normally, perfusion to organs within the abdominal compartment is MAP-RAP, when abdominal compartment pressure increases, perfusion pressure becomes MAP-Abdominal pressure
  • Normal intraabdominal pressure in adults is about 5 mmHg
  • Intraabdominal Hypertension in adults is >12 mmHg
  • Abdominal Compartment Syndrome in adults is defined as an intraabdominal pressure of >20 mmHg with evidence of organ dysfunction. In reality, a more relevant definition may be an elevated intraabdominal pressure with evidence of organ dysfunction. There are no clear values for intraabdominal hypertension or compartment syndrome in children
  • Increased abdominal wall compliance that develops over time (ie chronic cirrhosis with ascites) may be protective against abdominal compartment syndrome


  • Intraabdominal pressure rises due to ascites, bowel wall edema, organomegaly, intraabdominal bleeding, or some combination thereof
  • As intraabdominal pressure rises, it impairs perfusion pressure to vital organs (defined as MAP-Intraabdominal Pressure). In adults, a target of a abdominal perfusion pressure of 60 mmHg is generally quoted. 
  • Cardiac: impairs venous return (functionally obstructs IVC flow), pushes the diaphragm cephalad which can also cause cardiac compression
  • Pulmonary: Due to abdominal competition and pushing of the diaphragm cephalad, higher peak inspiratory and airway pressures, reduced chest wall compliance and lower tidal volumes. Pulmonary infection also more common with IAH
  • Renal: Renal vein compression increases venous resistance and impairs renal perfusion (major mechanism). The renin-angiotensin system is also upregulated due to low cardiac volume, leading to renal artery vasoconstriction. Hence, patients develop acute kidney injury and reduced urine output
  • Gastrointenstinal: Mesenteric blood flow and intestinal mucosal perfusion is decreased. Mesenteric veins are also compressed, impairing venous return and leading to intestinal edema, which further increases abdominal compartment pressures, inducing a vicious cycle
  • Hepatic: Hepatic clearance of lactic acid is reduced by increased intraabdominal pressure
  • CNS: ICP can also be elevated as a result of increased IA pressure


  • Tense, distended abdomen (not a very reliable physical exam finding for IAH)
  • Worsening oliguria and ventilatory requirements
  • Peripheral edema
  • Hypotension
  • Jugular venous distension


  • Imaging not always helpful
  • Measurement of IAP is key
  • Measurement technique: 
    • Bladder pressure: 
      • 1) Drainage catheter of Foley is clamped. 
      • 2) Sterile saline (1 cc/kg up to 25 cc) is instilled into the bladder via the aspiration port and the catheter also is filled with fluid 
      • 3) 18 gauge needle attached to pressure transducer is inserted into the aspiration port (or via the same set up as an arterial line transducer)
      • 4) Pressure is measured at end expiration in the supine position after ensuring no abdominal muscle contractions are present
      • 5) Zeroed at level of mid-axillary line
    • May not be accurate if there are intraperitoneal adhesions, a neurogenic bladder, or pelvic fractures/hematomas 
Reprinted from Journal of the American College of Cardiology, 51(3), Wilfried Mullens, Zuheir Abrahams, Hadi N. Skouri, Gary S. Francis, David O. Taylor, Randall C. Starling, et al., Elevated Intra-Abdominal Pressure in Acute Decompensated Heart Failure A Potential Contributor to Worsening Renal Function?, 300–306, Copyright 2008,


  • Supportive care including gastric and rectal decompression
  • Percutaneous drainage of ascites or intraperitoneal hematomas
  • Percutaneous catheter placement (we tend to place acute peritoneal dialysis catheters at the level of the linea alba (non vascular) below the umbilicus)
  • Sedation and chemical paralysis to relax the abdominal musculature
  • Ventilatory support as needed
  • Hemodynamic support as needed
  • Surgical decompression and usually maintenance of an open abdomen via a temporary abdominal wall closure is the definitive treatment


  1. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006; 32:1722.
  2. Vidal MG, Ruiz Weisser J, Gonzalez F, et al. Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Crit Care Med 2008; 36:1823.
  3. van Mook WN, Huslewe-Evers RP, Ramsay G. Abdominal compartment syndrome. Lancet 2002; 360:1502.
  4. Citerio G, Vascotto E, Villa F, et al. Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med 2001; 29:1466.
  5. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013; 39:1190.
  6. Cheatham ML, De Waele JJ, De Laet I, et al. The impact of body position on intra-abdominal pressure measurement: a multicenter analysis. Crit Care Med 2009; 37:2187.
  7. Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of elevated intraabdominal pressure. Chest 2011; 140:1428.
  8. An G, West MA. Abdominal compartment syndrome: a concise clinical review. Crit Care Med 2008; 36:1304.
  9. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med 2010; 38:402.