14/8/2018 Abdominal compartment syndrome in adults - UpToDate

Official reprint from UpToDate®

www.uptodate.com ©2018 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Abdominal compartment syndrome in adults

Author: Mark Gestring, MD

Section Editors: Hilary Sanfey, MD, 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: Jul 2018. | This topic last updated: Jan 29, 2018.

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].

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 1/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

● 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.

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 2/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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 "Treatment of 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 [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).

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 3/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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]

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 4/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

● 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
https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 5/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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 APPROACH — 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 [86,87].

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 6/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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 cause of ACS.

Hemoperitoneum, ascites, intra-abdominal abscess, and retroperitoneal hematoma occupy space and can
elevate 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
postdecompression was associated with failure and the urgent need for open abdominal decompression [84,85].

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 intra-abdominal pressure, and also impacts the measurement of intra-abdominal pressure
[74]. (See 'Measurement of intra-abdominal 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 during mechanical ventilation in adults" and "Clinical use of
neuromuscular blocking agents in critically ill patients".)

Positive end-expiratory pressure (PEEP) may reduce ventilation-perfusion mismatch and improve hypoxemia
[88]. (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 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 ACS even though central venous and pulmonary capillary
wedge pressures are usually elevated [89]. The only appropriate management is to open the abdomen. (See
'Abdominal decompression' below.)

ABDOMINAL DECOMPRESSION — 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 [90].

● 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.

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 7/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

● 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].

Most surgeons perform decompression and then maintain an open abdomen using temporary abdominal wall
closure [91]. 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".)

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 mm Hg in the first four
hours following decompression is associated with failure and should prompt urgent surgical decompression [85].

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

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

MORBIDITY AND MORTALITY — Failure to recognize 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 [92], mortality
for patients who have progressed to ACS is high, ranging from 40 to 100 percent [11,14,93-96].

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 [93]. 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.

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.)

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 8/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

● 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.)

● Management initially consists of careful observation and supportive care. In some cases, abdominal
compartment decompression is required. (See 'Ventilatory support' above and 'Abdominal decompression'
above.)

● 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 'Abdominal decompression' above.)

● Following surgical decompression, an open abdomen is maintained using a variety of temporary abdominal
closure techniques. (See 'Temporary closure techniques' above.)

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

Topic 2889 Version 16.0

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20comparti… 9/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20compar… 10/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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

↓ PaO 2 ↓ Compliance
↑ PaCO 2 ↓ Rectus sheath blood flow
↑ Shunt fraction

↑ Vd/Vt

Graphic 70250 Version 3.0

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20compar… 11/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20compar… 12/13
14/8/2018 Abdominal compartment syndrome in adults - UpToDate

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 3.0

https://www-uptodate-com.pbidi.unam.mx:2443/contents/abdominal-compartment-syndrome-in-adults/print?search=s%C3%ADndromes%20compar… 13/13