Abdominal compartment syndrome in adults

Author:
Mark Gestring, MD
Section Editors:
Amalia Cochran, MD, FACS, FCCM
Eileen M Bulger, MD, FACS
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2020. | This topic last updated: Mar 05, 2020.

INTRODUCTION Abdominal compartment syndrome refers to organ

dysfunction caused by intra-abdominal hypertension. It may be underrecognized

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 intra-abdominal
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 Intra-abdominal hypertension (IAH) and abdominal

compartment syndrome (ACS) are distinct clinical entities and should not be used
interchangeably.

Intra-abdominal pressure — Intra-abdominal 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 intra-
abdominal pressures. As an example, morbidly obese and pregnant individuals can
have chronically elevated intra-abdominal 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 intra-
abdominal 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].

Intra-abdominal hypertension — Intra-abdominal hypertension (IAH) is defined as a

sustained intra-abdominal 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 intra-abdominal pressure is inappropriately elevated. Intra-abdominal
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 intra-abdominal pressure lasting
only seconds. It is due to laughing, coughing, straining, sneezing, defecation,
or physical activity. IAH with ACS due to gastric overdistention following
endoscopy has been described [9].
●Acute IAH refers to elevation of the intra-abdominal pressure that develops
over hours. It is usually the result of trauma or intra-abdominal hemorrhage
and can lead to the rapid development of ACS.
●Subacute IAH refers to elevation of the intra-abdominal pressure that
develops over days. It is most common in medical patients and can also lead
to ACS.
●Chronic IAH refers to elevation of intra-abdominal 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 intra-abdominal 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 intra-abdominal pressure
threshold, since no intra-abdominal pressure can predictably diagnose ACS in all
patients [11-13].

Patients with an intra-abdominal pressure below 10 mmHg generally do not have ACS,
while patients with an intra-abdominal pressure above 25 mmHg usually have ACS
[4,5]. Patients with an intra-abdominal 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 intra-abdominal pressure is increased since the perfusion pressure
(APP) is the difference between the mean arterial pressure and the intra-
abdominal pressure. (See 'Abdominal perfusion pressure' above.)
●Abdominal wall compliance initially minimizes the extent to which an
increasing abdominal girth can elevate the intra-abdominal 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 intra-abdominal 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 intra-abdominal hypertension (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,
progressive 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 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 intra-abdominal problems
that occur in these critically ill patients (eg, necrotizing enterocolitis, ischemic
bowel).
●Liver transplantation – A prospective cohort study found intra-abdominal
hypertension (IAH; intra-abdominal pressure [IAP] >25 mmHg) following liver
transplantation in 32 percent of patients [26].
●Abdominal conditions – Massive ascites, abdominal surgery, or
intraperitoneal bleeding can increase intra-abdominal pressure [27,28].
●Retroperitoneal conditions – Retroperitoneal pathologies, such as ruptured
abdominal aortic aneurysm (rAAA), pelvic fracture with bleeding, and
pancreatitis, can lead to abdominal compartment syndrome [29-31]. In a
systematic review, the pooled rate of ACS following rAAA was 8 percent;
among those who developed ACS, nearly one half died.
●Medical illness – Conditions that require extensive fluid resuscitation (eg,
sepsis) and are associated with third spacing of fluids and tissue edema can
increase intra-abdominal pressure [1,32].
●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.

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).

The development of secondary ACS is often related to the need for and extent of
volume resuscitation [33-35]. 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 'Supportive care and temporizing
measures' below and "Treatment of severe hypovolemia or hypovolemic shock in
adults" and "Overview of inpatient management of 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 [34]. 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
[33]. 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 Intra-abdominal hypertension (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 [36,37]. Elevation of the diaphragm
may occur at pressures as low as 10 mmHg [38].
●Reduced venous return – IAH functionally obstructs blood flow in the inferior
vena cava, leading to diminished venous blood flow from the lower extremities
[39]. The resulting rise in lower extremity venous hydrostatic pressure
promotes the formation of peripheral edema and increases the risk of deep
vein thrombosis [40].
●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
intra-abdominal pressure if the patients are hypovolemic, receive excess applied PEEP,
or develop auto-PEEP [41-43]. (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 [44].
These effects are likely due to elevation of the diaphragm causing extrinsic compression
of the lung [45]. 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 [46]. These effects are accentuated by prior
hemorrhagic shock and resuscitation [47].

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 [48,49].
●Renal artery vasoconstriction is induced by the sympathetic nervous and
renin-angiotensin systems, which are stimulated by the fall in cardiac output
[50]. (See 'Cardiovascular' above.)

The end result is progressive reduction in both glomerular perfusion and urine output
[51]. Oliguria generally develops at an intra-abdominal pressure of approximately 15
mmHg, while anuria usually develops at an intra-abdominal pressure of approximately
30 mmHg [52].

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 [53]. These changes are reversible if the
IAH is recognized early and decompression is performed in a timely fashion [54].
(See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute
kidney injury in adults".)

Gastrointestinal — The gut appears to be one of the organs most sensitive to

increases in intra-abdominal pressure:
●Mesenteric blood flow was reduced at an intra-abdominal pressure as low as
10 mmHg in one animal study [55].
●Intestinal mucosal perfusion is decreased at an intra-abdominal pressure of
approximately 20 mmHg, according to both animal and human studies [56-
58].
●Celiac artery and superior mesenteric artery blood flow are decreased at an
intra-abdominal pressure of approximately 40 mmHg, according to one animal
study [6].

The impact of intra-abdominal pressure on mesenteric perfusion seems to be greatest

among patients who had hemorrhage or are hypovolemic [55,59].

IAH also compresses thin-walled mesenteric veins, which impairs venous flow from the
intestine and causes intestinal edema. The intestinal swelling further increases intra-
abdominal pressure, initiating a vicious cycle. The end result is worsened
hypoperfusion, bowel ischemia, decreased intramucosal pH, and lactic acidosis [60].

Hypoperfusion of the gut may incite loss of the mucosal barrier, with subsequent
bacterial translocation, sepsis, and multiple system organ failure [61]. Supporting this
notion, bacterial translocation has been shown to occur at an intra-abdominal pressure
of only 10 mmHg in the presence of hemorrhage [62].

Hepatic — The liver's ability to remove lactic acid is impaired by increases of intra-

abdominal pressure as small as 10 mmHg [63,64]. This occurs even in the presence of
a normal cardiac output and mean arterial blood pressure [63,64]. 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 intra-abdominal pressure that occurs with coughing, defecating,
or emesis [65]. 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 [66-68].
(See "Evaluation and management of elevated intracranial pressure in adults".)

CLINICAL PRESENTATION It is desirable to recognize intra-abdominal

hypertension (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 [1,69,70].
In a prospective cohort study of 42 adult blunt trauma victims, physical examination of
the abdomen identified a significantly elevated intra-abdominal 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
[69].

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 [71].

DIAGNOSTIC EVALUATION Definitive diagnosis of ACS requires

measurement of the intra-abdominal pressure, which should be performed with a low

threshold [72]. This is particularly true for patients who have trauma, liver
transplantation, bowel obstruction, pancreatitis, or other conditions that are known to be
associated with ACS. (See 'Etiology and risk factors' above.)

Measurement of intra-abdominal pressure — Intra-abdominal pressure can be

measured indirectly using intragastric, intracolonic, intravesical (bladder), or inferior
vena cava catheters [73]. 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
intra-abdominal hypertension (IAH) and ACS [74]. 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 [74-76].

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 intra-
abdominal pressure in both animals and humans [77-80]. 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 [73].

Chronically increased intra-abdominal pressure due to morbid obesity, pregnancy, or

ascites can complicate the diagnosis. Acute increases in intra-abdominal pressure may
be less well tolerated if superimposed on chronic IAH [81].

MANAGEMENT Management of intra-abdominal hypertension (IAH) and ACS

consists of supportive care and, when needed, abdominal decompression. Surgical

decompression of the abdominal cavity is considered definitive management (algorithm
1) [82]. Some exceptions include escharotomy release to relieve mechanical limitations
due to burn scars and percutaneous catheter decompression to relieve tense ascites
[83-85].

Supportive care and temporizing measures — The goals of supportive care in

patients with intra-abdominal hypertension include reduction of intra-abdominal volume
through avoidance of positive fluid balance after initial resuscitation, evacuation of
intraluminal contents, evacuation of intra-abdominal space-occupying lesions (eg,
ascites, hematoma) when possible, and measures to improve abdominal wall
compliance (pain control, sedation, paralysis, mechanical ventilation) [86,87].

Following certain surgeries (eg, complex ventral hernia repair), reopening the abdomen
is highly undesirable, and maximal supportive measures are undertaken to minimize the
need for abdominal decompression [88].

Supportive measures include:

 ●Proper positioning – Attention should be paid to patient positioning, and the
patient should be placed in a supine position. Elevation of the head of the bed
(>20°), which is commonly used to reduce the risk of ventilator-associated
pneumonia, increases intra-abdominal pressure and also impacts the
measurement of intra-abdominal pressure [74]. (See 'Measurement of intra-
abdominal pressure' above.)
●Drainage procedures – Nasogastric and rectal drainage is a simple
temporizing means for reducing intra-abdominal pressure in patients with
bowel distension. However, bowel distention alone is not a likely the cause of
ACS. Hemoperitoneum, ascites, intra-abdominal abscess, and retroperitoneal
hematoma also occupy space and can increase intra-abdominal pressure. In
cases where ACS and chronic ascites coexist, there may be a role for
paracentesis as a temporizing measure [74]. 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 intra-abdominal pressure (IAP) by at least
9 mmHg in the first four hours post-decompression was associated with
failure and the urgent need for open abdominal decompression [84,85].
●Pain control and sedation – Abdominal wall compliance can be improved
with adequate pain control and sedation. (See "Sedative-analgesic
medications in critically ill adults: Selection, initiation, maintenance, and
withdrawal" and "Sedative-analgesic medications in critically ill adults:
Properties, dosage regimens, and adverse effects".)
●Paralysis and 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. Pharmacologic paralysis, which
relaxes the abdominal wall and decreases carbon dioxide production to permit
better ventilation, may be required if hypercapnia is particularly severe.
(See "Neuromuscular blocking agents in critically ill patients: Use, agent
selection, administration, and adverse effects" and "Overview of initiating
invasive mechanical ventilation in adults in the intensive care
unit" and "Permissive hypercapnia during mechanical ventilation in adults".)
Positive end-expiratory pressure (PEEP) may reduce ventilation-perfusion
mismatch and improve hypoxemia [89]. (See "Positive end-expiratory
pressure (PEEP)".)
●Hemodynamic support – For patients with intra-abdominal 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, and visceral perfusion and negates some of the negative
effects of 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 ACS even though central venous
and pulmonary capillary wedge pressures are usually elevated [90].

Abdominal decompression
When to decompress the abdomen — There is general agreement that surgical
decompression is indicated for ACS (algorithm 1) [74]. However, a precise threshold for
surgical decompression has not been established. Various approaches include:

●Surgical decompression for all patients whose intra-abdominal pressure is

greater than 25 mmHg [91].
●Many clinicians suggest surgical decompression at a lower intra-abdominal
pressure (eg, 15 to 25 mmHg), based on their belief that surgical
decompression performed at an intra-abdominal 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 (MAP) and the intra-abdominal
pressure (IAP; 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 intra-abdominal pressure alone [15].

Techniques — 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.

Percutaneous decompression of the peritoneal cavity can be effective and is a less

invasive technique for treating patients with IAH/ACS where free intraperitoneal fluid or
blood is present as determined by bedside ultrasonography. Failure to drain at least
1000 mL of fluid and decrease IAP by at least 9 mmHg in the first four hours following
decompression is associated with failure and should prompt urgent surgical
decompression [85].

Temporary abdominal closure — Most surgeons perform decompression and then

maintain an open abdomen using temporary abdominal wall closure [92]. Several
techniques are available for temporary abdominal closure, but all require dressings that
bridge the fascial edges while preventing evisceration, retaining fluid, and retaining
heat. 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 intra-abdominal

hypertension (IAH) prior to the development of ACS causes tissue hypoperfusion, which
may lead to multisystem organ failure, and potentially death. The effect of
decompressive laparotomy on outcomes in patients with abdominal compartment
syndrome is not well studied. Although the development of IAH alone is not a predictor
of multiorgan failure [93], mortality for patients who have progressed to ACS is high,
ranging from 40 to 100 percent [11,14,94-97].

One prospective study measured intra-abdominal pressure in all patients admitted to

the intensive care unit and requiring a bladder catheter. Of the 83 patients studied, 33
percent developed intra-abdominal hypertension [7]. Logistic regression identified
maximal intra-abdominal 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).

Another prospective cohort study included 33 adult patients who underwent

decompressive laparotomy [94]. The overall 28 day mortality rate was 36 percent, which
increased to 55 percent at one year. Nonsurvivors tended to be older, and more
required mechanical ventilation compared with survivors. Median intra-abdominal
pressure was 23 mmHg (range: 21 to 27 mmHg) before decompressive laparotomy,
decreasing to 12 mmHg two hours after decompression, a level that was sustained
thereafter. Oxygenation and urinary output were significantly improved. Although
survivors showed improvement in organ function scores, nonsurvivors did not. The
abdomen could be closed primarily in 18 patients.

SOCIETY GUIDELINE LINKS Links to society and government-sponsored

guidelines from selected countries and regions around the world are provided
separately. (See "Society guideline links: Abdominal compartment
syndrome" and "Society guideline links: Ventral hernia".)

SUMMARY AND RECOMMENDATIONS

●Increased intra-abdominal pressure is called intra-abdominal hypertension

(IAH). Abdominal compartment syndrome (ACS) refers to organ dysfunction
caused by intra-abdominal 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 intra-abdominal pressure be measured.
Symptoms, physical signs, and imaging findings are insufficient to diagnose
ACS. Intra-abdominal pressure can be measured indirectly using intragastric,
intracolonic, intravesical (bladder), or inferior vena cava catheters.
Measurement of bladder pressure is the standard method to screen for IAH
and ACS. (See 'Diagnostic evaluation' above.)
●Initial management consists of supportive care and careful observation.
Surgical decompression should not be delayed in patients with ACS
(algorithm 1). We evaluate the patient for possible surgical decompression
when the intra-abdominal pressure is ≥20 mmHg and make our final decision
only after carefully weighing the potential benefits of decompression
compared with the risks of the proposed intervention in each individual
patient. (See 'Management' above.)
●Following surgical decompression, an open abdomen is maintained using a
variety of temporary abdominal closure techniques. (See 'Temporary
abdominal closure' above.)
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Topic 2889 Version 23.0

GRAPHICS
Intra-abdominal hypertension and abdominal compartment syndrome
Intra-abdominal hypertension (IAH) is defined as a sustained intra-abdominal pressure >12 mmHg.

Abdominal compartment syndrome (ACS) is defined as a sustained intra-abdominal pressure >20

mmHg that is associated with new organ dysfunction.

Based on information from: Abdominal perfusion pressure. AdominalCompartmentSyndrome.org

Graphic 69364 Version 4.0

Systemic effects of elevated intra-abdominal pressure

Central nervous system Gastrointestinal

↑ Intracranial pressure ↓ Celiac blood flow

↓ Cerebral perfusion pressure ↓ SMA blood flow

Cardiac ↓ Mucosal blood flow

Hypovolemia ↓ pHi

↓ Cardiac output Renal

↓ Venous return ↓ Urinary output

↑ PCWP and CVP ↓ Renal blood flow

↑ SVR ↓ GFR

Pulmonary Hepatic
↑ Intrathoracic pressure ↓ Portal blood flow

↑ Peak inspiratory pressure ↓ Mitochondrial function

↑ Airway pressures ↓ Lactate clearance

 ↓ Compliance Abdominal wall
↓ PaO2 ↓ Compliance

↑ PaCO2 ↓ Rectus sheath blood

flow
↑ Shunt fraction

↑ Vd/Vt
Graphic 70250 Version 3.0

Measurement of intra-abdominal pressure

1. Clamp the drainage tube of the Foley (bladder) catheter.

2. Instill up to 60 cc sterile saline into the bladder via the aspiration port of the Foley catheter. Be

certain the catheter is filled with fluid.

3. The pressure transducer can be held in place using an elastic strap as shown in the figure, or
alternatively, it can be attached to an intravenous pole at the height of the midaxillary line. Attach a

pressure transducer to an 18-gauge needle, and insert into the aspiration port. With some newer-style

Foley catheters, a needle-less connection system can be used.

4. Zero the transducer at the level of the midaxillary line.

5. With the patient in the supine position, ensure that abdominal muscle contractions are absent, and

measure the bladder pressure at end-expiration.

Graphic 56661 Version 6.0

Management of abdominal compartment syndrome and open abdomen

IAP: intra-abdominal pressure; OR: operating room.

* Severe injury, severe burns, liver transplantation, prolonged open surgery, massive resuscitation.
¶ For at-risk patients, bladder pressure measurements are obtained every four to six hours.

Δ Abdominal decompression can be considered in the absence of other obvious causes of organ dysfunction.

◊ Bladder pressure should be rechecked for new clinical findings (eg, abdominal tension, organ dysfunction).
Graphic 101881 Version 4.0