When rising intra-abdominal pressure turns silent killer: the abdominal compartment syndrome

The spectrum of clinical disorders arising from raised intra-abdominal pressure (IAP) was recognized from the 19thcentury onwards. Abdominal compartment syndrome (ACS) was first described three decades ago among four patients who underwent surgery for ruptured abdominal aortic aneurysm. ACS manifested within the first 24 hours postoperatively with massive abdominal distension and was characterized by rising ventilation pressures, central venous pressure, and oliguria.1 There is increasing awareness among clinicians that ACS may be the underlying cause for impaired cardiac output, renal function, and lead to metabolic acidosis. A high index of suspicion is called for as the consequences of ACS may be easily mistaken for hypovolemia; continued fluid resuscitation results in worsening of the clinical state. 

Retrospective studies have reported the presence of intra-abdominal hypertension (IAH) in 38–45% of adult critically ill patients.2 In a recent multicentric study of 491 mixed critically ill patients, IAH occurred in 34.0% of patients day 1 of ICU admission and in 48.9% of patients during the entire study period.3

Pathophysiology, causes, and risk factors 

The volume of the intra-abdominal compartment may increase due to fluid, air, tissue edema, or the presence of a solid tumor. As the intra-abdominal volume rises, the elastic recoil of the abdominal wall tends to mitigate any rise in pressure. However, the IAP rises steeply once compensatory mechanisms fail. Thus, ACS may occur due to an increase in the intra-abdominal volume, decreased compliance of the abdominal wall, or a combination of both mechanisms. Massive crystalloid fluid resuscitation and a positive fluid balance are being increasingly recognized as a trigger for raised IAP, probably due to visceral edema leading to an increase in the intra-abdominal volume.4 Tense ascites, hemoperitoneum, acute pancreatitis, and unrelieved ileus are common etiological factors for the development of ACS. Blunt trauma, sepsis, and massive blood transfusion can also trigger the development of ACS. 


The World Society of Abdominal Compartment Syndrome (WSACS) has formulated definitions and practice guidelines for IAP and ACS. IAH is defined as a sustained rise in IAP of higher than 12 mm Hg. IAH is classified into four grades of severity (Table 1). ACS is defined as a sustained rise in IAP greater than 20 mm Hg with or without an abdominal perfusion pressure (mean arterial pressure – IAP) less than 60 mm Hg and accompanied by end-organ dysfunction.5

Grade of intra-abdominal hypertensionIntra-abdominal pressure (mm Hg)
Grade I 12–15
Grade II16–20
Grade III21–25
Grade IV> 25

Table 1. The WSACS classification of intra-abdominal hypertension based on severity 

Organ dysfunction in ACS

IAH can impair the function of both ventricles and reduce cardiac output. There is an increase in the central venous and pulmonary artery pressures. Besides, the systemic vascular resistance rises, with an increase in the left ventricular afterload. The respiratory function is compromised, with the requirement for increased ventilation pressures. There is a reduction in the functional residual capacity, with impaired gas exchange, leading to hypoxia and hypercarbia. There may be a profound drop in the pH due to a combination of respiratory and metabolic acidosis. Increased IAP leads to compression of the renal parenchyma; furthermore, the renal blood flow decreases due to a fall in the cardiac output. The activation of the renin-angiotensin system results in salt and water retention. Oliguria in spite of the administration of fluids is a key early feature of ACS. IAH can lead to compromise of intestinal mucosal blood flow. This may precipitate gut ischemia and lead to translocation of bacteria, resulting in systemic sepsis. An increase in IAP leads to upward displacement of the diaphragm, with an increase in the intrathoracic and jugular venous pressures. The rise in jugular venous pressure impedes venous return from the brain and may precipitate severe intracranial hypertension in patients with traumatic brain injury.  

Measurement of IAP

Clinical examination alone is poorly sensitive in diagnosing IAH.6 Measurement of the intravesical pressure is the standard method followed to measure IAP. The urinary catheter is connected to a 3-way stopcock and transduced at the level of the midaxillary line. The intravesical pressure is measured after instillation of 20 ml of normal saline into the urinary bladder. A larger volume of normal saline may lead to erroneously high readings. There are commercially available kits that reduce the possibility of technical errors; however, a needle inserted into the sampling port of the urinary catheter is easy to use and usually allows accurate measurement of the intravesical pressure. 

Treatment of IAH 

Unrelieved, severe IAH has been shown to be an independent predictor of 28- and 90-day mortality among critically ill patients.3 Hence, it is important to monitor IAP in patients at risk and resort to early corrective intervention. Figure 1 illustrates a step-wise approach to the management of unrelieved IAH leading to ACS. 

Figure 1. A stepwise approach to the management of IAH and ACS


The abdominal perfusion pressure predicted survival from IAH and ACS and was found to be a useful endpoint of resuscitation in a retrospective observational study.7 However, abdominal perfusion pressure-based resuscitation has not been clinically validated. Evacuation of abdominal contents by gastric drainage, rectal tube insertion, and administration of enema may have a mitigating effect on IAH. The commonly recommended head-up position in ventilated patients may worsen IAH; hence, it may be appropriate to assume a reverse Trendelenburg position. The administration of analgesics, sedative medication, and neuromuscular blockade may offer temporary respite while the underlying problem is addressed. Large-volume paracentesis may also contribute significantly to a reduction in the IAP. It is important not to over-resuscitate patients who may have ACS; judicious use of diuretics may help de-resuscitate patients who are fluid overloaded, and reduce IAP.8 If renal function is compromised, fluid removal by ultrafiltration may be required.  


If medical therapies fail, surgical decompression with open abdomen must be carried out expeditiously. Surgical decompression combined with suction drainage may lead to a reduced incidence of septic complications and improve clinical outcomes.9 Managing a patient with open abdomen may be complicated by excessive protein loss, fistula formation, hemorrhage, and infection. Ventral hernias may also develop in the long-term.10 A patch closure is commonly resorted to for temporary closure of an open abdomen (Figure 2). The patch is interposed between facial edges and gradually approximated as the IAP resolves. The negative pressure vacuum system applies an airtight seal around the edges of the wound while suction is applied. This enables drainage of fluid and maintains tension on the facial edges and enables healing. It is preferable to close an open abdomen within 48 h. Maintaining an open abdomen for a longer duration may be required, while repeated surgical interventions are carried out. 

Figure 2. Decompressive laparotomy and open abdomen with mesh closure in a patient with necrotising pancreatitis

The bottom line

  • IAH is common in critically ill patients and is an independent predictor of mortality. 
  • Clinical examination is poorly sensitive for the diagnosis of IAH; intravesical pressure reflects IAP with reasonable accuracy. 
  • Common etiological factors for IAH and ACS include overexuberant fluid resuscitation, tense ascites, hemoperitoneum, acute pancreatitis, unrelieved ileus, blunt abdominal trauma, and sepsis.
  • Unrelieved IAH triggers organ failure, leading to ACS.
  • Early detection of IAH with an expeditious, stepwise approach is necessary to relieve rising IAP; unrelieved IAH with ACS requires surgical decompression and maintenance of an open abdomen.


1.         Fietsam R, Villalba M, Glover JL, Clark K. Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg. 1989;55(6):396-402.

2.         Murphy PB, Parry NG, Sela N, Leslie K, Vogt K, Ball I. Intra-abdominal hypertension is more common than previously thought: A prospective study in a mixed medical-surgical ICU. Crit Care Med. 2018;46(6):958-964. doi:10.1097/CCM.0000000000003122

3.         Reintam Blaser A, Regli A, De Keulenaer B, et al. Incidence, risk Factors, and outcomes of intra-abdominal hypertension in critically ill patients—a prospective multicenter study (IROI Study): Crit Care Med. 2019;47(4):535-542. doi:10.1097/CCM.0000000000003623

4.         Malbrain MLNG, Chiumello D, Cesana BM, et al. A systematic review and individual patient data meta-analysis on intra-abdominal hypertension in critically ill patients: the wake-up project. World initiative on Abdominal Hypertension Epidemiology, a Unifying Project (WAKE-Up!). Minerva Anestesiol. 2014;80(3):293-306.

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(7):1190-1206. doi:10.1007/s00134-013-2906-z

6.         Al-Dorzi HM, Tamim HM, Rishu AH, Aljumah A, Arabi YM. Intra-abdominal pressure and abdominal perfusion pressure in cirrhotic patients with septic shock. Ann Intensive Care. 2012;2 Suppl 1:S4. doi:10.1186/2110-5820-2-S1-S4

7.         Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49(4):621-626; discussion 626-627. doi:10.1097/00005373-200010000-00008

8.         Malbrain MLNG, Marik PE, Witters I, et al. Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic review with suggestions for clinical practice. Anaesthesiol Intensive Ther. 2014;46(5):361-380. doi:10.5603/AIT.2014.0060

9.         Cheatham ML, Demetriades D, Fabian TC, et al. Prospective study examining clinical outcomes associated with a negative pressure wound therapy system and Barker’s vacuum packing technique. World J Surg. 2013;37(9):2018-2030. doi:10.1007/s00268-013-2080-z

10.       Sugrue M. Abdominal compartment syndrome and the open abdomen: any unresolved issues? Curr Opin Crit Care. 2017;23(1):73-78. doi:10.1097/MCC.0000000000000371

1 thought on “When rising intra-abdominal pressure turns silent killer: the abdominal compartment syndrome”

  1. Sir is it necessary to monitor IAP in each pt with distension of abd and s/o organ failure or decreasing urine output, surgical abd, pancreatitis?

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