Official reprint from UpToDate® www.uptodate.com
©2012 UpToDate®
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use (click here) ©2012 UpToDate, Inc.
Abdominal compartment syndrome
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2012. | This topic last updated: May 18, 2011.

INTRODUCTION — Abdominal compartment syndrome refers to organ dysfunction caused by intraabdominal hypertension. It may be under-recognized because it primarily affects patients who are already quite ill and whose organ dysfunction may be incorrectly ascribed to progression of the primary illness. Since treatment can improve organ dysfunction, it is important that the diagnosis be considered in the appropriate clinical situation. The definition, incidence, risk factors, clinical presentation, diagnosis, management, and prognosis of intraabdominal hypertension and abdominal compartment syndrome are reviewed here.

The management of the open abdomen following abdominal decompression is discussed separately. (See "Management of the open abdomen in adults".)

DEFINITIONS — Intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are distinct clinical entities and should not be used interchangeably.

Intraabdominal pressure — Intraabdominal pressure (IAP) is the steady state pressure concealed within the abdominal cavity [1]. For most critically ill patients, an IAP of 5 to 7 mmHg is considered normal. In a prospective cohort study of 77 supine hospitalized patients, the IAP averaged 6.5 mmHg and was directly related to body mass index [2].

The normal range described above is not applicable for all patients. Patients with increased abdominal girth that developed slowly may have higher baseline intraabdominal pressures. As an example, morbidly obese and pregnant individuals can have chronically elevated intraabdominal pressure (as high as 10 to 15 mmHg) without adverse sequelae [1].

Abdominal perfusion pressure — Abdominal perfusion pressure (APP) is calculated as the mean arterial pressure (MAP) minus the IAP: APP = MAP - IAP. Elevated intraabdominal pressure reduces blood flow to the abdominal viscera [3]. Multiple regression analysis has found that APP is better than other resuscitation endpoints such as arterial pH, base deficit, arterial lactate, and hourly urinary output for predicting outcomes [4]. A target APP of at least 60 mmHg is correlated with improved survival from IAH and ACS [4-6].

Intraabdominal hypertension — Intraabdominal hypertension (IAH) is defined as a sustained intraabdominal pressure ≥12 mmHg (figure 1) [1,7,8]. Although this value was established arbitrarily, it is used in many research studies and distinguishes most patients whose intraabdominal pressure is inappropriately elevated. Intraabdominal pressure can be further graded as follows: Grade I = IAP 12 to 15 mmHg; Grade II = IAP 16 to 20 mmHg; Grade III = IAP 21 to 25 mmHg; Grade IV = IAP >25 mmHg [1].

  • Hyperacute IAH refers to elevation of the intraabdominal pressure lasting only seconds. It is due to laughing, coughing, straining, sneezing, defecation, or physical activity. IAH with ACS due to gastric over-distention following endoscopy has been described [9].
  • Acute IAH refers to elevation of the intraabdominal pressure that develops over hours. It is usually the result of trauma or intraabdominal hemorrhage and can lead to the rapid development of ACS.
  • Subacute IAH refers to elevation of the intraabdominal pressure that develops over days. It is most common in medical patients and can also lead to ACS.
  • Chronic IAH refers to elevation of intraabdominal pressure that develops over months (pregnancy) or years (morbid obesity) [10]. It does not cause ACS, but does place the individual at higher risk for ACS if they develop superimposed acute or subacute IAH.

Abdominal compartment syndrome — For research purposes, ACS is defined as a sustained intraabdominal pressure >20 mmHg (with or without APP <60 mmHg) that is associated with new organ dysfunction [1,7,8]. For clinical purposes, ACS is better defined as IAH-induced new organ dysfunction without a strict intraabdominal pressure threshold, since no intraabdominal pressure can predictably diagnose ACS in all patients [11-13].

Patients with an intraabdominal pressure below 10 mmHg generally do not have ACS, while patients with an intraabdominal pressure above 25 mmHg usually have ACS [4,5]. Patients with an intraabdominal pressure between 10 and 25 mmHg may or may not have ACS, depending upon individual variables such as blood pressure and abdominal wall compliance (figure 1) [11,14-16]:

  • Higher systemic blood pressure may maintain abdominal organ perfusion when the intraabdominal pressure is increased, since the perfusion pressure (APP) is the difference between the mean arterial pressure and the intraabdominal pressure. (See 'Abdominal perfusion pressure' above.)
  • Abdominal wall compliance initially minimizes the extent to which an increasing abdominal girth can elevate the intraabdominal pressure. But when a critical abdominal girth is reached, abdominal wall compliance decreases abruptly. Further increases in abdominal girth beyond this critical level result in a rapid rise of intraabdominal pressure and ACS if untreated. Increased abdominal wall compliance due to chronic increased abdominal girth (eg, pregnancy, cirrhosis with ascites, morbid obesity) may be protective against ACS [17].

EPIDEMIOLOGY — Most studies evaluating the incidence of ACS have been performed in trauma patients, with estimates of incidence varying considerably [18-21]. The largest study (n=706) reported an incidence of ACS of 1 percent [19]. In contrast, two smaller observational studies (n=128 and n=188) reported an incidence of ACS of 9 to 14 percent [20,21]. The incidence of IAH is less well characterized.

The variable estimates do not appear to be related to the definition of ACS because the studies defined ACS similarly. ACS was considered present if there was persistent IAH, progression organ dysfunction despite resuscitation, and improvement following decompression.

The different estimates likely relate to the different patient populations studied. The largest study enrolled all patients with trauma who were admitted to an intensive care unit. The smaller studies enrolled patients with major torso trauma (flail chest, two or more abdominal injuries, major vascular injury, complex pelvic fracture, or two or more long bone fractures), an early arterial base deficit (≥6 mEq/L), and either an age ≥65 years or the need for transfusion of ≥6 units of packed red blood cells. These different enrollment criteria suggest that the incidence of ACS is highest among the most critically ill patients.

ETIOLOGY AND RISK FACTORS — ACS can be classified as primary or secondary [1]. Primary ACS is due to injury or disease in the abdominopelvic region (eg, abdominal trauma, hemoperitoneum, pancreatitis); intervention (surgical or radiologic) of the primary condition is often needed. Secondary ACS refers to conditions that do not originate in the abdomen or pelvis (eg, fluid resuscitation, sepsis, burns). Recurrent ACS defines a condition in which ACS develops again following previous surgical or medical treatment of primary or secondary ACS.

ACS generally occurs in patients who are critically ill due to any of a wide variety of medical and surgical conditions [14,18]. Some of these include:

  • Trauma – Injured patients in shock who require aggressive fluid resuscitation are at risk for ACS [22,23].
  • Burns – Patients with severe burns (>30 percent total body surface area) with or without concomitant trauma are also at risk for ACS [24,25]. Importantly, ACS must be distinguished from other intraabdominal problems that occur in these critically ill patients (eg, necrotizing enterocolitis, ischemic bowel).
  • Liver transplantation – A prospective cohort study found IAH (IAP >25 mmHg) following liver transplantation in 32 percent of patients [26].
  • Abdominal conditions – Massive ascites, bowel distension, abdominal surgery, or intraperitoneal bleeding can increase intraabdominal pressure [27,28].
  • Retroperitoneal conditions – Retroperitoneal pathologies, such as ruptured abdominal aortic aneurysm, pelvic fracture with bleeding, and pancreatitis, can lead to abdominal compartment syndrome [29,30].
  • Medical illness – Conditions that require extensive fluid resuscitation (eg, sepsis) and are associated with third spacing of fluids and tissue edema can increase intraabdominal pressure [1,31].
  • Post-surgical patients – Patients undergoing operations in which they are given large volume resuscitation, particularly with crystalloid in the face of hemorrhagic or septic shock, are at risk for ACS.

The development of secondary ACS is often related to the need for and extent of volume resuscitation [32-34]. Careful attention needs to be paid to the amount of fluid being administered and alterations in fluid management may be needed in patients who are exhibiting early signs/symptoms of ACS. The fluid management of hypovolemic patients is discussed elsewhere. (See "Treatment of severe hypovolemia or hypovolemic shock in adults" and 'Hemodynamic support' below and "Overview of inpatient management in trauma patients".)

The following trials illustrate the correlation between fluid administration and ACS:

  • One trial randomly assigned 71 patients with severe acute pancreatitis to rapid fluid expansion or controlled fluid expansion [33]. The rapid expansion group received significantly greater volumes of crystalloid (4028 versus 2472 mL) and colloid (1336 versus 970 mL) on the day of admission with no differences after four days. The incidence of abdominal compartment syndrome was higher in the rapid expansion group (72 versus 38 percent).
  • Abdominal compartment pressures were measured (bladder catheter transduction) in 31 severely burned patients who were randomly assigned to resuscitation using crystalloid (Parkland formula) or plasma administration [32]. Significantly increased abdominal compartment pressure (27 versus 11 mmHg) was found in the group receiving crystalloid which correlated to increased volume of administered fluid (0.26 L/kg versus 0.21 L/kg).

PHYSIOLOGIC CONSEQUENCES — IAH can impair the function of nearly every organ system, thereby causing ACS (table 1).

Cardiovascular — IAH decreases cardiac output by impairing cardiac function and reducing venous return:

  • Impaired cardiac function — IAH causes cephalad movement of the diaphragm, which leads to cardiac compression. The end result is reduced ventricular compliance and contractility [35,36]. Elevation of the diaphragm may occur at pressures as low as 10 mmHg [37].
  • Reduced venous return — IAH functionally obstructs blood flow in the inferior vena cava, leading to diminished venous blood flow from the lower extremities [38]. The resulting rise in lower extremity venous hydrostatic pressure promotes the formation of peripheral edema and increases the risk of deep vein thrombosis [39].
  • IAH generally causes an elevated central venous pressure and pulmonary capillary wedge pressure impairing cardiac function because of diminished venous return.

Intravascular volume and positive end-expiratory pressure (PEEP) influence the degree to which IAH decreases cardiac output. Specifically, cardiac output is reduced at a lower intraabdominal pressure if the patients are hypovolemic, receive excess applied PEEP, or develop auto-PEEP [40-42]. (See "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Auto-PEEP' and "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Hemodynamics'.)

Pulmonary — Mechanically ventilated patients with IAH have increased peak inspiratory and mean airway pressures, which can cause alveolar barotrauma. They also have reduced chest wall compliance and spontaneous tidal volumes, which combine to cause arterial hypoxemia and hypercarbia. Pulmonary infection is more common among patients with IAH [43].

These effects are likely due to elevation of the diaphragm causing extrinsic compression of the lung [44]. According to animal studies, compression of the lung leads to atelectasis, edema, decreased oxygen diffusion, an increased intrapulmonary shunt fraction, and increased alveolar dead space [45]. These effects are accentuated by prior hemorrhagic shock and resuscitation [46].

Renal — Several mechanisms contribute to renal impairment in patients with IAH:

  • Renal vein compression increases venous resistance, which impairs venous drainage. This appears to be the major cause of renal impairment [47,48]
  • Renal artery vasoconstriction is induced by the sympathetic nervous and renin-angiotensin systems, which are stimulated by the fall in cardiac output [49] (see 'Cardiovascular' above)

The end result is progressive reduction in both glomerular perfusion and urine output [50]. Oliguria generally develops at an intraabdominal pressure of approximately 15 mmHg, while anuria usually develops at an intraabdominal pressure of approximately 30 mmHg [51].

Similar to renal impairment induced by other causes of reduced perfusion, the urine sodium and chloride concentrations are usually decreased. In addition, plasma renin activity, aldosterone concentration, and antidiuretic hormone concentration are increased to more than twice baseline levels [52]. These changes are reversible if the IAH is recognized early and decompression is performed in a timely fashion [53]. (See "Etiology and diagnosis of acute tubular necrosis and prerenal disease".)

Gastrointestinal — The gut appears to be one of the organs most sensitive to increases in intraabdominal pressure:

  • Mesenteric blood flow was reduced at an intraabdominal pressure as low as 10 mmHg in one animal study [54]
  • Intestinal mucosal perfusion is decreased at an intraabdominal pressure of approximately 20 mmHg, according to both animal and human studies [55-57]
  • Celiac artery and superior mesenteric artery blood flow are decreased at an intraabdominal pressure of approximately 40 mmHg, according to one animal study [6]

The impact of intraabdominal pressure on mesenteric perfusion seems to be greatest among patients who had hemorrhage or are hypovolemic [54,58].

IAH also compresses thin-walled mesenteric veins, which impairs venous flow from the intestine and causes intestinal edema. The intestinal swelling further increases intraabdominal pressure, initiating a vicious cycle. The end result is worsened hypoperfusion, bowel ischemia, decreased intramucosal pH, and lactic acidosis [59].

Hypoperfusion of the gut may incite loss of the mucosal barrier, with subsequent bacterial translocation, sepsis, and multiple system organ failure [60]. Supporting this notion, bacterial translocation has been shown to occur at an intraabdominal pressure of only 10 mmHg in the presence of hemorrhage [61].

Hepatic — The liver's ability to remove lactic acid is impaired by increases of intraabdominal pressure as small as 10 mmHg [62,63]. This occurs even in the presence of a normal cardiac output and mean arterial blood pressure [62,63]. Thus, lactic acidosis may clear more slowly than expected despite adequate resuscitation.

Central nervous system — Intracranial pressure (ICP) transiently increases during the short-lived elevation of intraabdominal pressure that occurs with coughing, defecating, or emesis [64]. ICP similarly appears to be elevated in the presence of persistent IAH. The elevated ICP is sustained as long as IAH exists, which can lead to a critical decrease in cerebral perfusion and progressive cerebral ischemia [65-67]. (See "Evaluation and management of elevated intracranial pressure in adults".)

CLINICAL PRESENTATION — It is desirable to recognize IAH early, so it can be treated before progressing to ACS.

Symptoms — Most patients who develop ACS are critically ill and unable to communicate. The rare patient who is able to convey symptoms may complain of malaise, weakness, lightheadedness, dyspnea, abdominal bloating, or abdominal pain.

Physical signs — Nearly all patients with ACS have a tensely distended abdomen. Despite this, physical examination of the abdomen is a poor predictor of ACS [1,68,69]. In a prospective cohort study of 42 adult blunt trauma victims, physical examination of the abdomen identified a significantly elevated intraabdominal pressure (defined as >15 mmHg) with a sensitivity of 56 percent, specificity of 87 percent, positive predictive value of 35 percent, negative predictive value of 94 percent, and accuracy of 84 percent [68].

Progressive oliguria and increased ventilatory requirements are also common in patients with ACS. Other findings may include hypotension, tachycardia, an elevated jugular venous pressure, jugular venous distension, peripheral edema, abdominal tenderness, or acute pulmonary decompensation. There may also be evidence of hypoperfusion, including cool skin, obtundation, restlessness, or lactic acidosis.

Imaging findings — Imaging is not helpful in the diagnosis of ACS. A chest radiograph may show decreased lung volumes, atelectasis, or elevated hemidiaphragms. Chest computed tomography (CT) may demonstrate tense infiltration of the retroperitoneum that is out of proportion to peritoneal disease, extrinsic compression of the inferior vena cava, massive abdominal distention, direct renal compression or displacement, bowel wall thickening, or bilateral inguinal herniation [70].

DIAGNOSTIC EVALUATION — Definitive diagnosis of ACS requires measurement of the intraabdominal pressure, which should be performed with a low threshold [71]. This is particularly true for patients who have trauma, liver transplantation, bowel obstruction, pancreatitis, or peritonitis because these conditions are known to be associated with ACS. (See 'Etiology and risk factors' above.)

Measurement of intraabdominal pressure — Intraabdominal pressure can be measured indirectly using intragastric, intracolonic, intravesical (bladder), or inferior vena cava catheters [72]. The wall of the hollow viscus or vascular structure acts as a membrane to transduce pressure.

Measurement of bladder (ie, intravesical) pressure is the standard method to screen for IAH and ACS. It is simple, minimally invasive, and accurate (additional pressure is not imparted from its own musculature). Because differences in recorded intravesical pressure occur with varying head position, care must be taken to ensure consistent head and body positioning from one measurement to another [73,74].

Commercial products are available to simplify measurement, however, bladder pressure measurement can be performed with supplies routinely available in the intensive care unit using the following steps (figure 2) [1]:

  • The drainage tube of the patient's Foley (bladder) catheter is clamped.
  • Sterile saline (up to 25 mL) is instilled into the bladder via the aspiration port of the Foley catheter and the catheter filled with fluid [1].
  • An 18-gauge needle attached to a pressure transducer is inserted into the aspiration port. With some newer style Foley catheters, this can be done using a needle-less connection system.
  • The pressure is measured at end-expiration in the supine position after ensuring that abdominal muscle contractions are absent. The transducer should be zeroed at the level of the midaxillary line.

These steps require the aspiration port to be punctured twice. Three-way stopcocks can be used to avoid repeated puncturing of the aspiration port. Commercially available systems have also been developed to simplify measurement.

There is strong correlation between the bladder pressure and directly measured intraabdominal pressure in both animals and humans [75-78]. However, the bladder pressure may not be accurate in the presence of intraperitoneal adhesions, pelvic hematomas, pelvic fractures, abdominal packs, or a neurogenic bladder because accurate measurement requires free movement of the bladder wall [72].

Chronically increased intraabdominal pressure due to morbid obesity, pregnancy, or ascites can complicate the diagnosis. Acute increases in intraabdominal pressure may be less well tolerated if superimposed on chronic IAH [79].

MANAGEMENT APPROACH — Management of IAH and ACS consists of supportive care and, when needed, abdominal decompression. Surgical decompression of the abdominal cavity is considered definitive management [80].

Some exceptions include escharotomy release to relieve mechanical limitations due to burn scars and percutaneous catheter decompression to relieve tense ascites [81-83].

Supportive care — The goals of supportive care in patients with intraabdominal hypertension include reduction of intraabdominal volume through evacuation of intraluminal contents, evacuation of intraabdominal space-occupying lesions (eg, ascites, hematoma) when possible, and measures to improve abdominal wall compliance [84,85].

Nasogastric and rectal drainage are a simple means for reducing intraabdominal pressure in patients with bowel distension. Hemoperitoneum, ascites, intraabdominal abscess and retroperitoneal hematoma occupy space and can elevate intraabdominal pressure. In some cases, these collections can be evacuated using percutaneous techniques. In one study, percutaneous catheter drainage (PCD) avoided the need for subsequent open abdominal decompression in 81 percent of patients treated. However, failure to drain at least 1000 mL of fluid and decrease intraabdominal pressure (IAP) by at least 9 mmHg in the first four hours postdecompression was associated with failure and the urgent need for open abdominal decompression [82,83].

Attention should be paid to patient positioning and the patient should be placed in a supine position since elevation of the head of the bed (>20°), which is commonly used to reduce the risk of ventilator-associated pneumonia, increases intraabdominal pressure and also impacts the measurement of intraabdominal pressure. (See 'Measurement of intraabdominal pressure' above.)

Abdominal wall compliance can be improved with adequate pain control and sedation, but for some patients, chemical paralysis will be needed to achieve abdominal wall relaxation and ventilatory support will be indicated. (See "Overview of mechanical ventilation".)

Ventilatory support — High peak and mean airway pressures can be problematic. Tidal volume reduction, a pressure-limited mode, and/or permissive hypercapnia may be necessary. Chemical paralysis, which will decrease carbon dioxide production and permit better ventilation, may be required if hypercapnia is particularly severe. (See "Permissive hypercapnia" and "Use of neuromuscular blocking medications in critically ill patients".)

Positive end-expiratory pressure (PEEP) may reduce ventilation-perfusion mismatch and improve hypoxemia [86] (see "Positive end-expiratory pressure (PEEP)").

Hemodynamic support — For patients with intraabdominal hypertension, limiting the amount of fluid administration may decrease the risk of developing ACS. Some clinicians prefer to use colloids under this circumstance; however, although there are accumulating data that large-volume crystalloid resuscitation for shock can lead to ACS, it is not clear that substituting colloid offers any protection, and once the patient develops ACS, the treatment is decompression and the type of fluid is of no consequence.

For patients with ACS, volume administration temporarily improves cardiac output, renal blood flow, urine output, visceral perfusion and negates some of the negative effects of positive-end expiratory pressure (PEEP), but compartment syndrome cannot be treated by administration of fluid (regardless of type). Also, there is no role for diuretic therapy in the resuscitation of patients with acute compartment syndrome (ACS) even though central venous and pulmonary capillary wedge pressures are usually elevated [87]. The only appropriate management is to open the abdomen. (See 'Surgical decompression' below.)

SURGICAL DECOMPRESSION — There is general agreement that surgical decompression is indicated for ACS. However, a precise threshold for surgical decompression has not been established. Decompressing the abdomen prior to the development of ACS is becoming increasingly common and may improve survival [73]. Various approaches include:

  • Surgical decompression for all patients whose intraabdominal pressure is greater than 25 mmHg [88]
  • Many clinicians suggest surgical decompression at a lower intraabdominal pressure (eg, 15 to 25 mmHg), based on their belief that surgical decompression performed at an intraabdominal pressure lower than 25 mmHg is associated with improved organ perfusion, patient outcome, and prevention of ACS.
  • Other clinicians believe that the need for surgical decompression should be determined by the pressure gradient for abdominal perfusion, also called the abdominal perfusion pressure (APP). As described above, the APP is the difference between the mean arterial pressure and the intraabdominal pressure (APP = MAP - IAP). In a retrospective study, an APP below 50 mmHg predicted mortality with greater sensitivity and specificity than either the mean arterial pressure or the intraabdominal pressure alone [15].

In our clinical practice, we begin to consider surgical decompression when the intraabdominal pressure is 20 mmHg or greater, regardless of whether there are signs of ACS. We make our final decision after carefully weighing the potential benefits and the perioperative risks related to this procedure in each individual case.

Most surgeons perform decompression and then maintain an open abdomen using temporary abdominal wall closure [89]. Maintenance of an open abdomen using temporary abdominal wall closure requires dressings that bridge the fascial edges while preventing evisceration, retaining fluid, and retaining heat. (See "Management of the open abdomen in adults".)

Surgical decompression can be performed in the operating room if the patient is medically stable for transfer or at the bedside in the intensive care unit. The standard technique is to make a midline incision through the linea alba to open the abdominal cavity.

Temporary closure techniques — Several techniques are available for temporary abdominal closure. In some patients, delayed primary closure of the abdominal fascia is possible once edema subsides. However, if closure is premature, abdominal compartment syndrome can recur. Techniques for temporary abdominal closure and timing of closure are discussed in detail elsewhere. (See "Management of the open abdomen in adults", section on 'Temporary abdominal closure'.)

MORBIDITY AND MORTALITY — Failure to recognize IAH prior to the development of ACS causes tissue hypoperfusion, which may lead to multisystem organ failure, and potentially death. Although the development of IAH alone is not a predictor of multiorgan failure [90], mortality for patients who have progressed to ACS range from 40 to 100 percent [11,14,91-93].

One prospective study measured intraabdominal pressure in all patients admitted to the intensive care unit and requiring a bladder catheter. Of the 83 patients studied, 33 percent developed intraabdominal hypertension [7]. Logistic regression identified maximal intraabdominal pressure as a significant predictor of mortality (odds ratio [OR], 1.17 95% CI 1.05-1.3), which remained significant after adjusting with Acute Physiology and Chronic Health Evaluation II (APACHE II) (OR, 1.15 95% CI 1.06-1.25) and comorbidities (OR, 2.68 95% CI 1.27-5.67).

SUMMARY AND RECOMMENDATIONS

  • Increased intraabdominal pressure is called intraabdominal hypertension (IAH). Abdominal compartment syndrome (ACS) refers to organ dysfunction caused by intraabdominal hypertension. (See 'Definitions' above.)
  • ACS can impair the function of nearly every organ system. Physiologic consequences include impaired cardiac function, decreased venous return, hypoxemia, hypercarbia, renal impairment, diminished gut perfusion, and elevated intracranial pressure. (See 'Physiologic consequences' above.)
  • Diagnosis of ACS requires that intraabdominal pressure be measured. Symptoms, physical signs, and imaging findings are insufficient to diagnose ACS. (See 'Diagnostic evaluation' above.)
  • Management initially consists of careful observation and supportive care. In some cases abdominal compartment decompression is required. (See 'Ventilatory support' above and 'Surgical decompression' above.)
  • We suggest that surgical decompression is not delayed until the development of ACS (Grade 2C). We evaluate the patient for possible surgical decompression when the intraabdominal pressure is ≥20 mmHg, regardless of whether ACS exists. We make our final decision only after carefully weighing the potential benefits and the perioperative risks related to the individual patient. (See 'Surgical decompression' above.)
  • Following surgical decompression, an open abdomen is maintained using a variety of temporary abdominal closure techniques. (See 'Temporary closure techniques' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

  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. Sanchez NC, Tenofsky PL, Dort JM, et al. What is normal intra-abdominal pressure? Am Surg 2001; 67:243.
  3. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma 1992; 33:45.
  4. Schein M, Ivatury R. Intra-abdominal hypertension and the abdominal compartment syndrome. Br J Surg 1998; 85:1027.
  5. Ivatury RR, Diebel L, Porter JM, Simon RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 1997; 77:783.
  6. Caldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res 1987; 43:14.
  7. 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.
  8. http://www.wsacs.org/consensus_summary.php (Accessed on October 11, 2011).
  9. van Mook WN, Huslewe-Evers RP, Ramsay G. Abdominal compartment syndrome. Lancet 2002; 360:1502.
  10. Wilson A, Longhi J, Goldman C, McNatt S. Intra-abdominal pressure and the morbidly obese patients: the effect of body mass index. J Trauma 2010; 69:78.
  11. Sugrue M. Abdominal compartment syndrome. Curr Opin Crit Care 2005; 11:333.
  12. Bailey J, Shapiro MJ. Abdominal compartment syndrome. Crit Care 2000; 4:23.
  13. Malbrain ML, Deeren D, De Potter TJ. Intra-abdominal hypertension in the critically ill: it is time to pay attention. Curr Opin Crit Care 2005; 11:156.
  14. Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med 2005; 33:315.
  15. Cheatham ML, White MW, Sagraves SG, et al. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma 2000; 49:621.
  16. Moore AF, Hargest R, Martin M, Delicata RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Br J Surg 2004; 91:1102.
  17. Sugerman HJ, DeMaria EJ, Felton WL 3rd, et al. Increased intra-abdominal pressure and cardiac filling pressures in obesity-associated pseudotumor cerebri. Neurology 1997; 49:507.
  18. Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre epidemiological study. Intensive Care Med 2004; 30:822.
  19. Hong JJ, Cohn SM, Perez JM, et al. Prospective study of the incidence and outcome of intra-abdominal hypertension and the abdominal compartment syndrome. Br J Surg 2002; 89:591.
  20. Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003; 54:848.
  21. Balogh Z, McKinley BA, Cocanour CS, et al. Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation. Am J Surg 2002; 184:538.
  22. Balogh Z, McKinley BA, Cocanour CS, et al. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg 2003; 138:637.
  23. Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the abdominal compartment syndrome after "damage-control" laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000; 28:1747.
  24. Markell KW, Renz EM, White CE, et al. Abdominal complications after severe burns. J Am Coll Surg 2009; 208:940.
  25. Kirkpatrick AW, Ball CG, Nickerson D, D'Amours SK. Intraabdominal hypertension and the abdominal compartment syndrome in burn patients. World J Surg 2009; 33:1142.
  26. Biancofiore G, Bindi ML, Romanelli AM, et al. Intra-abdominal pressure monitoring in liver transplant recipients: a prospective study. Intensive Care Med 2003; 29:30.
  27. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdominal compartment syndrome. J Trauma 1998; 45:597.
  28. Morken J, West MA. Abdominal compartment syndrome in the intensive care unit. Curr Opin Crit Care 2001; 7:268.
  29. Djavani Gidlund K, Wanhainen A, Björck M. Intra-abdominal hypertension and abdominal compartment syndrome after endovascular repair of ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2011; 41:742.
  30. Mentula P, Hienonen P, Kemppainen E, et al. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg 2010; 145:764.
  31. Regueira T, Bruhn A, Hasbun P, et al. Intra-abdominal hypertension: incidence and association with organ dysfunction during early septic shock. J Crit Care 2008; 23:461.
  32. O'Mara MS, Slater H, Goldfarb IW, Caushaj PF. A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma 2005; 58:1011.
  33. Mao EQ, Tang YQ, Fei J, et al. Fluid therapy for severe acute pancreatitis in acute response stage. Chin Med J (Engl) 2009; 122:169.
  34. Oda J, Yamashita K, Inoue T, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns 2006; 32:151.
  35. Coombs, HC. The mechanism of the regulation of intra-abdominal pressure. Am J Physiol 1922; 61:159.
  36. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med 1989; 17:118.
  37. Richardson JD, Trinkle JK. Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res 1976; 20:401.
  38. Barnes GE, Laine GA, Giam PY, et al. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol 1985; 248:R208.
  39. MacDonnell SP, Lalude OA, Davidson AC. The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 1996; 183:419.
  40. Kashtan J, Green JF, Parsons EQ, Holcroft JW. Hemodynamic effect of increased abdominal pressure. J Surg Res 1981; 30:249.
  41. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma 1995; 39:1071.
  42. Burchard KW, Ciombor DM, McLeod MK, et al. Positive end expiratory pressure with increased intra-abdominal pressure. Surg Gynecol Obstet 1985; 161:313.
  43. Aprahamian C, Wittmann DH, Bergstein JM, Quebbeman EJ. Temporary abdominal closure (TAC) for planned relaparotomy (etappenlavage) in trauma. J Trauma 1990; 30:719.
  44. Obeid F, Saba A, Fath J, et al. Increases in intra-abdominal pressure affect pulmonary compliance. Arch Surg 1995; 130:544.
  45. Quintel M, Pelosi P, Caironi P, et al. An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury. Am J Respir Crit Care Med 2004; 169:534.
  46. Simon RJ, Friedlander MH, Ivatury RR, et al. Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma 1997; 42:398.
  47. Doty JM, Saggi BH, Blocher CR, et al. Effects of increased renal parenchymal pressure on renal function. J Trauma 2000; 48:874.
  48. Doty JM, Saggi BH, Sugerman HJ, et al. Effect of increased renal venous pressure on renal function. J Trauma 1999; 47:1000.
  49. Shenasky JH 2nd. The renal hemodynamic and functional effects of external counterpressure. Surg Gynecol Obstet 1972; 134:253.
  50. Bloomfield GL, Blocher CR, Fakhry IF, et al. Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma 1997; 42:997.
  51. Richards WO, Scovill W, Shin B, Reed W. Acute renal failure associated with increased intra-abdominal pressure. Ann Surg 1983; 197:183.
  52. Le Roith D, Bark H, Nyska M, Glick SM. The effect of abdominal pressure on plasma antidiuretic hormone levels in the dog. J Surg Res 1982; 32:65.
  53. Smith JH, Merrell RC, Raffin TA. Reversal of postoperative anuria by decompressive celiotomy. Arch Intern Med 1985; 145:553.
  54. Friedlander MH, Simon RJ, Ivatury R, et al. Effect of hemorrhage on superior mesenteric artery flow during increased intra-abdominal pressures. J Trauma 1998; 45:433.
  55. Chang MC, Cheatham ML, Nelson LD, et al. Gastric tonometry supplements information provided by systemic indicators of oxygen transport. J Trauma 1994; 37:488.
  56. Diebel LN, Myers T, Dulchavsky S. Effects of increasing airway pressure and PEEP on the assessment of cardiac preload. J Trauma 1997; 42:585.
  57. Samel ST, Neufang T, Mueller A, et al. A new abdominal cavity chamber to study the impact of increased intra-abdominal pressure on microcirculation of gut mucosa by using video microscopy in rats. Crit Care Med 2002; 30:1854.
  58. Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma 1998; 44:1016.
  59. Diebel LN, Wilson RF, Dulchavsky SA, Saxe J. Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma 1992; 33:279.
  60. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma 1997; 43:852.
  61. Gargiulo NJ 3rd, Simon RJ, Leon W, Machiedo GW. Hemorrhage exacerbates bacterial translocation at low levels of intra-abdominal pressure. Arch Surg 1998; 133:1351.
  62. Luca A, Cirera I, García-Pagán JC, et al. Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis. Gastroenterology 1993; 104:222.
  63. Nakatani T, Sakamoto Y, Kaneko I, et al. Effects of intra-abdominal hypertension on hepatic energy metabolism in a rabbit model. J Trauma 1998; 44:446.
  64. Luce JM, Huseby JS, Kirk W, Butler J. Mechanism by which positive end-expiratory pressure increases cerebrospinal fluid pressure in dogs. J Appl Physiol 1982; 52:231.
  65. Bloomfield GL, Dalton JM, Sugerman HJ, et al. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma 1995; 39:1168.
  66. 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.
  67. Joseph DK, Dutton RP, Aarabi B, Scalea TM. Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma 2004; 57:687.
  68. Kirkpatrick AW, Brenneman FD, McLean RF, et al. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg 2000; 43:207.
  69. Sugrue M, Bauman A, Jones F, et al. Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg 2002; 26:1428.
  70. Pickhardt PJ, Shimony JS, Heiken JP, et al. The abdominal compartment syndrome: CT findings. AJR Am J Roentgenol 1999; 173:575.
  71. Malbrain ML. Is it wise not to think about intraabdominal hypertension in the ICU? Curr Opin Crit Care 2004; 10:132.
  72. Malbrain ML. Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Intensive Care Med 2004; 30:357.
  73. 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.
  74. De Keulenaer BL, De Waele JJ, Powell B, Malbrain ML. What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure? Intensive Care Med 2009; 35:969.
  75. Iberti TJ, Lieber CE, Benjamin E. Determination of intra-abdominal pressure using a transurethral bladder catheter: clinical validation of the technique. Anesthesiology 1989; 70:47.
  76. Iberti TJ, Kelly KM, Gentili DR, et al. A simple technique to accurately determine intra-abdominal pressure. Crit Care Med 1987; 15:1140.
  77. Fusco MA, Martin RS, Chang MC. Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. J Trauma 2001; 50:297.
  78. Lacey SR, Bruce J, Brooks SP, et al. The relative merits of various methods of indirect measurement of intraabdominal pressure as a guide to closure of abdominal wall defects. J Pediatr Surg 1987; 22:1207.
  79. Sugerman HJ. Effects of increased intra-abdominal pressure in severe obesity. Surg Clin North Am 2001; 81:1063.
  80. Chang MC, Miller PR, D'Agostino R Jr, Meredith JW. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma 1998; 44:440.
  81. Hobson KG, Young KM, Ciraulo A, et al. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002; 53:1129.
  82. Dries DJ. Abdominal compartment syndrome: toward less-invasive management. Chest 2011; 140:1396.
  83. Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of elevated intraabdominal pressure. Chest 2011; 140:1428.
  84. Cheatham ML. Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg 2009; 33:1116.
  85. Cheatham ML. Abdominal compartment syndrome. Curr Opin Crit Care 2009; 15:154.
  86. Smith PK, Tyson GS Jr, Hammon JW Jr, et al. Cardiovascular effects of ventilation with positive expiratory airway pressure. Ann Surg 1982; 195:121.
  87. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 1997; 174:667.
  88. Burch JM, Moore EE, Moore FA, Franciose R. The abdominal compartment syndrome. Surg Clin North Am 1996; 76:833.
  89. Mayberry JC, Goldman RK, Mullins RJ, et al. Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment syndrome. J Trauma 1999; 47:509.
  90. Balogh ZJ, Martin A, van Wessem KP, et al. Mission to eliminate postinjury abdominal compartment syndrome. Arch Surg 2011; 146:938.
  91. An G, West MA. Abdominal compartment syndrome: a concise clinical review. Crit Care Med 2008; 36:1304.
  92. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg 1984; 199:28.
  93. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med 2010; 38:402.
Topic 2889 Version 6.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.