Abdominal compartment syndrome

Abdominal compartment syndrome

Author
Mark Gestring, MD
Section Editors
Hilary Sanfey, MD
Heidi L Frankel, MD, FACS
Deputy Editor
Kathryn A Collins, MD, PhD, FACS
Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2013. | This topic last updated: Aug 8, 2012.

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 ].

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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.)

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  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.

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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.

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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 patient" .)

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

5
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 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
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 ]

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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" .)

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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 ].

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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 ].

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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

10
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

11
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.)

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  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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