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Síndrome compartimental abdominal en adultos

Autor: Mark Gestring, MD
Editores de secciones: Amalia Cochran, MD, FACS, FCCM, Eileen M Bulger, MD, FACS
Editor Adjunto: Kathryn A Collins, MD, PhD, FACS

Todos los temas se actualizan a medida que se dispone de nueva evidencia y se completa nuestro proceso de revisión
por pares .

Revisión de literatura vigente hasta mayo de 2019. | Este tema fue actualizado por última vez el 12 de junio de
2019.

INTRODUCCIÓN El

síndrome del compartimiento abdominal se refiere a la disfunción orgánica causada por la

hipertensión intraabdominal. Puede ser poco reconocido porque afecta principalmente a pacientes
que ya están bastante enfermos y cuya disfunción orgánica puede atribuirse incorrectamente a la
progresión de la enfermedad primaria. Dado que el tratamiento puede mejorar la disfunción del
órgano, es importante que el diagnóstico se considere en la situación clínica adecuada. Aquí se
revisan la definición, la incidencia, los factores de riesgo, la presentación clínica, el diagnóstico, el
tratamiento y el pronóstico de la hipertensión intraabdominal y el síndrome del compartimento
abdominal.

El manejo del abdomen abierto después de la descompresión abdominal se discute por separado.
(Ver "Manejo del abdomen abierto en adultos" .)

DEFINICIONES

La hipertensión intraabdominal (IAH, por sus siglas en inglés) y el síndrome compartimental

abdominal (SCA) son entidades clínicas distintas y no se deben usar de manera intercambiable.

Presión intraabdominal : la presión intraabdominal (PIA) es la presión de estado estable oculta

dentro de la cavidad abdominal [ 1 ]. Para la mayoría de los pacientes críticamente enfermos, una
PIA de 5 a 7 mmHg se considera normal. En un estudio de cohorte prospectivo de 77 pacientes
hospitalizados en posición supina, el IAP promedió 6.5 mmHg y se relacionó directamente con el
índice de masa corporal [ 2 ].

El rango normal descrito anteriormente no es aplicable para todos los pacientes. Los pacientes con
un aumento de la circunferencia abdominal que se desarrolló lentamente pueden tener presiones
intraabdominales basales más altas. Como ejemplo, las personas con obesidad mórbida y
embarazadas pueden tener una presión intraabdominal crónica elevada (hasta 10 a 15 mmHg) sin
secuelas adversas [ 1 ].

Abdominal presión de perfusión - presión de perfusión abdominal (APP) se calcula como la

presión arterial media (MAP) menos el IAP: APP = MAP - IAP. La presión intraabdominal elevada
reduce el flujo de sangre a las vísceras abdominales [ 3 ]. El análisis de regresión múltiple ha
encontrado que la APP es mejor que otros puntos finales de reanimación, como el pH arterial, el
déficit de base, el lactato arterial y la producción de orina por hora para predecir los resultados [ 4 ].
Una APP objetivo de al menos 60 mmHg se correlaciona con una mejor supervivencia de IAH y ACS
[ 4-6 ].

Hipertensión intraabdominal : la hipertensión intraabdominal (IAH, por sus siglas en inglés) se

define como una presión intraabdominal sostenida ≥12 mmHg ( figura 1 ) [ 1,7,8 ]. Aunque este valor
se estableció arbitrariamente, se usa en muchos estudios de investigación y distingue a la mayoría
de los pacientes cuya presión intraabdominal está inadecuadamente elevada. La presión
intraabdominal se puede clasificar de la siguiente manera: Grado I = IAP 12 a 15 mmHg, Grado II =
IAP 16 a 20 mmHg, Grado III = IAP 21 a 25 mmHg, Grado IV = IAP> 25 mmHg [ 1 ].

IAH
● La hiperaguda se refiere a la elevación de la presión intraabdominal que dura solo unos
segundos. Se debe a la risa, la tos, la tensión, los estornudos, la defecación o la actividad física.
Se ha descrito la IAH con SCA debido a una sobredistensión gástrica después de la endoscopia
[ 9 ].

● La IAH aguda se refiere a la elevación de la presión intraabdominal que se desarrolla durante

horas. Por lo general, es el resultado de un traumatismo o una hemorragia intraabdominal y
puede conducir al rápido desarrollo de SCA.

● La IAH subaguda se refiere a la elevación de la presión intraabdominal que se desarrolla a lo

largo de los días. Es más común en pacientes médicos y también puede conducir a SCA.

● La IAH crónica se refiere a la elevación de la presión intraabdominal que se desarrolla durante

meses (embarazo) o años (obesidad mórbida) [ 10 ]. No causa SCA, pero coloca al individuo en
mayor riesgo de SCA si desarrolla IAH superpuesta o subaguda superpuesta.
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 "Treatment of severe hypovolemia or hypovolemic shock in adults" and 'Hemodynamic support'
below 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 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].

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 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.

● 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 mmHg 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.

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.)

● 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.)

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Topic 2889 Version 21.0

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

↓ PaO 2 ↓ Compliance
↑ PaCO 2 ↓ 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

Contributor Disclosures
Mark Gestring, MD Nothing to disclose Amalia Cochran, MD, FACS, FCCM Other Financial Interest: JAMA
Surgery (Web and social media editor). Eileen M Bulger, MD, FACS Grant/Research/Clinical Trial Support: Atox
Bio [Necrotizing soft tissue infections (AB103)]. Consultant/Advisory Boards: Hemanext [Transfusion therapy
(Anaerobic storage system for blood products)]; Opticyte [Shock (Direct cellular oximeter)]. Equity
Ownership/Stock Options: Opticyte [Shock (Direct cellular oximeter)]. Kathryn A Collins, MD, PhD,
FACS Nothing to disclose

Las revelaciones de los contribuyentes son revisadas para los conflictos de interés por el grupo editorial.
Cuando se encuentran, estos se abordan examinando un proceso de revisión multinivel y los requisitos para que
se proporcionen referencias que respalden el contenido. El contenido referenciado adecuadamente es requerido
por todos los autores y debe cumplir con los estándares de evidencia UpToDate.

Política de conflicto de intereses.