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Mark Gestring, MD
Hilary Sanfey, MD
Heidi L Frankel, MD, FACS
Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is
Literature review current through: Dec 2013. | This topic last updated: Jan 23, 2014.
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 . 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 .
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 .
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 . 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 . 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 .
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 .
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) . 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)
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 .
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 . 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 .
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 .
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
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 the adult trauma
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 . 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 . 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
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
Reduced venous return — IAH functionally obstructs blood flow in the inferior vena
cava, leading to diminished venous blood flow from the lower extremities . The
resulting rise in lower extremity venous hydrostatic pressure promotes the formation of
peripheral edema and increases the risk of deep vein thrombosis .
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 .
These effects are likely due to elevation of the diaphragm causing extrinsic compression of the
lung . 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 . These effects are accentuated by prior hemorrhagic shock and resuscitation
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  (see
The end result is progressive reduction in both glomerular perfusion and urine output .
Oliguria generally develops at an intraabdominal pressure of approximately 15 mmHg, while
anuria usually develops at an intraabdominal pressure of approximately 30 mmHg .
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 . These changes are reversible if the IAH is recognized early and decompression is
performed in a timely fashion . (See "Etiology and diagnosis of prerenal disease and acute
tubular necrosis in acute kidney injury (acute renal failure)".)
Gastrointestinal — The gut appears to be one of the organs most sensitive to increases in
Mesenteric blood flow was reduced at an intraabdominal pressure as low as 10 mmHg in
one animal study 
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 
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 .
Hypoperfusion of the gut may incite loss of the mucosal barrier, with subsequent bacterial
translocation, sepsis, and multiple system organ failure . Supporting this notion, bacterial
translocation has been shown to occur at an intraabdominal pressure of only 10 mmHg in the
presence of hemorrhage .
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 . 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
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 .
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 .
DIAGNOSTIC EVALUATION — Definitive diagnosis of ACS requires measurement of the
intraabdominal pressure, which should be performed with a low threshold . 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 . 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 [73-75].
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) :
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 .
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
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 [76-79]. 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 .
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 .
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 .
Some exceptions include escharotomy release to relieve mechanical limitations due to burn scars
and percutaneous catheter decompression to relieve tense ascites [82-84].
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 [85,86].
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
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'
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  (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 . 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 . Various approaches include:
Surgical decompression for all patients whose intraabdominal pressure is greater than 25
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 .
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 . 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
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 ,
mortality for patients who have progressed to ACS range from 40 to 100 percent [11,14,92-94].
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 . 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
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.)
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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;
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;
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;
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
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
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;
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;
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 Respir Environ
Exerc 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;
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
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. 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.
74. 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.
75. 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.
76. Iberti TJ, Lieber CE, Benjamin E. Determination of intra-abdominal pressure using a
transurethral bladder catheter: clinical validation of the technique. Anesthesiology 1989;
77. Iberti TJ, Kelly KM, Gentili DR, et al. A simple technique to accurately determine intra-
abdominal pressure. Crit Care Med 1987; 15:1140.
78. Fusco MA, Martin RS, Chang MC. Estimation of intra-abdominal pressure by bladder
pressure measurement: validity and methodology. J Trauma 2001; 50:297.
79. 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.
80. Sugerman HJ. Effects of increased intra-abdominal pressure in severe obesity. Surg Clin
North Am 2001; 81:1063.
81. 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.
82. 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.
83. Dries DJ. Abdominal compartment syndrome: toward less-invasive management. Chest
84. Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of
elevated intraabdominal pressure. Chest 2011; 140:1428.
85. Cheatham ML. Nonoperative management of intraabdominal hypertension and
abdominal compartment syndrome. World J Surg 2009; 33:1116.
86. Cheatham ML. Abdominal compartment syndrome. Curr Opin Crit Care 2009; 15:154.
87. Smith PK, Tyson GS Jr, Hammon JW Jr, et al. Cardiovascular effects of ventilation with
positive expiratory airway pressure. Ann Surg 1982; 195:121.
88. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective
management of the abdominal compartment syndrome. Am J Surg 1997; 174:667.
89. Burch JM, Moore EE, Moore FA, Franciose R. The abdominal compartment syndrome.
Surg Clin North Am 1996; 76:833.
90. 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;
91. Balogh ZJ, Martin A, van Wessem KP, et al. Mission to eliminate postinjury abdominal
compartment syndrome. Arch Surg 2011; 146:938.
92. An G, West MA. Abdominal compartment syndrome: a concise clinical review. Crit Care
Med 2008; 36:1304.
93. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a
criterion for abdominal re-exploration. Ann Surg 1984; 199:28.
94. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension
and abdominal compartment syndrome improving survival? Crit Care Med 2010; 38:402.
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