Intra-abdominal hypertension in the critically ill: it is time

to pay attention
Manu L. N. G. Malbraina, Dries Deerenb and Tom J. R. De Potterc

Care Medicine, Amsterdam, The Netherlands, October 5 8, 2003; at the 24th

Purpose of the review
There has been an exponentially increasing interest in
intra-abdominal hypertension (IAH). Comparison of the
published data however is difficult due to the lack of
consensus definitions. This review will focus on the
available literature from the last 2 years. A Medline and
PubMed search was performed using intra-abdominal
International Symposium on Intensive Care and Emergency Medicine, Brussels,
Belgium, March 30 April 2, 2004; and at the 17th Annual Congress of the
European Society of Intensive Care Medicine, Berlin, Germany, October 1013,
2004.
Correspondence to Manu Malbrain, MD, ICU Director, Intensive Care Unit,
ZiekenhuisNetwerk Antwerpen, Campus Stuivenberg, Lange Beeldekensstraat
267, B-2060 Antwerpen 6, Belgium
Tel: +32 3 217 7399; fax: +32 3 217 7279; e-mail: manu.malbrain@skynet.be

pressure (IAP), intra-abdominal hypertension (IAH), and Current Opinion in Critical Care 2005, 11:156
171
abdominal compartment syndrome (ACS) as search
Abbreviations
items. The aim was to find an answer to the question Isnt it
ACS abdominal compartment syndrome
time to pay attention to intra-abdominal pressure in the ALI acute lung injury
critically ill? APP abdominal perfusion pressure
ARDS acute respiratory distress syndrome
Recent findings BT bacterial translocation
Although the number of studies published on this topic is BMI body mass index
CVP central venous pressure
steadily increasing and confirms the pathophysiologic IAH intra-abdominal hypertension
implications of IAH on end-organ function within and IAP intra-abdominal pressure
ICU intensive-care unit
outside the abdominal cavity it remains difficult to compare MAP mean arterial pressure
the literature data because the measurement methods and MOF multiple organ system failure
PAOP pulmonary artery occlusion pressure
definitions used are not uniform. Provocative data have PEEP positive end expiratory pressure
been published regarding the interactions between the Pplat plateau pressure
SOFA sepsis and organ failure assessment
abdominal and thoracic compartments especially in
patients with capillary leak and fluid overload; most of this
2005 Lippincott Williams & Wilkins.
data raises even more questions than it gives answers and 1070-5295
may therefore strengthen the nonbelievers who consider
IAP, IAH and ACS as epiphenomena in critically ill patients. Introduction
Unless the international scientific community does not There has been increasing interest in intra-abdominal
come forward with clear-cut definitions we will keep hypertension (IAH) and the abdominal compartment
comparing apples with oranges. syndrome (ACS) over the last decade, however until
Summary now no uniform definitions have been suggested. Defini-
It is time to pay attention to intra-abdominal pressure in the tions of IAH or ACS stand or fall with the accuracy and
critically ill. It is also time for standardized IAP measurement reproducibility of the intra-abdominal pressure measure-
methods, good consensus definitions and randomized ment method [1]. Not only the absolute numbers but
interventional studies. also the use of mean, median or maximal IAP values will
influence the prevalence and incidence of IAH [2]. Dif-
Keywords ferent threshold values have been suggested for IAH and
abdominal compartment, abdominal hypertension, ACS and some have interchanged the terms IAH and ACS.
abdominal pressure, diagnosis, pathophysiology, treatment Others have suggested terms such as surgical or medical
ACS, or abdominal and extra-abdominal ACS, but with ever-
171. 2005 Lippincott Williams & Wilkins.
Curr Opin Crit Care 11:156 changing definitions. To date, it is therefore very difficult
a
to interpret the literature data and a consensus on defini-
Intensive Care Unit, ZiekenhuisNetwerk Antwerpen, Campus Stuivenberg, Lange
Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium, bDepartment of Internal
tions of issues related to IAH is needed to approach sci-
Medicine, ZiekenhuisNetwerk Antwerpen, campus Stuivenberg, Lange entific accuracy in comparing different clinical reports
Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium, and cDepartment of
Cardiology, Cardiovascular Center, OLV Hospital, Moorselbaan 164, B-9300 Aalst,
and to plan for future clinical trials. These definitions
Belgium should be comprehensive, detailed, simple, practical
and acceptable to most of the scientific community work-
Part of this work was presented at the 14th Annual Congress of the European
Society of Intensive Care Medicine, Geneva, Switzerland, September 30
October
ing in this field. Until such a consensus is achieved, this
3, 2001; at the 22nd International Symposium on Intensive Care and Emergency article will provide some suggestions for definitions, so
Medicine, Brussels, Belgium, March 19 22, 2002; at the 23rd International
Symposium on Intensive Care and Emergency Medicine, Brussels, Belgium, March
that the data and results from future studies can be more
1821, 2003; at the 16th Annual Congress of the European Society of Intensive easily compared [3].
156

Intra-abdominal pressure
Intra-abdominal pressure (IAP) is the steady state pres-
sure concealed within the abdominal cavity. The IAP
shifts with respiration as evidenced by an inspiratory
increase (diaphragmatic contraction) and an expiratory
decrease (relaxation). A normal IAP value is around
5 mm Hg, but can be substantially higher in the morbidly
obese or the postoperative period [46]. Before the diag-
nosis of pathologic IAP or IAH, which may potentially re-
quire therapeutic intervention, can be made, a sustained
increase in the IAP reflecting a new pathologic phe-
nomenon or entity in the abdominal cavity needs to be
demonstrated [7].
Intra-abdominal pressure measurement
Clinical examination of the abdomen or the abdominal pe-
rimeter is an inaccurate way to estimate IAP [812]. This
was recently shown in a study by Castren and co-workers
who found that for patients with end-stage renal disease on
peritoneal dialysis, measuring the abdominal circumference
was not a good diagnostic tool to predict intra-abdominal
bleeding [13].
To obtain a correct IAP value, a pressure needs to be mea-
sured. Various direct and indirect measurement methods
via different routes have been suggested in the literature
and most of the currently used indirect methods were
summarized in a recent review on this topic [1]. The
IAP should be expressed in mm Hg and measured at
end-expiration in the complete supine position, ensuring
that abdominal muscle contractions are absent and the
transducer zeroed at the level of mid-axillary line (conver-
sion factor from mm Hg to cm H2O is 1.36 and conversely,
from cm H2O to mm Hg is 0.74).
Until other methods are validated, the bladder method is
considered as the de facto indirect gold standard for inter-
mittent IAP measurement (the direct measurement gold
standard being intraperitoneal pressure measurement).
Figure 1 depicts an intermittent bladder pressure measure-
ment method. Recently, new measurement kits, either via
a Foley Manometer (Holtech Medical, Kopenhagen, Den-
mark; www.holtech-medical.com), AbViser-valve (Wolfe
Tory Medical, Salt Lake City, UH, USA; www.wolfetory.
com) or continuous IAP measurement via a balloon-tipped
stomach catheter (Spiegelberg, Hamburg, Germany; www.
spiegelberg.de) have become commercially available [1].
A continuous IAP tracing can also be obtained via a standard
18 Fr three-way Foley bladder catheter. The continuous
IAP measurement is performed via the irrigation port of
the three-way catheter, in which continuous sterile normal
saline irrigation is maintained and connected through
a two-way stopcock and normal saline-filled tubing to a
pressure transducer placed in-line with the iliac crest at
Intra-abdominal hypertension in the critically ill Malbrain et al. 157
the mid axillary line [14]. The transducer is zeroed and
the continuous IAP measurement is recorded on the bed-
side monitor.
Abdominal perfusion pressure
Analogous to the widely accepted and used concept of ce-
rebral perfusion pressure (CPP), calculated as mean arte-
rial pressure (MAP) minus intracranial pressure (ICP)
(CPP = MAP ICP), the abdominal perfusion pressure
(APP), calculated as MAP minus IAP (APP = MAP
IAP), has been suggested as a useful endpoint for resus-
citation [15,16]. Likewise, the renal (abdominal) filtration
gradient is defined as MAP minus 2 times IAP (FG =
MAP 2 3 IAP).
Intra-abdominal hypertension
The exact level of IAP that defines intra-abdominal hyper-
tension (IAH) still remains a subject of debate. In the early
surgical literature the level of 1518 mm Hg (20 to 25 cm
H2O) came forward. Burch and co-authors defined a grad-
ing system of IAH/ACS to guide therapy: Grade I corre-
sponds to a bladder pressure of 7.511 mm Hg, Grade II
to 1118 mm Hg, Grade III to 1825 mm Hg, and Grade
IV >25 mm Hg [17]. Obviously, pathologic IAP is a
continuum ranging from mild increases without clinical
adverse effects to a substantial elevation, with grave conse-
quences to all organ systems. Although the use of a single
IAP parameter to define IAH could be questioned, it is
important that a consensus on this point is reached in
the future.
Currently, the IAP threshold (either mean or maximal
values) for the definition of IAH in the literature varies
most commonly between 12 and 25 mm Hg [2,9,18
27,24,26]. Some studies have shown deleterious effects
on organ function after increases in IAP as low as 10 or
15 mm Hg, respectively [3,16,2831,29]. A recent, and
so far the only, multicenter study aimed at establishing
the prevalence, etiology and predisposing factors associat-
ed with IAH in a mixed population of intensive care
patients defined IAH as a maximal IAP value of 12 mm
Hg or more in at least one measurement [2]. With the
lack of a consensus, and to exclude brief, temporary ele-
vations of IAP which are not clinically significant, we sug-
gest that IAH be defined as follows:
IAH is a consistent increased IAP value of $12 mm Hg,
which is recorded by a minimum of three standardized
pressure measurements that are conducted 46 hours
apart.
After establishing this minimum threshold for defining
IAH, stratification or gradation of the pathologic IAP
values as Burch suggested is probably needed to calibrate
and quantify the threat of the insult to produce clinically
significant manifestations (see above).
158 Gastrointestinal system

Figure 1. A closed needle-free revised method for measurement of intra-abdominal pressure

(a) A Foley catheter is connected to the urine

collection bag with a ramp with 3 stopcocks. A
standard intravenous (IV) infusion set is connected
to a bag of 1000mL of saline and attached to the
first stopcock. A 60-mL syringe is connected to the
second stopcock and the third stopcock
is connected to a pressure. The system is flushed
and the pressure transducer is zeroed at the
symphysis pubis. At rest the 3 stopcocks give an
open way for urine flow. To measure IAP, the
urinary drainage tubing is clamped and the third
stopcock is turned on to the transducer. The first
stopcock is turned off to the patient, the second
stopcock is turned on to the 60-mL syringe and
50ml of saline is aspirated into the syringe and
instilled into the bladder. The third stopcock being
turned on to the transducer allows immediate IAP
reading on the monitor. Reproduced with
permission [1].
(b) Mounted patient view of the device and close
up of manifold and conical connection pieces.
Reproduced with permission [1].

Abdominal compartment syndrome
Abdominal compartment syndrome (ACS) is a syndrome
and not a disease; therefore it can have different causes.
Most syndromes are preceded by a prodromal phase dur-
ing which a number of nonspecific symptoms and signs
appear. The ACS is no exception to this general rule,
and IAH represents the prodromal phase of ACS. Within
the last statement rests the theoretical distinction be-
tween IAH and ACS, namely that IAH in combination
with overt organ dysfunction represents ACS (Fig. 2).
A more accurate definition of the ACS will require a com-
bination of a numerical value identified with increased
IAP with the significant clinical consequences of the pro-
longed IAH, that is the development of disturbances in
the different organ systems. In a recent study [2], ACS
was defined as IAP $20 mm Hg with failure of one or
more organ systems, and organ failure was defined as a
Sequential Organ Failure Assessment (SOFA) organ sub-
score $3 [32]. Until a consensus agreement on a definition
of ACS is reached, we submit the following to be used in
future clinical studies:
ACS is defined as IAH with a gradual and consistent
increased IAP value of $20 mm Hg recorded during a -
minimum of three standardized measurements that are
performed 16 hours apart and that is directly associated
with single or multiple organ system failure that was not
previously present (as assessed by the daily SOFA
or equivalent scoring system, organ failure is defined as
a SOFA organ system score of $3).

Figure 2. Distinctions between normal intra-abdominal
pressure (IAP), intra-abdominal hypertension (IAH)
and abdominal compartment syndrome (ACS)
The shaded area illustrating IAH may undergo shifts to the right
or left depending on the clinical scenario. Reproduced by courtesy
of David J.J. Muckart, MD, University of Natal Medical School,
Republic of South Africa, and Rao Ivatury, MD, PhD, Virginia
Commonwealth University, Virginia, USA.
In contrast to IAH, the ACS should not be graded, since
ACS is an all-or-nothing phenomenon. Further assessment
of organ function can be done by examining the direct
clinical effects of ACS on different variables (see the
below section Organ function assessment).
Classification of intra-abdominal
hypertension and abdominal
compartment syndrome
With the increasing recognition of ACS as a significant
contributor to the development of multiple organ failure
(MOF) in critically ill patients, and the multitude of con-
ditions associated with ACS, it is useful to categorize ACS
according to the underlying pathology [3,26,33,34]. This
overlap of clinical conditions and potential etiologies has
added to the confusion regarding the definitions. Addi-
tional difficulty arises when patients develop ACS after
previous surgical treatment for the prevention of IAH
[22,3537].
For further fine-tuning and classification of IAH/ACS
other questions need to be answered with regard to the
duration (chronic, acute, subacute, hyperacute), the ini-
tial underlying problem (intra- or extra-abdominal), the
etiology (medical, surgical, trauma or burn) and the local-
ized or generalized character.
Some examples and suggestions for definitions were
recently given and are summarized below [3,31]:
Intra-abdominal hypertension in the critically ill Malbrain et al. 159
Hyperacute IAH lasts only seconds or minutes: laughing,
straining, coughing, sneezing, defecation or physical
activity.
Acute IAH occurs within hours: trauma or intra-abdominal
hemorrhage of any cause (e.g. ruptured abdominal aor-
tic aneurysm).
Subacute IAH occurs within days: most medical causes
(e.g. fluid resuscitation and capillary leak).
Chronic IAH occurs within months or years: morbid
obesity, intra-abdominal tumor (large ovarian cyst,
fibroma.), chronic ascites (liver cirrhosis or chronic
ambulatory peritoneal dialysis [CAPD]), or pregnancy.
Primary ACS: defined as a condition associated with injury
or disease in the abdomino-pelvic region (e.g. severe
acute pancreatitis, spleen rupture).
Secondary ACS: refers to conditions that do not originate
from the abdominal cavity (such as pneumonia with
sepsis and capillary leak, major burns and other condi-
tions requiring massive fluid resuscitation).
Tertiary ACS: refers solely to the condition where ACS
develops following prophylactic or therapeutic surgical
or medical treatment of primary or secondary ACS (e.g.
persistence of ACS after decompressive laparotomy,
formerly termed the open or recurrent abdominal
compartment syndrome) [35].
Intra-abdominal hypertension and
abdominal compartment syndrome
prevalence and incidence
In a recent, and so far the only multicenter study, IAP was
measured through a Foley bladder catheter according to
the modified Kron technique [1] every 6 hours during
a 24-hour period in all patients hospitalized for more than
24 hours in 13 ICUs [2]. IAH was defined as a maximal
IAP of 12 mm Hg or more, and ACS as a maximal IAP of
20 mm Hg or more, with at least one organ failure as de-
fined by a SOFA subscore of more than 3. The mean IAP
was 9.8 mm Hg ( 4.7 SD). In medical ICU patients, the
prevalence of IAH was 54.4% (31 of 57 patients), whereas
this percentage was higher (65% or 26 of 40 patients) in
surgical ICU patients. Overall, the prevalence of IAH
was 57 of 97 patients or 58.8%, and 8.2% of these patients
were classified as ACS (Table 1). The mean coefficient
of variation (COVA, defined as the standard deviation di-
vided by the mean value) was 25%, but ranged from 11.8%
to 46.3% among different centers, and from 4% to 66%
among different patients [3].
We recently determined the COVA of two techniques for
IAP measurement in 15 sedated and ventilated patients
through a novel bladder Foley manometer (Holtech Med-
ical, Copenhagen, Denmark) and with a fully automated
continuous technique using a balloon-tipped gastric cath-
eter, connected to an IAP monitor (Spiegelberg, Hamburg,
Germany) [38]. The COVA for the IAP was 17.1% and
160 Gastrointestinal system

18.7%, respectively. These variations may be even more Abdominal assessment

pronounced in nonsedated patients. Thus, intermittent
measurements are only snapshots, and may underestimate
the true prevalence or incidence of IAH and ACS. This
explains why the interpretation and comparison of litera-
ture data are so difficult.
The one-day snapshot prevalence study was followed by
a one-month incidence study [39]. In this multicenter
study conducted in 14 ICUs 265 patients were enrolled
and 4513 IAP measurements were performed during the
study period. The mean IAP was 10 4.8 mm Hg for
all measurements. The mean IAP value on admission dif-
fered from center to center between 6 3.6 mm Hg and
15.1 4.7 mm Hg (Fig. 3). Table 2 summarizes the inci-
dence of IAH for different cut-offs. The incidence differs
in relation to the cut-offs used and whether mean or max-
imal IAP values were used.
On admission, 166 patients (62.6%) had a normal IAPmax
(< 12 mm Hg), 99 (37.4%) had IAH above 12 mm Hg, 52
(19.6%) had IAH above 15 mm Hg and 18 (6.8%) pre-
sented with an ACS cut-off above 20 mm Hg. With
a cut-off of 12 mm Hg the incidence increased from
37% on day 1 to 57% after 1 week, and from 20% to
40% with a cut-off of 15 mm Hg. The incidence showed
a plateau after day 3 (Fig. 4, Panel A).
On admission, 140 patients (67.9%) had a normal IAP-
mean (< 12 mm Hg), 85 (32.1%) had IAH above 12
mm Hg, 43 (16.2%) had IAH above 15 mm Hg and 11
(4.2%) presented with an ACS cut-off above 20 mm Hg.
The incidence remained quite stable during the following
days (Fig. 4, Panel B).
Recently, the incidence of IAH was studied prospectively
in orthotopic liver transplant recipients [40]. IAH (de-
fined in this study as an IAP of 25 mm Hg or higher) de-
veloped in 32% of the cases.
Organ function assessment
After identification of the at-risk patient by means of IAP
thresholds and SOFA score, the impact of IAH on the dif-
ferent organ specific parameters should be assessed.
Table 1. Prevalence of intra-abdominal hypertension and
abdominal compartment syndrome in different patient groups,
according to different thresholds for mean (IAPmean) and
maximal intraabdominal pressure (IAPmax). Adapted from [2]
Ongoing assessment of IAP should be done either by in-
termittent or continuous IAP monitoring, together with
APP. However the bladder pressure alone can never be
considered as a surrogate tool for the clinical examination
of the patient at the bedside. IAH should be seen as an
organ failure for which specific interventions may be con-
sidered depending on the actual IAP level, such as diag-
nostic (CT scan [41], echocardiography [42], correct
interpretation of intrathoracic blood and filling pressures
[3,43]), therapeutic (the use of higher PEEP levels
[3,44], the application of externally continuous negative
abdominal pressure [45]) and surgical (damage control
surgery, decompressive laparotomy).
Neurologic assessment
Neurologic failure is defined by the SOFA score as
a Glasgow coma scale <10. Neurologic dysfunction is de-
fined by the SOFA score as a Glasgow coma scale <13.
There is accumulating evidence of a link between IAP and
ICP. Numerous animal studies found a positive correlation
between the two pressures [4656]. In an elegant non-
head-injury model, Bloomfield et al. acutely increased
IAP by inflation of an intraperitoneal balloon in three pigs
after sternotomy and pleuropericardiotomy, and in nine
control pigs. Sternotomy and pleuropericardiotomy before
inflation of the balloon prevented the increase in ICP and
decrease in CPP observed in the control pigs [46]. These
results suggest that raised ICP resulting from a rise in IAP
is mediated by raised intrathoracic pressure. The hypoth-
esis was that IAH causes an upward displacement of the
diaphragm, resulting in increased pleural pressure, in-
creased central venous pressure, impaired cerebral venous
outflow and intracranial congestion.
In humans, this correlation was confirmed in 15 patients
with traumatic brain injury by placing weights on the
patients abdomens [57]. It was also described in a few
case reports [58,60]. We recently confirmed the positive
correlation between IAP and ICP in ventilated patients
with nontraumatic brain injury by continuously measuring
both parameters and without interventions. We found
that increases in IAP were associated with increases in
ICP and decreases in CPP in these patients, even at only
slightly elevated IAP levels (mean IAP SD in our study:
8.13 3.66 mm Hg) [61].

Total Medical Surgical According to the modified MonroKellie doctrine, the in-
Cut-off (n = 97) (n = 57) (n = 40)
tracranial contents are divided into four compartments:
IAPmax $ 12 mm Hg 57 (58.8%) 31 (54.4%) 26 (65%) osseous, vascular, cerebrospinal fluid and parenchymal
IAPmax $ 15 mm Hg 28 (28.9%) 17 (29.8%) 11 (27.5%)
IAPmax $ 20 mm Hg 8 (8.2%) 6 (10.5%) 2 (5%)
[47]. The ICP reflects the relation between these vol-
IAPmean $ 12 mm Hg 23 (23.7%) 14 (24.6%) 9 (22.5%) umes and intracranial compliance [62]. The intracranial
IAPmean $ 15 mm Hg 9 (9.3%) 7 (12.3%) 2 (5%) pressure-volume curve is not linear. In the physiologic
IAPmean $ 20 mm Hg 4 (4.1%) 2 (3.5%) 2 (5%)
range, small volume increases do not cause substantial
 Intra-abdominal hypertension in the critically ill Malbrain et al. 161

Figure 3. Differences in mean intra-abdominal pressure values injured patients [63]. Hence, measurement and control
of IAP may also be important for these patients, and others
at risk for developing intracranial hypertension.

In summary IAH increases ICP by transdiaphragmatic IAP

Box plot illustrating the differences in mean intra-abdominal pressure
values according to the participating center on the first day of ICU
admission in the multicenter incidence study from the Critically Ill and
Abdominal Hypertension (CIAH) study group Adapted from [39].
pressure increases until a point of decompensation, after
which each small increase in volume results in a large
increase in intracranial pressure [62].
transmission leading to an elevation of pleural and central
venous pressure; these elevations are sustained as long as
the IAH is present [46,49]. The combination of elevated
central venous pressure and increased ICP can lead to
a substantial decrease in CPP, especially in hypotensive,
hypovolemic patients where it can lead to progressive
cerebral ischemia. The IAP has also been suggested as
the cause of idiopathic intracranial hypertension in the
morbidly obese [4,6466] or the neurologic deterioration
in patients with multiple trauma but without overt
neurotrauma [59]. This hypothesis makes laparoscopy
less indicated and less safe in patients with intracranial
pathology [3].
Cardiovascular assessment
Cardiovascular failure is defined by the SOFA score as the
need for vasopressors (either dopamine >5 mg/kg/min(g)
or (nor)epinephrine <0.1g). Cardiovascular dysfunction is
defined by the SOFA score as the need for vasopressors
(either dopamine >5g or dobutamine at any dose).

If traumatic or nontraumatic brain injury causes an
enlargement of one of the intracranial compartments
or if it adds an extra volume (for example, hematoma
or edema), intracranial compliance can be reduced. In
that situation, it seems plausible that even minor
congestion, caused by increases in IAP, may lead to
a marked increase in ICP. The combination of elevated
central venous pressure and increased ICP can lead to
a substantial decrease in CPP, especially in hypotensive,
hypovolemic patients where it can lead to progressive
cerebral ischemia.
High ICP and low CPP have been shown to be associated
with increased morbidity and mortality in traumatic head-
The multiple assumptions linking central venous pres-
sure (CVP) and pulmonary artery occlusion pressure
(PAOP) to myocardial fiber length (preload) are debatable
even in healthy individuals [67]. They are especially
compromised in the setting of IAH. We refer to a recent
book chapter on optimal preload indicators in IAH [43].
In summary, IAH decreases venous return and cardiac out-
put, while systemic and pulmonary vascular resistances in-
crease, heart rate remains stable or may increase, the mean
arterial pressure initially increases but afterwards decreases,
and pulmonary arterial pressure increases. The left ventric-
ular compliance and regional wall motion decreases. Most of
the effects of raised IAP are markedly more pronounced in

Table 2. Incidence of intra-abdominal hypertension and abdominal compartment syndrome in different patient groups,
according to different thresholds for mean (IAPmean) and maximal intra-abdominal pressure (IAPmax)

IAPmean > 12 IAPmean >15 IAPmean >20

day 1 day 2 day 3 day 1 day 2 day 3 day 1 day 2 day 3
Surgical 48 (18.1%) 47 (17.7%) 44 (16.6%) 27 (10.2%) 27 (10.2%) 25 (9.4%) 7 (2.6%) 4 (1.5%) 4 (1.5%)
Medical 37 (14%) 35 (13.2%) 35 (13.2%) 16 (6%) 12 (4.5%) 12 (4.5%) 4 (1.5%) 4 (1.5%) 4 (1.5%)
Total 85 (32.1%) 82 (30.9%) 79 (29.8%) 43 (16.2%) 39 (14.7%) 37 (14%) 11 (4.2%) 8 (3%) 8 (3%)
IAPmax > 12 IAPmax >15 IAPmax >20
day 1 day 2 day 3 day 1 day 2 day 3 day 1 day 2 day 3
Surgical 56 (21.1%) 70 (26.4%) 77 (29.1%) 32 (12.1%) 44 (16.6%) 48 (18.1%) 10 (3.8%) 13 (4.9%) 18 (6.8%)
Medical 43 (16.2%) 55 (20.8%) 64 (24.2%) 20 (7.5%) 35 (13.2%) 41 (15.5%) 8 (3%) 12 (4.5%) 14 (5.3%)
Total 99 (37.4%) 125 (47.2%) 141 (53.2%) 52 (19.6%) 79 (39.8%) 89 (33.6%) 18 (6.8%) 25 (9.4%) 32 (12.1%)
Adapted from [39].
162 Gastrointestinal system
Figure 4. Evolution of the incidence (%) of intra-abdominal
hypertension during the first week of ICU stay according to
different thresholds for maximal (IAPmax) and mean
(IAPmean) intra-abdominal pressure (IAP)
(a) With an IAPmax cut-off of 12 mm Hg the incidence increased from
37% on day 1 to 57% after 1 week, with an IAPmax cut-off of 15 mm Hg
the incidence ranged from 20% on day 1 to 40% after 1 week. The
incidence reached a plateau after day 3. (b) With an IAPmean cut-off of
12 mm Hg the incidence decreased from 32.1% on day 1 to 26.8%
after 1 week, with an IAPmean cut-off of 15 mm Hg the incidence ranged
from 16.2% on day 1 to 12.8% after 1 week. The incidence remained
stable after day 3. Adapted from [39].
hypovolemic patients, resulting in a greater compromise
of ventricular function at equal IAP levels. As a result
IAH makes preload assessment difficult because PAOP
and CVP rise despite the reduced venous return and cardiac
output, while transmural filling pressures usually remain
stable or may even decrease. Intravascular pressures are
thus not reflective of intravascular volumes. Volumetric
and functional hemodynamic parameters, adjusted for ejec-
tion fraction, on the other hand, will better reflect the true
volemic status and the volume responsiveness of the pa-
tient: In IAH global and right ventricular end-diastolic
and intrathoracic blood volumes remain stable or may de-
crease, extravascular lung water increases (in the presence
of capillary leak), stroke volume and pulse pressure varia-
tions remain stable or may increase. Finally there is an in-
creased risk for peripheral edema and venous thrombosis
due to the increased femoral vein pressures and the re-
duced venous blood flow and the resulting rise in venous
hydrostatic pressure. This may lead to fatal pulmonary
embolism on decompression [3].
Pulmonary assessment
Respiratory failure is defined by the SOFA score as a
paO2/FiO2 ratio <200 with the need for respiratory sup-
port in the form of mechanical ventilation. Respiratory
dysfunction is defined by the SOFA score as a paO2/FiO2
ratio <300 regardless of the need for respiratory support.
The total elastance (elastance = 1/compliance) of the re-
spiratory system is the sum of the lung elastance and the
chest wall elastance [68]. The chest wall comprises the
anterior and posterior thoracic cage and the diaphragm,
which is mechanically coupled to the abdomen. It has
been shown that the increase in elastance in acute lung
injury (ALI) and acute respiratory distress syndrome
(ARDS) is caused by increased elastance of both the lung
and chest wall compartment. The distending force of the
lung is the transpulmonary pressure (alveolar minus pleu-
ral pressure), which depends on the pressure applied to
the airways and the ratio between lung and chest wall ela-
stance. This means that the same applied airway pressure
may result in a substantially lower transpulmonary pres-
sure, higher pleural pressure, less lung distension and
more profound hemodynamic effects if the chest wall ela-
stance is high instead of low. Not surprisingly, since the
strain on lung structures leading to ventilator-induced
lung injury (VILI) depends on transpulmonary pressure,
not only recruitment maneuvers [69] but also safe pla-
teau pressures depend on chest wall elastance and pleural
pressure.
The most common cause of increased chest wall elastance
in ALI/ARDS patients is IAH [6971]. Compared with
pulmonary ARDS, patients with extrapulmonary ARDS
have a decreased chest wall elastance and a higher pleural
pressure that is positively and linearly correlated with IAP
[69,72]. We showed in ventilated patients that abdominal
compression resulted in decreased total respiratory sys-
tem static compliance and flattening and rightward shift
of the inspiratory PV curve of the total respiratory system
[44]. This was solely due to decreased chest wall compli-
ance, while lung compliance remained unchanged. We also
found a strong positive correlation (r2 = 0.93, P < 0.0001)
between IAP and the lower inflection point of the total
respiratory system PV curve, especially in conditions with
increased IAP. The latter suggested that the IAP level may
be correlated with the best PEEP in ventilated patients
with secondary ARDS and IAH.
The correlation between IAP and chest wall elastance
had previously been described in pigs [73] and in
patients undergoing laparoscopic cholecystectomy [74],

in which IAH was shown to decrease functional residual
capacity (promoting ventilation-perfusion mismatch).
CT studies have shown that in deeply sedated ARDS
patients, the diaphragm behaves as a passive structure,
which moves upward in the rib cage and transmits in-
creased IAP to the lower lung lobes, causing compression
atelectasis [71]. Indeed, surgical abdominal decompres-
sion was shown to recruit lung volume and to increase the
PaO2/FiO2 ratio [70]. In accordance, in animal models,
high PEEP ventilation was demonstrated to improve
pulmonary gas exchange during CO2 pneumoperito-
neum, resulting in a decreased alveolo-arterial oxygen
pressure difference, increased oxygenation and CO2
elimination [75,76].
We demonstrated in 22 ventilated patients that putting
the patient in an upright position increased IAP and de-
creased the static compliance of the total respiratory sys-
tem [77]. This suggests that putting a patient upright, as
is frequently done, may deteriorate respiratory function.
In a porcine model, Quintel et al. recently found that the
application of an IAP of 20 cm H2O after oleic acid-in-
duced lung injury resulted in a more than twofold increase
of pulmonary oedema [41]. The authors proposed two
possible explanations for this phenomenon: first, in-
creased cardiac filling pressures induced by IAH, and
second, decreased clearance of pulmonary edema by lym-
phatic pathways, pulmonary and pleural capillaries, all of
which leads to the thoracic veins, and are subjected to
raised intrathoracic pressures.
In summary, IAH increases intrathoracic and pleural pres-
sure leading to edema and atelectasis causing a decrease
in functional residual capacity and all other lung volumes
(mimicking restrictive lung disease). In mechanically venti-
lated patients auto-PEEP, peak, plateau and mean airway
pressures increase (possibly leading to alveolar barotrauma),
while dynamic and static total respiratory system compli-
ance drop (due to a diminished chest wall compliance (with
reduced spontaneous tidal volumes) while lung compliance
remains unchanged, thus the lower inflection point in-
creases while the upper inflection point shifts to the left).
IAH hence results in hypercarbia, hypoxia with a drop in
paO2/FiO2 ratio, increased dead-space ventilation and intra-
pulmonary shunt. Lung neutrophils are activated with in-
creased pulmonary inflammatory infiltration and alveolar
edema (extravascular lung water increases), increased risk
for pulmonary infection and compression atelectasis, all
resulting in difficult and prolonged ventilation and weaning
[3].
Renal assessment
Renal failure is defined by the SOFA score as a serum
creatinine level $3.5 mg/dL ($300 mmol/L) or oliguria
Intra-abdominal hypertension in the critically ill Malbrain et al. 163
<500 ml/d. Renal dysfunction is defined by the SOFA score
as a serum creatinine level $2 mg/dL ($170 mmol/L).
Pivotal work on this topic was done by Sugrue et al. [78,79]
from Australia. Recently, others confirmed these initial
observations [80,81]. Within this concept, abdominal or
renal perfusion pressure, calculated as mean arterial pres-
sure minus IAP, and the filtration gradient, calculated as
MAP minus 2 times the IAP, have gained acceptance as
useful clinical and prognostic parameters.
In summary IAH decreases renal perfusion pressure, the
filtration gradient, and renal blood flow. Oliguria develops,
tubular dysfunction increases, glomerular filtration rate
drops, renal vascular resistance increases, renal vein and
ureter compression increases, renin, aldosteron and anti-
diuretic hormone levels increase, while adrenal blood flow
usually remains preserved [3].
Gastrointestinal assessment
Gastrointestinal failure is not defined by a SOFA subscore.
However, perfusion of the gastrointestinal system is sen-
sitive to increases in IAP as low as 10 mm Hg [82].
Bacterial translocation
Bacterial translocation (BT) refers to the process by which
bacteria that reside within the gastrointestinal lumen, or
endotoxin cross intact intestine into normally sterile tis-
sue [83]. It is caused by increased gut permeability, as
can be induced by splanchnic ischemia with and without
reperfusion [84,85]. In the 1990s, several authors ob-
served a positive correlation between BT and IAP in ani-
mal models, even when it was raised for less than one hour.
IAH was shown to be associated with increased BT to
mesenteric lymph nodes, liver and spleen [8688]. This
increase was more pronounced when the rise in IAP was
preceded by hemorrhage-resuscitation [86] and after sev-
eral hours of increased IAP, the bacteria were not found in
the mesenteric lymph nodes anymore, but in the liver and
spleen [88]. This correlation was not found by others [89].
In more recent animal studies, two authors confirmed the
correlation [90,91]. Doty et al. found no correlation be-
tween IAP and BT in pigs in the context of hemorrhage-
resuscitation followed by IAH (IAP 30 mm Hg above base-
line for one hour) [92]. Interestingly, they documented
BT to mesenteric lymph nodes (5 of 9 animals) and portal
vein (1 of 9) in the control group, subjected neither to
hemorrhage-resuscitation, nor to IAH [92]. We were not
able to find any studies in humans in this context.
BT has recently been linked to injuries the mesenteric
microcirculation [93]. However, although the gut clearly
plays a major role in the development of multiple organ
failure (MOF), it has been difficult to document BT as
a pathogenic event [83,94,95].
164 Gastrointestinal system
Splanchnic ischemia
The APP was shown to be a better predictor of survival
than lowest MAP, highest IAP, highest lactate, highest
base deficit and lowest urine output in surgical ICU
patients with an IAP of 15 mm Hg or more [15]. An
APP during ICU stay of 50 mm Hg or more had a sensitiv-
ity of 76% and specificity of 55% for predicting survival.
However, APP is simply the calculation of MAP minus
IAP, and an APP of more than 50 mm Hg does not mean
that the gut is adequately perfused.
Intramucosal acidosis is a marker of local hypoperfusion
and gastric intramucosal pH does not necessarily reflect
similar changes in splanchnic blood flow [84]. Several
investigators demonstrated that abdominal insufflation
was associated with a decrease in gastric intramucosal
pH or oxygen saturation [9699,98]. Sugrue et al. identi-
fied in 73 patients after major abdominal surgery a signif-
icant association between a decreased gastric intramucosal
pH at any given moment during ICU stay, and increased
IAP (20 mm Hg or more) during ICU stay [18].
A lot of animal studies demonstrated a link between IAH
and decreased intestinal blood flow. In an important study
in dogs, Caldwell showed that IAH (20 mm Hg or more)
was associated with decreased flow to stomach, duode-
num, jejunum, ileum, colon, pancreas, liver, spleen and
kidney, but with increased flow to the adrenal glands
[100]. This correlation was confirmed in the context of
decreased mesenteric artery blood flow [82,101104],
celiac artery blood flow [103], intestinal mucosal blood
flow [87,88,101,102,104,105], intestinal intramucosal pH
[101,106] and blood flow to small and large bowel
[107], spleen [105,107] and pancreas [105,107]. The de-
crease in intestinal blood flow was shown to be more se-
vere if IAH was preceded by hemorrhage-resuscitation
[82].
Interpreting these data, we have to keep in mind that the
method for obtaining IAH may affect splanchnic blood
flow. Blobner et al. showed in pigs that at an IAP of
12 mm Hg or less, CO2 and not air insufflation resulted
in moderate splanchnic hyperemia [108]. Furthermore,
the insufflation of CO2 affects arterial pCO2, pCO2 of
the tonometry sample and intramucosal pH, as was shown
in patients undergoing laparoscopic cholecystectomy.
When arterial pCO2 was kept constant by ventilatory
adjustment, gastric intramucosal pH did not change at
an IAP of 12 mm Hg [109].
Several factors may contribute to the decrease in splanch-
nic blood flow from increased IAP. These include a
mechanical compression of the splanchnic bed, and mesen-
teric vasoconstriction induced by vasopressin [110,111].
The effect of IAH on blood flow or thus cardiac output
(CO) depends on intravascular volume status. IAH causes
a decrease in CO in the case of hypovolemia and an in-
crease in case of hypervolemia [112]. In two studies, the
reduction in splanchnic blood flow was greater than the re-
duction in CO. This led to the conclusion that optimizing
CO alone may be inadequate to normalize intestinal blood
flow in case of IAH [82,100]. This was confirmed in anoth-
er animal study that showed that dobutamine infusion re-
versed the decrease in CO induced by IAH, but failed to
restore superior mesenteric artery blood flow [102].
Multiple organ failure
In addition to splanchnic ischemia and bacterial transloca-
tion, IAH has been shown to provoke the release of pro-
inflammatory cytokines, which may serve as a second
insult for the induction of multiple organ failure (MOF)
[113]. Sequential insults of hemorrhage-resuscitation
or ischemia-reperfusion and ACS were associated with sig-
nificantly increased portal and central venous cytokine
levels and more severe lung injury than hemorrhage-
resuscitation or ACS alone [114].
In summary IAH decreases abdominal perfusion pressure,
as well as celiac blood flow, superior mesenteric artery
blood flow, the blood flow to all intraabdominal organs,
and in particular mucosal blood flow. Intramucosal gastric
pH drops, while regional CO2 and the CO2-gap increase.
IAH also leads to mesenteric vein compression promoting
venous hypertension and intestinal edema and visceral
swelling triggering a vicious cycle. Enteral feeding be-
comes difficult, intestinal permeability increases and bac-
terial translocation may occur finally leading to multiple
system organ failure. IAH increases the risk for gastroin-
testinal ulcer (re)bleeding, and the increased variceal wall
stress may lead to varciceal (re)bleeding. Finally, there is
an increased risk for peritoneal adhesions [3].
Hepatic assessment
Hepatic failure is defined by the SOFA score as a se-
rum bilirubin level $6 mg/dL ($102 mmol/L). Hepatic
dysfunction is defined by the SOFA score as a serum bil-
irubin level $2 mg/dL ($33 mmol/L).
Hepatic blood flow
In the literature, conflicting results are reported, possibly
caused by the different types of animals, volume status,
methods used to increase IAP (with or without CO2),
and body position [115], making it very difficult to draw
conclusions. Animal studies, showed a decrease in total
blood flow to the liver during IAH [100]. This parallels
the decrease in hepatic microcirculation and hepatic mi-
tochondrial redox status found by others [88,116]. Most
authors found that IAH causes a decrease in portal venous
blood flow [104,107,117] and that the decrease in total
hepatic blood flow was predominantly caused by a de-
crease in portal blood flow, although there was also a less
pronounced decrease in hepatic artery blood flow

[104,107,117]. Possibly, the differential effect of IAH on
hepatic artery and portal venous flow can be explained
by the hepatic artery buffer response that initially protects
the liver against hypoperfusion, but that can get ex-
hausted [84].
These results do not agree with a previous study that did
not show a decrease in total hepatic or portal venous blood
flow during IAH [115]. Nor was this the case in a study of
human patients undergoing laparoscopic cholecystectomy
at an IAP of 1113 mm Hg. No flow changes could be
detected with hepatic artery and vein catheterization
[118].
Cirrhosis and esophageal varices
A group of Spanish investigators increased IAP by 10 mm
Hg with an inflatable girdle in 14 patients with cirrhosis
and esophageal varices. This caused a marked increase
in variceal pressure, wall tension, radius and volume, prob-
ably contributing to the risk of rupture [119]. This agrees
with the finding that abdominal paracentesis causes a de-
crease in wedged hepatic venous pressure and hepatic ve-
nous pressure gradient in cirrhotic patients with tense
ascites [120]. In patients with ascites, reduction of IAP
by paracenthesis resulted in a significant reduction in gas-
troesophageal reflux [121].
Indocyanine green clearance
We recently found a significant but poor negative correla-
tion between IAP and plasma disappearance rate of indoc-
yanine green (PDR-ICG) (LiMON
, Pulsion Medical
Systems, Munich, Germany) [122]. After bolus injection,
indocyanine green binds immediately to plasma proteins
and is exclusively eliminated by the liver without entero-
hepatic circulation. Its clearance is dependent on both he-
patic blood flow and hepatic cellular function. PDR-ICG
correlates well with the SOFA score and a low PDR is
a poor prognostic sign [123].
In summary IAH decreases hepatic artery flow and portal
venous blood flow while portocollateral flow increases,
lactate clearance drops, glucose metabolism diminishes,
mitochondrial and cytochrome P450 function decreases
as well as the plasma disappearance rate for indocyanine
green [3].
Prognosis
Nonsurvivors had a significantly higher mean IAP on ad-
mission than survivors 11.4 4.8 versus 9.5 4.8 mm
Hg in the recent incidence study conducted by the crit-
ically ill and abdominal hypertension (CIAH) study group
[39]. Independent predictors for mortality were age
(odds ratio (OR) = 1.04, 95% confidence interval (CI)
1.011.06, P = 0.003), APACHE II score (OR = 1.1,
95% CI 1.051.15, P <0.0001), type of ICU admission
Intra-abdominal hypertension in the critically ill Malbrain et al. 165
(OR = 2.5 medical vs. surgical, 95% CI 1.245.16, P =
0.01), and the presence of liver dysfunction (OR = 2.5,
95% CI 1.065.8, P = 0.04). The occurrence of IAH dur-
ing the ICU stay was also an independent predictor
of mortality (relative risk = 1.85 95% CI 1.123.06,
P = 0.01).
A total of 73 patients died after the index admission
(27.5% of the study population). Forty of 180 patients
(22.2%) who had a normal IAPmean on admission died
versus 33 of 85 patients (38.8%) with IAH (OR = 2.2
[1.33.9]; P = 0.005). Fifteen of 124 patients (12.1%)
who had a normal IAPmax within the first 3 days died ver-
sus 51 of 141 patients (41.1%) with IAH (OR = 5.1 [2.7
9.6]; P <0.0001). The higher the IAP, the poorer the sur-
vival rate (Fig. 5, Panel A). The length of ICU stay was not
significantly different but survivors reached the maximal
IAP earlier than nonsurvivors. The maximal IAP remained
associated with mortality after stratification in quartiles
of admission APACHE II (adjusted OR from 1.5 to 9.5)
or SAPS II (adjusted OR from 1.7 to 7.5) (Fig. 5, Panel B).
During intensive-care stay nonsurvivors had a significantly
higher IAP, SOFA score, daily fluid balance and net cumu-
lative fluid balance compared with survivors (Fig. 6).
The maximal IAP was higher in medical, elective surgery
and trauma patients who died versus survivors but did not
differ between emergency surgery patients who died or
not (Fig. 7).
Patients with IAH presented a higher total SOFA score
and SOFA subscores on admission (except cardiovascular
and neurologic), a higher number of organ failures, a lower
APP, a higher CVP and PAOP, a greater rate of abdominal
surgery, hemoperitoneum, fluid resuscitation, ileus, acido-
sis, polytransfusion, coagulopathy, sepsis and liver dys-
function compared with patients without IAH. The
higher the number of organs in failure the higher the max-
imal IAP (Fig. 8). Independent predictors for IAH were
liver dysfunction (OR = 2.25, 95% CI 1.14.58, P =
0.03), abdominal surgery (OR = 1.96, 95% CI 1.05
3.64, P = 0.03), fluid resuscitation (OR = 1.88, 95% CI
1.043.42, P = 0.04), and ileus (OR = 2.07, 95% CI
1.153.72, P = 0.02).
Treatment
Patients with organ dysfunction and an IAP above 20 mm
Hg should probably undergo decompressive surgery [124].
But what of those between 15 to 20 mm Hg with mild
organ dysfunctions? This defines the group with IAH
but potential ACS. As shown above, splanchnic hypoper-
fusion and acidosis start occurring at pressures from 10 to
15 mm Hg. The earlier treatment is instituted, the more
likely a progression to irreversible damage is prevented. A
judgment call between risk and benefit is required. On
166 Gastrointestinal system
Figure 5. Distribution of 28-day motility according
to intra-abdominal pressure (IAP) and simplified acute
physiology score (SAPS) II quartiles
(a) Distribution of mortality according to IAP quartiles. The higher
the mean or maximal IAP, the poorer the survival (P = 0.002 for IAPmax).
(b) Relative hospital mortality according to admission SAPS II
quartiles, subdivided according to maximal IAP value (grey bars: patients
with IAP $12 mm Hg, white bars: patients with normal IAP). Odds
ratios for patients with versus patients without IAH were 1.2 (95%
CI, 11.4, P = 0.013) for the first quartile (SAPS II from 0 to 26),
7.5 (95% CI, 1.537.3, P = 0.006) for the second quartile (SAPS II from
26 to 36), 3.3 (95%CI, 1.110.5, P = 0.035) for the third quartile
(SAPS II from 36 to 50) and 3.4 (95%CI, 1.110.2, P = 0.03) for the
fourth quartile (SAPS II above 50). Adapted from [39].
balance, from the available accumulating evidence, such
patients should probably be decompressed and the diag-
nosis confirmed or refuted retrospectively. However, some
may benefit from volume resuscitation at the beginning of
oliguria, in itself not without risks [125]. It is within this
narrow no-mans land of IAH between normal IAP and
ACS that our efforts should be concentrated in an attempt
to clarify definitions and thereby treatment options. Reli-
ance on standard hemodynamic parameters is too crude
but measurement of splanchnic perfusion too difficult
in the clinical scenario to be currently applicable. The
Figure 6. Evolution of daily and cumulative fluid balance
during the first week of ICU stay
(a) Evolution of daily fluid balance during the first week of ICU stay in
survivors (open squares) and nonsurvivors (closed squares).
Nonsurvivors had significantly greater positive daily fluid balances
during the first week, except on day 1 and 5 (P < 0.01). (b) Evolution of
net cumulative fluid balance during the first week of ICU stay in survivors
(open squares) and nonsurvivors (closed squares). Nonsurvivors had
significantly greater positive net cumulative fluid balances during the first
week (P < 0.01 for all comparisons). Adapted from [39].
exact causative role of bacterial and vasoactive mediator
translocation in the genesis and evolution of multi-system
organ failure is a further controversial area of critical care
medicine [87,92]. It is indisputable though that the gut
is sensitive to low-flow states and is rendered ischemic
at pressures below those expected to induce the ACS,
therefore any attempt should be made to prevent the de-
velopment of overt ACS.
Different medical treatment procedures have been sug-
gested to decrease IAP [16]. These include the use of

Figure 7. Box plots showing maximal IAP values in different
patient groups split into two groups of survivors and
nonsurvivors
P = 0.21, one-way ANOVA. Adapted from [39].
paracenthesis, gastric suctioning, rectal enemas, gastropro-
kinetics (cisapride, metoclopramide, domperidone, eryth-
romycin), colonoprokinetics (prostygmine), furosemide
either alone or in combination with human albumin 20%,
continuous venovenous hemofiltration with aggressive ultra-
filtration, continuous negative abdominal pressure, and
finally sedation and curarization [3].
Figure 8. Box plot of maximal IAP values according to total
number of organ failures
The higher the number of organ failures, the higher the IAP. P < 0.0001,
one-way ANOVA. Adapted from [39].
Intra-abdominal hypertension in the critically ill Malbrain et al. 167
Implications for future research?
Studies examining the prevalence and incidence of
IAH/ACS should be based on the above cited definitions
and classifications. The results should be given for mean,
median and maximal IAP values on admission and during
the study stay. The ideal frequency for IAP measurement
also needs to be elucidated as well as the diurnal and noc-
turnal variations during continuous IAP monitoring, since
this may affect the mean and maximal daily IAP-levels
as well as the incidence and prevalence of IAH when dif-
ferent thresholds are used.
Studies looking at IAP thresholds should be based on the
analysis of receiver operating characteristics (ROC) and
the area under the ROC-curve (Fig. 9) [126]. ROC curves
graph the sensitivity of a diagnostic test (true positive pro-
portion) versus 1 minus specificity (false positive propor-
tion) and provide an improved measure of the overall
discriminatory power of a test as they assess all possible
threshold values. A test that always predicts survival has
an area under the ROC curve of 1.0 and a test that pre-
dicts survival no more often than would be done by chance
has an area under the ROC curve of 0.5. The point on the
ROC curve closest to the upper left corner is generally
considered to optimize the sensitivity and specificity of
the test.
Studies examining new devices to measure IAP should
always compare the new IAP measurement method with
some form of gold standard. The validation of the new
technique should not be limited to the analysis of (signif-
icant) correlation coefficients with R2 (since a good corre-
lation coefficient is not enough to compare two different
methods) but should go further into detail with an analysis
according to Bland and Altman who proposed to test for
a systematic bias, precision and agreement between two
methods by plotting the mean difference against the
mean of two measurements [127].
Future research should not only focus on epidemiol-
ogy. The crucial question before widespread acceptance,
practice and clinical use of IAP still remains unanswered
to date, Is IAP a phenomenon or an epi-phenomenon?
The impact that IAP has on therapeutic decision-making
and outcome when an intervention is undertaken to influ-
ence IAP have still to be studied. Before IAP is accepted
as a valid tool in practice, it has to be demonstrated that
any intervention to treat ACS alters patient outcome
(if not mortality then at least morbidity). Maybe it is
now time for such multicenter, multinational interven-
tional studies.
Summary
Every definition of a clinical situation or syndrome fails to
include all possible conditions and variations of an
168 Gastrointestinal system
Figure 9. Receiver operator characteristic (ROC) curves for
IAP and APP with clinically useful decision points
IAP has been plotted against mortality instead of survival as in the
original study while APP is plotted against survival. (a) Sensitivity and
specificity of maximal IAP, SAPS II and APACHE II score with respect to
mortality according to receiver operating characteristics in 265
patients. The best cut-off for IAP was 12 mm Hg with a sensitivity of
79.5% and a specificity of 56.8%. The area under the curve was .776
(.716.836) for SAPS II, .771 (.710.832) for APACHE II and .685
(.617.753) for IAP. (b) Sensitivity and specificity of abdominal
perfusion pressure on admission with respect to mortality according to
receiver operating characteristics in 235 patients. The best cut-off for
APP was 60 mm Hg with a sensitivity of 72.2% and a specificity of
72.7%. The area under the curve was .777 (.709.844). IAP,
intra-abdominal pressure; APP, abdominal perfusion pressure. Adapted
from [39].
inherently complex phenomenon. Nevertheless, to ap-
proach scientific accuracy in comparing different clinical
reports, and to plan for future clinical trials, definitions
are required which are comprehensive, detailed, simple,
practical and acceptable to most of the scientific commu-
nity working in the particular field. This review does not,
and cannot, provide bullet-proof definitions for all issues
associated with increased IAP, but puts forward arguments
and suggestions that may serve as a springboard for further
consensus-building endeavors. These definitions also
allow better comparisons of data between groups of
researchers and may lead to refined and better definitions
themselves.
Acknowledgements
The corresponding author is indebted to the study coordinators, clinical research
associates, medicine residents, and pulmonary/critical care fellows who partici-
pated in the data collection for the Critically Ill and Abdominal Hypertension
(CIAH) prevalence study. The corresponding author also wishes to thank all the
nurses from the participating ICUs for the IAP measurements. The corresponding
author is indebted to his wife Miss Bieke Depre for her advice and technical
assistance with the preparation of the manuscript. The corresponding author is
also very grateful to all faculty members and ACS book authors for their feedback
and comments during the second World Congress of Abdominal Compartment
Syndrome held in Noosa, Australia, Dec. 6 8, 2004 (www.wsacs.org).
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
1 Malbrain ML. Different techniques to measure intra-abdominal pressure
(IAP): time for a critical re-appraisal. Intensive Care Med 2004; 30:357
371.
A must-read for everyone who starts thinking about IAP, wants to measure it or
wants to do a study on IAH or ACS
2 Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intra-abdominal
hypertension in critically ill patients: a multicentre epidemiological study.
Intensive Care Med 2004; 30:822 829.
The first, and for the time being, the only multicenter study on the prevalence of
IAH in 97 critically ill patients. The only independent predictor for IAH was BMI
while massive fluid resuscitation, renal and coagulation impairment as assessed
by SOFA score were only at the limit of significance. The study raises questions
about the accuracy and reproducibility of standard IVP measurements because
the coefficient of variation was quite high in some centers.
3 Malbrain ML. Is it wise not to think about intraabdominal hypertension in the
ICU? Curr Opin Crit Care 2004; 10:132 145.
A good overview of the latest literature on intra-abdominal pressure and intra-
abdominal hypertension, with an emphasis on measurement and recent patho-
physiologic implications and a nice summary of clinical key-messages. It also gives
some suggestions for consensus definitions.
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A nice study validating the use of a continuous IAP measurement method via the
bladder via a standard 18 Fr three-way Foley bladder catheter. The continuous IAP
measurement is performed via the irrigation port of the three-way catheter, in
which continuous sterile normal saline irrigation is maintained and connected
through a two-way stopcock and normal saline-filled tubing to a pressure trans-
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mucosal pH: is there an association? World J Surg 1996; 20:988 991.
19 Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and
selective management of the abdominal compartment syndrome. Am J Surg
1997; 174:667 672.
20 Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-
threatening penetrating abdominal trauma: prophylaxis, incidence, and clin-
ical relevance to gastric mucosal pH and abdominal compartment syndrome.
J Trauma 1998; 44:1016 1021.
21 Ivy ME, Atweh NA, Palmer J, et al. Intra-abdominal hypertension and ab-
dominal compartment syndrome in burn patients. J Trauma 2000; 49:
387391.
22 Raeburn CD, Moore EE, Biffl WL, et al. The abdominal compartment syn-
drome is a morbid complication of postinjury damage control surgery. Am
J Surg 2001; 182:542546.
23 McNelis J, Marini CP, Jurkiewicz A, et al. Predictive factors associated with
the development of abdominal compartment syndrome in the surgical inten-
sive care unit. Arch Surg 2002; 137:133 136.
24 Loftus IM, Thompson MM. The abdominal compartment syndrome following
aortic surgery. Eur J Vasc Endovasc Surg 2003; 25:97 109.
An excellent review on the topic from a surgical point of view.
25 Hong JJ, Cohn SM, Perez JM, et al. Prospective study of the incidence and
outcome of intra-abdominal hypertension and the abdominal compartment
syndrome. Br J Surg 2002; 89:591 596.
26 Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and secondary ab-
dominal compartment syndrome can be predicted early and are harbingers
of multiple organ failure. J Trauma 2003; 54:848 859.
An interesting, prospective study stressing the fact that not all ACS patients are
the same. Differences with regard to primary and secondary ARDS are described,
however both have similar demographics, injury severity, time to decompression
from hospital admit, and both are associated with bad outcome. Secondary ACS
seems to an earlier ICU event preceded by more crystalloid administration.
27 Offner PJ, de Souza AL, Moore EE, et al. Avoidance of abdominal compart-
ment syndrome in damage-control laparotomy after trauma. Arch Surg 2001;
136:676681.
28 Cheatham M. Intra-abdominal hypertension and abdominal compartment
syndrome. New Horiz 1999; 7:96
115.
29 Papavassiliou V, Anderton M, Loftus IM, et al. The physiological effects
of elevated intra-abdominal pressure following aneurysm repair. Eur J Vasc
Endovasc Surg 2003; 26:293 298.
A nice study on 75 patients undergoing aneurysm repair that showed that IAP was
significantly higher in ruptured infrarenal aneurysms compared to nonruptured or
endovascular techniques.
30 Malbrain ML. Abdominal pressure in the critically ill: measurement and clin-
ical relevance. Intensive Care Med 1999; 25:1453 1458.
31 Malbrain ML. Intra-abdominal pressure in the intensive care unit: Clinical tool
or toy? In: Vincent JL, editor. Yearbook of Intensive Care and Emergency
Medicine. Berlin: Springer-Verlag, 2001: 547-585.
32 Vincent JL, Moreno R, Takala J, et al. The SOFA (Sepsis-related Organ
Failure Assessment) score to describe organ dysfunction/failure. Intensive
Care Med 1996; 22:707 710.
33 Balogh Z, McKinley BA, Cocanour CS, et al. Secondary abdominal compart-
ment syndrome is an elusive early complication of traumatic shock resusci-
tation. Am J Surg 2002; 184:538 543.
34 Biffl WL, Moore EE, Burch JM, et al. Secondary abdominal compartment
syndrome is a highly lethal event. Am J Surg 2001; 182:645
648.
Intra-abdominal hypertension in the critically ill Malbrain et al. 169
35 Gracias VH, Braslow B, Johnson J, et al. Abdominal compartment syndrome
in the open abdomen. Arch Surg 2002; 137:1298 1300.
36 Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the
abdominal compartment syndrome after damage-control laparotomy in
311 patients with severe abdominal and/or pelvic trauma. Crit Care Med
2000; 28:17471753.
37 Maxwell RA, Fabian TC, Croce MA, et al. Secondary abdominal compartment
syndrome: an underappreciated manifestation of severe hemorrhagic shock.
J Trauma 1999; 47:995 999.
38 Malbrain MLNG, Deeren D, De Potter T, et al. Coefficient of variation (COVA)
during continuous intra-abdominal pressure (IAP) and abdominal perfusion
pressure (APP) monitoring. Crit Care 2004; 8:171.
39 Malbrain MLNG, Chiumello D, Pelosi P, et al. Incidence and prognosis of
intraabdominal hypertension in a mixed population of critically ill patients:
a multicenter epidemiological study. Crit Care Med 2005; 33:315 322.
The first, and for the time being, the only multicenter epidemiologic study on the
incidence of IAH in 265 critically ill patients. The presence of IAH (defined via
receiver operating characteristics curve analysis as an IAP above 12 mm Hg)
on admission was associated with severe organ dysfunction during the ICU stay.
The mean IAP on admission was not an independent risk factor for mortality,
however the occurrence of IAH during ICU stay was an independent outcome
predictor.
40 Biancofiore G, Bindi ML, Romanelli AM, et al. Intra-abdominal pressure mon-
itoring in liver transplant recipients: a prospective study. Intensive Care Med
2003; 29:30 36.
An interesting prospective study and the first in liver transplant patients depicting
the timely association between IAH, fluid balance, organ failure and adverse out-
come.
41 Quintel M, Pelosi P, Caironi P, et al. An increase of abdominal pressure in-
creases pulmonary edema in oleic acid induced lung injury. Am J Respir Crit
Care Med 2004; 169:534 541.
A must-read for anyone who is concerned about lung protective ventilation in con-
ditions of intra-abdominal hypertension. The study showed that increased IAP in
the presence of capillary leak (oleic acid injury model) was associated with a tre-
mendous (exponential) increase in interstitial edema (extravascular lung water).
The clinical consequences of this provocative animal study may be substantial,
although they need to be proved in humans.
42 Sakka SG, Huettemann E, Petrat G, et al. Transoesophageal echocardio-
graphic assessment of haemodynamic changes during laparoscopic hernior-
rhaphy in small children. Br J Anaesth 2000; 84:330
334.
43 Malbrain ML, Cheatham ML. Cardiovascular effects and optimal preload
markers in intra-abdominal hypertension. In: Vincent JL, editor. Yearbook
of Intensive Care and Emergency Medicine. Berlin: Springer-Verlag, 2004:
519-543.
A nice overview of the different cardiovascular pathophysiologic complications
of IAH followed by a discussion on the validity of the different preload indices
(pressures vs. volumes) in conditions with increased IAP.
44 Malbrain ML, Deeren D, Nieuwendijk R, et al. Partitioning of respiratory
mechanics in intra-abdominal hypertension. Intensive Care Med 2003; 29:
S85.
45 Valenza F, Bottino N, Canavesi K, et al. Intra-abdominal pressure may be de-
creased non-invasively by continuous negative extra-abdominal pressure
(NEXAP). Intensive Care Med 2003; 29:2063 2067.
An original study of 30 ICU patients looking at the hemodynamic and respiratory
effects of applying extra-abdominal negative pressure. A drawback was that mean
baseline IAP values were quite low.
46 Bloomfield GL, Ridings PC, Blocher CR, et al. A proposed relationship be-
tween increased intra-abdominal, intrathoracic, and intracranial pressure.
Crit Care Med 1997; 25:496 503.
47 Josephs LG, Este-McDonald JR, Birkett DH, et al. Diagnostic laparoscopy
increases intracranial pressure. J Trauma 1994; 36:815
818.
48 Holthausen UH, Nagelschmidt M, Troidl H. CO(2) pneumoperitoneum: what
we know and what we need to know. World J Surg 1999; 23:794 800.
49 Bloomfield GL, Ridings PC, Blocher CR, et al. Effects of increased intra-
abdominal pressure upon intracranial and cerebral perfusion pressure before
and after volume expansion. J Trauma 1996; 40:936 941.
50 Saggi BH, Bloomfield GL, Sugerman HJ, et al. Treatment of intracranial hyper-
tension using nonsurgical abdominal decompression. J Trauma 1999; 46:
646651.
51 Bloomfield G, Saggi B, Blocher C, et al. Physiologic effects of externally ap-
plied continuous negative abdominal pressure for intra-abdominal hyperten-
sion. J Trauma 1999; 46:1009 1014.
52 Schob OM, Allen DC, Benzel E, et al. A comparison of the pathophysiologic
effects of carbon dioxide, nitrous oxide, and helium pneumoperitoneum on
intracranial pressure. Am J Surg 1996; 172:248 253.
170 Gastrointestinal system
53 Rosenthal RJ, Friedman RL, Kahn AM, et al. Reasons for intracranial hyperten-
sion and hemodynamic instability during acute elevations of intra-abdominal
pressure: observations in a large animal model. J Gastrointest Surg 1998;
2:415425.
54 Ben Haim M, Mandeli J, Friedman RL, et al. Mechanisms of systemic hyper-
tension during acute elevation of intraabdominal pressure. J Surg Res 2000;
91:101 105.
55 Rosenthal RJ, Hiatt JR, Phillips EH, et al. Intracranial pressure. Effects of pneu-
moperitoneum in a large-animal model. Surg Endosc 1997; 11:376 380.
56 Halverson A, Buchanan R, Jacobs L, et al. Evaluation of mechanism of in-
creased intracranial pressure with insufflation. Surg Endosc 1998; 12:266
269.
57 Citerio G, Vascotto E, Villa F, et al. Induced abdominal compartment syn-
drome increases intracranial pressure in neurotrauma patients: a prospective
study. Crit Care Med 2001; 29:1466 1471.
58 Miglietta MA, Salzano LJ, Chiu WC, et al. Decompressive laparotomy: a novel
approach in the management of severe intracranial hypertension. J Trauma
2003; 55:551 554.
A nice article followed by an interesting discussion and editorial comment describ-
ing 2 patients treated with decompressive celiotomy in the treatment of intracranial
hypertension in the absence of intra-abdominal pathology.
59 Bloomfield GL, Dalton JM, Sugerman HJ, et al. Treatment of increasing intra-
cranial pressure secondary to the acute abdominal compartment syndrome
in a patient with combined abdominal and head trauma. J Trauma 1995;
39:1168 1170.
60 Irgau I, Koyfman Y, Tikellis JI. Elective intraoperative intracranial pressure
monitoring during laparoscopic cholecystectomy. Arch Surg 1995; 130:
1011 1013.
61 Deeren D, Leijs J, Van den Brande E, et al. Relationship between intracranial
and intra-abdominal pressure in ICU patients. Crit Care Med 2003; 31:A89.
62 Andrews PJ, Citerio G. Intracranial pressure. Part one: historical overview
and basic concepts. Intensive Care Med 2004; 30:1730 1733.
Elegant discussion on the aspects of intracranial pressure that are important for
the ICU physician.
63 Citerio G, Andrews PJ. Intracranial pressure. Part two: Clinical applications
and technology. Intensive Care Med 2004; 30:1882 1885.
Elegant discussion on the aspects of intracranial pressure that are important for
the ICU physician.
64 Sugerman HJ. Effects of increased intra-abdominal pressure in severe
obesity. Surg Clin North Am 2001; 81:1063
1075. (vi.)
65 Sugerman HJ. Increased intra-abdominal pressure in obesity. Int J Obes
Relat Metab Disord 1998; 22:1138.
66 Sugerman HJ, DeMaria EJ, Felton WL III, et al. Increased intra-abdominal
pressure and cardiac filling pressures in obesity-associated pseudotumor
cerebri. Neurology 1997; 49:507 511.
67 Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and
central venous pressure fail to predict ventricular filling volume, cardiac per-
formance, or the response to volume infusion in normal subjects. Crit Care
Med 2004; 32:691 699.
An elegant study in healthy volunteers showing that neither central venous pres-
sure nor pulmonary artery occlusion pressure are useful predictors of ventricular
preload with respect to optimizing cardiac performance.
68 Gattinoni L, Chiumello D, Carlesso E, et al. Bench-to-bedside review: chest
wall elastance in acute lung injury/acute respiratory distress syndrome
patients. Crit Care 2004; 8:350355.
An excellent and comprehensive review of the pathophysiology of changes in ela-
stance in ALI/ARDS patients, highlighting the role of IAH. It summarizes a large
number of studies performed by different groups and provides insights into the
clinical consequences.
69 Gattinoni L, Pelosi P, Suter PM, et al. Acute respiratory distress syndrome
caused by pulmonary and extrapulmonary disease. Different syndromes?
Am J Respir Crit Care Med 1998; 158:3 11.
70 Ranieri VM, Brienza N, Santostasi S, et al. Impairment of lung and chest wall
mechanics in patients with acute respiratory distress syndrome: role of abdo-
minal distension. Am J Respir Crit Care Med 1997; 156:1082 1091.
71 Rouby JJ, Puybasset L, Nieszkowska A, et al. Acute respiratory distress syn-
drome: lessons from computed tomography of the whole lung. Crit Care Med
2003; 31:S285 S295.
A concise and complete overview on the topic of acute lung injury and acute
respiratory distress syndrome by an expert in the field. The importance of IAP
on respiratory mechanics is nicely addressed.
72 Pelosi P, Cereda M, Foti G, et al. Alterations of lung and chest wall mechan-
ics in patients with acute lung injury: effects of positive end-expiratory
pressure. Am J Respir Crit Care Med 1995; 152:531 537.
73 Mutoh T, Lamm WJ, Embree LJ, et al. Volume infusion produces abdominal
distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol
1992; 72:575 582.
74 Pelosi P, Foti G, Cereda M, et al. Effects of carbon dioxide insufflation for
laparoscopic cholecystectomy on the respiratory system. Anaesthesia
1996; 51:744 749.
75 Loeckinger A, Kleinsasser A, Hoermann C, et al. Inert gas exchange during
pneumoperitoneum at incremental values of positive end-expiratory pressure.
Anesth Analg 2000; 90:466 471.
76 Hazebroek EJ, Haitsma JJ, Lachmann B, et al. Mechanical ventilation with
positive end-expiratory pressure preserves arterial oxygenation during pro-
longed pneumoperitoneum. Surg Endosc 2002; 16:685 689.
77 Malbrain MLNG, Van Mieghem N, Verbrugghe W, et al. Effects of different
body positions on intra-abdominal pressure and dynamic respiratory compli-
ance. Crit Care 2003; 7:179.
78 Sugrue M, Jones F, Deane SA, et al. Intra-abdominal hypertension is an
independent cause of postoperative renal impairment. Arch Surg 1999;
134:10821085.
79 Sugrue M, Buist MD, Hourihan F, et al. Prospective study of intra-abdominal
hypertension and renal function after laparotomy. Br J Surg 1995; 82:235
238.
80 Biancofiore G, Bindi ML, Romanelli AM, et al. Postoperative intra-abdominal
pressure and renal function after liver transplantation. Arch Surg 2003;
138:703 706.
81 Biancofiore G, Bindi L, Romanelli AM, et al. Renal failure and abdominal hy-
pertension after liver transplantation: determination of critical intra-abdominal
pressure. Liver Transpl 2002; 8:1175 1181.
82 Friedlander MH, Simon RJ, Ivatury R, et al. Effect of hemorrhage on superior
mesenteric artery flow during increased intra-abdominal pressures. J Trauma
1998; 45:433 489.
83 Steinberg SM. Bacterial translocation: what it is and what it is not. Am J Surg
2003; 186:301 305.
This paper gives an overview of the concept of bacterial translocation and puts it in
perspective. It attempts to review the clinically relevant information that supports
and refutes the concept of bacterial translocation as a cause of our critically ill
patients to exhibit the symptoms and signs of sepsis, develop organ failure,
and ultimately die.
84 Jakob SM. Clinical review: splanchnic ischaemia. Crit Care 2002; 6:306
312.
85 Khanna A, Rossman JE, Fung HL, et al. Intestinal and hemodynamic impair-
ment following mesenteric ischemia/reperfusion. J Surg Res 2001; 99:
114
119.
86 Gargiulo NJ III, Simon RJ, Leon W, et al. Hemorrhage exacerbates bacterial
translocation at low levels of intra-abdominal pressure. Arch Surg 1998;
133:1351 1355.
87 Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial
translocation in the abdominal compartment syndrome. J Trauma 1997;
43:852 855.
88 Eleftheriadis E, Kotzampassi K, Papanotas K, et al. Gut ischemia, oxidative
stress, and bacterial translocation in elevated abdominal pressure in rats.
World J Surg 1996; 20:11 16.
89 Tug T, Ozbas S, Tekeli A, et al. Does pneumoperitoneum cause bacterial
translocation? J Laparoendosc Adv Surg Tech A 1998; 8:401407.
90 Cheng JT, Xiao GX, Xia PY, et al. [Influence of intra-abdominal hypertension
on the intestinal permeability and endotoxin/bacteria translocation in rabbits].
Zhonghua Shao Shang Za Zhi 2003; 19:229 232.
91 Polat C, Aktepe OC, Akbulut G, et al. The effects of increased intra-abdom-
inal pressure on bacterial translocation. Yonsei Med J 2003; 44:259 264.
A good animal study, although in an unknown journal; but I couldnt find anything
wrong with it. The authors nicely show the appearance of bacterial translocation at
an IAP above 14 mm Hg.
92 Doty JM, Oda J, Ivatury RR, et al. The effects of hemodynamic shock and
increased intra-abdominal pressure on bacterial translocation. J Trauma
2002; 52:13 17.
A negative study in which hemorrhage followed by reperfusion and a subsequent
insult of IAH caused significant GI mucosal acidosis, hypoperfusion, as well as
systemic acidosis. These changes however did not appear to be associated with
a significant bacterial translocation as judged by PCR measurements, tissue, or
blood cultures.
93 Koh IH, Menchaca-Diaz JL, Farsky SH, et al. Injuries to the mesenteric
microcirculation due to bacterial translocation. Transplant Proc 2002; 34:
10031004.
94 Moore FA. The role of the gastrointestinal tract in postinjury multiple organ
failure. Am J Surg 1999; 178:449 453.

95 Alverdy JC, Laughlin RS, Wu L. Influence of the critically ill state on host-
pathogen interactions within the intestine: gut-derived sepsis redefined. Crit
Care Med 2003; 31:598 607.
This evidence-based review posits that gut-derived bacteremia, even with potent
nosocomial pathogens, is an event of low proinflammatory potential and, itself, is
an insufficient stimulus for the systemic inflammatory response and organ failure
state typically seen after severe and prolonged catabolic stress. Mechanisms of
this apparent paradox are discussed.
96 Koivusalo AM, Kellokumpu I, Ristkari S, et al. Splanchnic and renal deterio-
ration during and after laparoscopic cholecystectomy: a comparison of the
carbon dioxide pneumoperitoneum and the abdominal wall lift method.
Anesth Analg 1997; 85:886 891.
97 Eleftheriadis E, Kotzampassi K, Botsios D, et al. Splanchnic ischemia during
laparoscopic cholecystectomy. Surg Endosc 1996; 10:324 326.
98 Schwarte LA, Scheeren TW, Lorenz C, et al. Moderate increase in intraab-
dominal pressure attenuates gastric mucosal oxygen saturation in patients
undergoing laparoscopy. Anesthesiology 2004; 100:1081 1087.
The results of this study in 16 patients undergoing elective laparoscopy suggest that
increasing intraabdominal pressure to moderate levels, commonly applied to induce
a surgical pneumoperitoneum, decreases gastric mucosal oxygen saturation.
99 Knolmayer TJ, Bowyer MW, Egan JC, et al. The effects of pneumoperitoneum
on gastric blood flow and traditional hemodynamic measurements. Surg
Endosc 1998; 12:115 118.
100 Caldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intra-
abdominal pressure. J Surg Res 1987; 43:14 20.
101 Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intra-abdominal
pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma
1992; 33:4548.
102 Agusti M, Elizalde JI, Adalia R, et al. Dobutamine restores intestinal mucosal
blood flow in a porcine model of intra-abdominal hyperpressure. Crit Care
Med 2000; 28:467 472.
103 Barnes GE, Laine GA, Giam PY, et al. Cardiovascular responses to elevation of
intra-abdominal hydrostatic pressure. Am J Physiol 1985; 248:R208 R213.
104 Kotzampassi K, Paramythiotis D, Eleftheriadis E. Deterioration of visceral
perfusion caused by intra-abdominal hypertension in pigs ventilated with
positive end-expiratory pressure. Surg Today 2000; 30:987992.
105 Yavuz Y, Ronning K, Lyng O, et al. Effect of carbon dioxide pneumoperito-
neum on tissue blood flow in the peritoneum, rectus abdominis, and dia-
phragm muscles. Surg Endosc 2003.
106 Windberger UB, Auer R, Keplinger F, et al. The role of intra-abdominal pressure
on splanchnic and pulmonary hemodynamic and metabolic changes during
carbon dioxide pneumoperitoneum. Gastrointest Endosc 1999; 49:84 91.
107 Schafer M, Sagesser H, Reichen J, et al. Alterations in hemodynamics and
hepatic and splanchnic circulation during laparoscopy in rats. Surg Endosc
2001; 15:1197 1201.
108 Blobner M, Bogdanski R, Kochs E, et al. Effects of intraabdominally insuf-
flated carbon dioxide and elevated intraabdominal pressure on splanchnic
circulation: an experimental study in pigs. Anesthesiology 1998; 89:475
482.
109 Makinen MT, Heinonen PO, Klemola UM, et al. Gastric air tonometry during
laparoscopic cholecystectomy: a comparison of two PaCO2 levels. Can
J Anaesth 2001; 48:121128.
110 Le Roith D, Bark H, Nyska M, et al. The effect of abdominal pressure on plas-
ma antidiuretic hormone levels in the dog. J Surg Res 1982; 32:65 69.
111 Rosin D, Rosenthal RJ. Adverse hemodynamic effects of intraabdominal
pressure- is it all in the head? Int J Surg Investig 2001; 2:335
345.
112 Kashtan J, Green JF, Parsons EQ, et al. Hemodynamic effect of increased
abdominal pressure. J Surg Res 1981; 30:249255.
113 Rezende-Neto JB, Moore EE, Melo de Andrade MV, et al. Systemic inflam-
matory response secondary to abdominal compartment syndrome: stage for
multiple organ failure. J Trauma 2002; 53:1121 1128.
An innovative and the first study so far that demonstrates that IAH provokes the
release of pro-inflammatory cytokines (IL-1b, IL-6 and TNF-a), which may serve as
a second insult for the induction of MODS.
Intra-abdominal hypertension in the critically ill Malbrain et al. 171
114 Oda J, Ivatury RR, Blocher CR, et al. Amplified cytokine response and lung
injury by sequential hemorrhagic shock and abdominal compartment syn-
drome in a laboratory model of ischemia-reperfusion. J Trauma 2002; 52:
625 631.
A very interesting animal study. In this clinically relevant model, sequential insults of
ischemia-reperfusion (hemorrhagic shock and resuscitation) and ACS were
associated with significantly increased portal and central venous cytokine levels and
more severe lung injury than hemorrhagic shock or ACS alone, suggesting a synergistic
effect.
115 Klopfenstein CE, Morel DR, Clergue F, et al. Effects of abdominal CO2 in-
sufflation and changes of position on hepatic blood flow in anesthetized pigs.
Am J Physiol 1998; 275:H900 H905.
116 Nakatani T, Sakamoto Y, Kaneko I, et al. Effects of intra-abdominal hyperten-
sion on hepatic energy metabolism in a rabbit model. J Trauma 1998;
44:446453.
117 Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intra-
abdominal pressure on hepatic arterial, portal venous, and hepatic microcir-
culatory blood flow. J Trauma 1992; 33:279 282.
118 Odeberg S, Ljungqvist O, Sollevi A. Pneumoperitoneum for laparoscopic
cholecystectomy is not associated with compromised splanchnic circulation.
Eur J Surg 1998; 164:843 848.
119 Escorsell A, Gines A, Llach J, et al. Increasing intra-abdominal pressure
increases pressure, volume, and wall tension in esophageal varices. Hepa-
tology 2002; 36:936 940.
A provocative study in a highly rated gastrointestinal journal about the effects of
IAH on esophageal variceal wall tension and volume in cirrhotic patients. The bot-
tom line is that IAH may trigger variceal rupture and bleeding. So why shouldnt we
intensivists ask for a nasogastric tube to decompress the stomach after repetitive
endoscopic procedures have been done for sclerotherapy or banding to prevent
rebleeding? This study is hopefully the necessarily push for gastroenterologists
and hepatologists to start thinking of IAP.
120 Luca A, Feu F, Garcia-Pagan JC, et al. Favorable effects of total paracentesis
on splanchnic hemodynamics in cirrhotic patients with tense ascites. Hep-
atology 1994; 20:30 33.
121 Navarro-Rodriguez T, Hashimoto CL, Carrilho FJ, et al. Reduction of abdom-
inal pressure in patients with ascites reduces gastroesophageal reflux. Dis
Esophagus 2003; 16:77 82.
Another push for gastroenterologists to start thinking and maybe measuring IAP
since it can trigger gastroesophageal reflux. So lets go for a paracenthesis instead
of proton pump inhibitors.
122 Deeren D, Daelemans R, Lins RL, et al. Correlation between LIMON
de-
rived liver function parameters and classic liver function tests, intra-abdom-
inal pressure (IAP) and organ failure in mixed ICU patients. Crit Care Med
2003; 31:A84.
123 Kimura S, Yoshioka T, Shibuya M, et al. Indocyanine green elimination rate
detects hepatocellular dysfunction early in septic shock and correlates with
survival. Crit Care Med 2001; 29:1159 1163.
124 Ghimenton F, Thomson SR, Muckart DJ, et al. Abdominal content contain-
ment: practicalities and outcome. Br J Surg 2000; 87:106
109.
125 Balogh Z, McKinley BA, Cocanour CS, et al. Supranormal trauma resuscita-
tion causes more cases of abdominal compartment syndrome. Arch Surg
2003; 138:637 642.
A very nice retrospective analysis of prospectively collected data confirming pre-
vious results with regard to the correlation between positive fluid balance,
increased IAP and organ failure. Supranormal resuscitation, compared with normal
resuscitation, was associated with more lactated Ringer infusion, decreased intes-
tinal perfusion (higher CO2-gap), and an increased incidence of IAH, ACS, mul-
tiple organ failure, and death. This study questions the recent early goal oriented
driven protocol for the care of septic patients in the emergency room as recently
written by Rivers in the New England Journal of Medicine.
126 Pepe MS, Janes H, Longton G, et al. Limitations of the odds ratio in gauging
the performance of a diagnostic, prognostic, or screening marker. Am J Epi-
demiol 2004; 159:882 890.
127 Bland JM, Altman DG. Statistical methods for assessing agreement be-
tween two methods of clinical measurement. Lancet 1986; 1:307
310.