Blackwell Science, LtdOxford, UKBJUBJU International1464-410XBJU InternationalMarch 2003
924
Review Article
ABDOMINAL COMPARTMENT SYNDROME
R. TAL
et al.
Abdominal compartment syndrome: urological aspects
R. TAL, D.M. LASK, J. KESLIN* and P.M. LIVNE
Institute of Urology and *General Intensive Care Unit, Rabin Medical Center, Golda-Hasharon Campus, Petah Tikva, and Sackler School of Medicine,
Tel Aviv University, Tel Aviv, Israel
Accepted for publication 9 August 2003
KEYWORDS
abdominal compartment syndrome,
intra-abdominal pressure, kidney function.
INTRODUCTION
The term abdominal compartment syndrome
(ACS) describes the effects of elevated intra-
abdominal pressure (IAP) on multiple-organ
systems. This article reviews the clinical
presentation, monitoring and treatment of
ACS, emphasising its urological implications.
HISTORY
Although the term ACS was introduced only
in the 1980s, the disorder has been recognized
since 1863, when Marey and Burt described
the respiratory effects of elevated IAP. In
1876, Wendt reported an association of
elevated IAP with renal dysfunction, which
was later corroborated by others. In 1890,
Heinricius showed that in animal models an
increase in IAP led to death, presumably from
respiratory failure, and in 1911 Emerson
described the cardiovascular derangements
caused by a high IAP in animals. Early in
World War II, Ogilvie detailed the surgical
management of the ‘burst abdomen’ and in
1940 Gross was the first to advocate a two-
stage repair of omphalocele, describing the
‘continual battle, often somewhat brutal,
while trying to pack intestinal loops into a
cavity which was too small to receive them’.
He also identified the clinical triad that could
be anticipated when the abdominal cavity is
overfilled; respiratory failure (caused by
upward displacement of the diaphragm),
impaired venous return (from pressure on the
inferior vena cava) and intestinal obstruction
(from compression of the viscera).
DEFINITION AND AETIOLOGY
The term ACS was first used by Kron et al.
[1] in the early 1980s to describe the
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pathophysiology of elevated IAP. Currently,
ACS is defined as the cardiovascular,
pulmonary, renal, splanchnic, gastrointestinal,
abdominal wall/wound and intracranial
disturbances resulting from an acute and
rapid increase in IAP [2]. The normal IAP is
atmospheric (zero) or sub-atmospheric
(negative) when measured in spontaneously
breathing animals [2]. Mechanical ventilation
produces a positive IAP close to the end-
expiratory pressure, with values of up to
10 mmHg considered normal. After
abdominal surgery pressures are typically
3–15 mmHg [3]. ACS is diagnosed when the
IAP is >25 mmHg in the presence of one of
the following signs of clinical deterioration;
oliguria, raised pulmonary pressure, hypoxia,
decreased cardiac output, hypotension or
acidosis. The diagnosis is confirmed when
abdominal decompression results in clinical
improvement [4]. In current publications,
different definitions for ACS are used.
Meldrum et al. [5] defined ACS as an IAP
of >20 mmHg complicated by one of
the following: a peak airway pressure
of >40 cmH2O, oxygen delivery index
<600 mL O2/min/m2, or urine output
<0.5 mL/kg/h, while Ertel et al. [6] defined ACS
as the development of significant respiratory
compromise, including elevated inspiratory
pressure of >35 mbar, a decreased Horowitz
quotient (<150 Torr, or <20 kPa), renal
dysfunction (urine output <30 mL/h),
haemodynamic instability necessitating
catecholamines and a rigid or tense abdomen.
ACS may follow many diverse insults and
clinical scenarios [2,3]. ACS and resultant
renal dysfunction have been described in
trauma patients with intraperitoneal,
extraperitoneal or pelvic injuries, and in
atraumatic conditions. The most common
cause is increased IAP from intraperitoneal
conditions, e.g. haemorrhage, oedema, bowel
distension, mesenteric venous obstruction,
abdominal packs, tense ascites, peritonitis
and tumours. Pneumoperitoneum, induced
and widely used for various laparoscopic
procedures, has been shown to cause
high IAPs with adverse effects on the
cardiovascular system and renal function,
© 2 0 0 4 B J U I N T E R N A T I O N A L | 9 3 , 4 7 4 – 4 7 7 | doi:10.1111/j.1464-410X.2004.04654.x
including decreased aortic and inferior vena
cava blood flow and oliguria [7,8]. However,
unilateral pneumoretroperitoneum causes
lesser systemic and renal haemodynamic
alterations [9]. The effects produced by the
gas insufflation are reversible, with complete
resolution at 2–24 h after decompression
[8,9]. ACS has also been described
after ureteric perforation, leading to
intraperitoneal urine leakage and as a
consequence of increased retroperitoneal
volume secondary to pancreatitis,
haemorrhage or oedema after pelvic trauma
or abdominal aortic surgery [2,10]. Our group
encountered ACS as a complication of a large
retroperitoneal haematoma resulting from
percutaneous nephrostomy insertion
(unpublished). A review of the literature
revealed no additional reports of ACS caused
by percutaneous access to the kidney.
Extrinsic abdominal compression can also
lead to ACS; IAP may rise in patients with
burns and abdominal eschars or after a tight
surgical abdominal closure.
In most critically ill patients, the development
of the ACS is multifactorial. Massive fluid
resuscitation, for any reason, combined
with capillary leak (e.g. in shock, sepsis,
burns or reperfusion injury), leads to visceral
oedema, an increase in visceral volume
and IAP. Poor pulmonary compliance from
acute lung dysfunction requires high
positive-pressure ventilation. This pressure
is transmitted to the abdominal cavity,
exacerbating the existing increase in IAP.
The circulatory effects of elevated IAP further
compromise abdominal wall and visceral
perfusion, leading to a vicious cycle of
increased oedema, decreased abdominal
wall compliance and in turn increasing
IAP [2]. The diagnosis of ACS should be
considered in any traumatised or critically
ill patient in the setting of abdominal
distension and deteriorating cardiac,
pulmonary or renal function [11]. The
incidence of elevated IAP in surgical patients
admitted to an intensive care unit has been
reported to be as high as 33%. Among
patients with renal functional impairment,
69% had increased IAP [12].

MEASURING THE IAP
Several methods of measuring IAP have been
described; Kron et al. [1] used intravesical
pressure to represent IAP, measuring the
intravesical pressure with a manometer
attached to a Foley catheter placed in the
bladder. Cheatham et al. [13] revised that
technique and described a closed-system
device that enabled repeated measurements
of the intravesical pressure and thereby, close,
convenient and safe monitoring of the IAP.
Johna et al. [14], comparing direct IAP
measurements during laparoscopy with
intravesical measurements, found that the
bladder had higher pressures than the
abdomen but the two were highly and
positively correlated in individual patients.
Fusco et al. [15] showed that intravesical
pressure closely approximated IAP and that
the instillation of 50 mL of liquid into the
bladder improved the accuracy of the IAP
measurement. Other techniques include
intragastric pressure measurement obtained
by nasogastric tube, and intrarectal pressure
obtained by introducing a 12 F balloon-tipped
catheter into the rectum 8–10 cm above the
anal verge, but these methods seem to be
technically less reliable [16]. Another method
of indirectly measuring IAP by inserting an
inferior vena caval catheter was attempted in
animal models but it is not clinically used
because it is invasive [2]. Measuring the IAP is
essential, as the clinical examination cannot
reliably identify patients with elevated IAP.
Kirkpatrick et al. [17] conducted a prospective
blinded study and found that the sensitivity
of the clinical examination was only 40%
for an IAP of >10 mmHg, and 56% for
>15 mmHg.
ACS and its pathophysiological derangements
appear above a critical IAP that varies among
patients and even within a given patient.
Burch et al. [18] described a grading system
for IAP depending on the pressure (in cmH2O)
as follows: grade I, 10–15; grade II, 16–25;
grade III, 26–35; and grade IV, >35. Although
physiological changes could be detected
already in association with grade I increases,
decompression was clinically insignificant
and unwarranted. The authors recommended
that at higher pressures treatment should be
determined on the basis of the patient’s
physiological responses. Meldrom et al. [5],
from their finding that renal dysfunction
(defined as a urine output of <0.5 mL/kg/h)
was absent in patients with grades I and II
ACS but present in 65% and all patients with
© 2004 BJU INTERNATIONAL
ABDOMINAL COMPARTMENT SYNDROME
grades III and IV, respectively, concluded that
most grade III and all grade IV increases
required operative intervention and
decompression. Cheatham et al. [19] proposed
a new variable for assessing the IAP, termed
‘abdominal perfusion pressure’, defined as the
mean arterial pressure minus the IAP. These
authors showed that the abdominal perfusion
pressure was better than the IAP for
predicting survival, and served as a clinically
useful resuscitation endpoint in patients with
ACS.
PATHOGENESIS AND TREATMENT
The deleterious consequences of a high IAP on
the abdominal viscera, abdominal wall,
respiratory system, cardiovascular system,
CNS and urinary system are well described
[2,3]. The cause of the urinary system
dysfunction is probably multifactorial. The
renal dysfunction of ACS is characterized
by oliguria progressing to anuria and
unresponsiveness to volume expansion
[2]. Oliguria can be seen at an IAP of 15–
20 mmHg, and anuria at ≥ 30 mmHg. Harman
et al. [20] studied the haemodynamic effects
of elevated IAP on renal function and cardiac
output in dogs. At 20 mmHg renal blood flow
and the GFR were 25% lower than the values
measured at 0 mmHg, and renal vascular
resistance was 15 times higher than systemic
vascular resistance. At 40 mmHg the dogs
became anuric and the renal blood flow and
GFRs were 7% of the baseline with a cardiac
output of 37% of the baseline. Volume
expansion corrected the deficit in cardiac
output but renal blood flow and GFR
remained at <25% of the normal value. These
findings suggest that renal dysfunction
secondary to elevated IAP is not related only
to reduced cardiac output. Indeed, at an IAP
of >20 mmHg all intraperitoneal and
retroperitoneal viscera show a markedly
reduced blood flow. The one exception is the
adrenal gland, for which measurements of
perfusion clearly indicate a paradoxical
increase in blood flow even at IAPs of up to
40 mmHg [3]. Biancofiore et al. [21] studied
the effects of elevated IAP on renal function
in subjects undergoing liver transplantation.
Using receiver operator characteristic curve
analysis they showed that an abdominal
pressure of 25 mmHg had the best sensitivity/
specificity ratio for renal failure. The
pathogenesis of these renal derangements is
probably multifactorial; a combination of
reduced cardiac output, elevated renal venous
pressure, increased renal parenchymal
pressure and direct compression of the renal
vein. Elevated IAP compresses the resistance
vessels, increasing afterload, and compresses
the inferior vena cava, decreasing pre-load.
These processes result in decreased cardiac
output and reduced renal blood flow with
activation of the renin-angiotensin-
aldosterone system. The combination of
decreased renal blood flow, increased renal
parenchymal pressure and direct renal vein
compression reduces the pressure gradient
across the glomerular membrane and thereby
the GFR, leading to changes in intrarenal
blood flow and corticomedullary blood
shunting. These haemodynamic alterations
promote the release of renin, with the
formation of angiotensin II, a potent
vasoconstrictor, further reducing renal blood
flow and GFR. With reduced GFR there is a
reduction of sodium delivery to the macula
densa and further release of renin from the
juxtaglomerular cells, leading to a vicious
cycle [22]. Aldosterone secretion mediates
sodium and water retention, contributing to
oliguria [2]. The reduction in GFR in ACS is
refractory to volume loading, suggesting that
the renal vein hypertension may be more
important than the reduction in renal blood
flow [3]. This assumption is also supported by
the general ineffectiveness of treatment with
dopaminergic agonists and loop diuretics [2].
Doty et al. [22,23] showed that high renal
parenchymal pressure alone does not
lead to renal dysfunction, whereas renal
vein compression alone creates the
pathophysiological derangements seen in
ACS, suggesting that renal vein compression
is the most important factor. Ureteric
compression has also been implicated as a
contributory factor in the development of
oliguria and urinary system dysfunction, but
inserting ureteric catheters has no favourable
effect [2,3].
The cornerstones of managing ACS are
prevention, a high index of suspicion, early
recognition and prompt decompressive
laparotomy to reverse the urinary system
dysfunction. Prolonged fluid resuscitation to
maintain intravascular volume and cardiac
output may aggravate bowel oedema and
ascites, resulting in a vicious cycle with
aggravation of the ACS [11]. ACS can be
prevented by an awareness of its high
prevalence, reportedly 5–15% among patients
with severe abdominal trauma, and knowing
the risk factors associated with ACS [6]. Ertel
et al. [6] found that the risk factors associated
475
R . TA L ET AL.
with ACS are active bleeding requiring
damage control laparotomy and packing,
combined abdominal and pelvic injuries,
primary abdominal fascial closure (in contrast
to mesh closure), massive bowel distension
secondary to reperfusion injury after fluid
resuscitation and resolution of shock, and
uncontrolled intra-abdominal bleeding, not
uncommonly caused by coagulopathy,
necessitating re-exploration. The early
diagnosis of ACS mandates close monitoring
of IAP in every patient at risk, as it may occur
within a few hours. In certain circumstances
the development of ACS can be prevented by
simple measures such as avoiding tense
abdominal closure, but the presence of active
bleeding poses a real challenge because of the
conflict between the need to achieve pressure
to tamponade the bleeding and to avoid
increasing the IAP. The treatment of ACS is
prompt surgical decompressive laparotomy
and temporary abdominal-wall closure using
a mesh or a ‘Bogota bag’ (various techniques
are described but are beyond the scope of this
review). Minimally invasive decompression
techniques, i.e. laparoscopic and
percutaneous procedures, for selected
indications have been described but they are
not widely used [24,25]. Kopelman et al. [11]
noted that survivors of ACS underwent
surgical decompression earlier than those not
surviving, and suggested that the length of
time a patient remains intra-abdominally
hypertensive is more significant than the
absolute increase in abdominal pressure. Early
recognition of predictive variables and
identifying patients at risk will hopefully lead
to early treatment and avoid the morbidity
and mortality associated with ACS.
SUMMARY
ACS is prevalent in various surgical conditions
and in a large percentage of critically ill
patients. Measuring the IAP is important in
the early diagnosis of ACS and can be easily
done by measuring the intravesical pressure.
ACS adversely affects many organ systems;
the pathogenesis of renal dysfunction is
probably multifactorial, from a combination
of reduced cardiac output, reduced GFR
mediated by secretion of renin and
angiotensin, aldosterone-mediated water
reabsorption, increased renal parenchymal
pressure and direct compression of the renal
vein. Successful treatment requires a high
index of suspicion, prompt recognition and
early surgical abdominal decompression.
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© 2004 BJU INTERNATIONAL
ABDOMINAL COMPARTMENT SYNDROME
Correspondence: Dr R. Tal, Institute of Abbreviations: ACS, abdominal compartment
Urology, Rabin Medical Center, Golda- syndrome; IAP, intra-abdominal pressure.
Hasharon Campus, 7 Kakal St., 49372 Petah
Tikva, Israel.
e-mail: raanant@post.tau.ac.il
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