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MINERVA ANESTESIOL 2008;74:657-73

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E X PE RT O PI N I O N

Acute intestinal distress syndrome: the importance

of intra-abdominal pressure
M. L. N. G. MALBRAIN 1, W. VIDTS 1, M. RAVYTS 1, I. DE LAET 1, J. DE WAELE 2
1Intensive Care Unit, Ziekenhuis Netwerk Antwerpen, Antwerpen, Belgium; 2Surgical ICU, Ghent Un i versity Hospital, Ghent,
Be l g i u m

ABSTRACT
This review article will focus primarily on the recent literature on abdominal compartment syndrome (ACS) as well
as the definitions and recommendations published by the World Society for the Abdominal Compartment Syndrome
(W S ACS, www.wsacs.org). The risk factors for intra-abdominal hypertension (IAH) and the definitions re g a rd i n g
increased intra-abdominal pressure (IAP) will be listed, followed by a brief but comprehensive overview of the differ-
ent mechanisms of end-organ dysfunction associated with IAH. Measurement techniques for IAP will be discussed,
as well as recommendations for organ function support in patients with IAH. Finally, noninvasive medical manage-
ment options for IAH, surgical treatment for ACS and management of the open abdomen will be briefly discussed.
Key words: Abdomen - Pressure - Risk factors - Compartment syndromes - Multiple organ failure, diagnosis - Multiple
organ failure, therapy.

A c o m p a rtment syndrome exists when

increased pressure in a closed anatomic space
t h reatens the viability of surrounding tissue.
When this occurs in the abdomen, the impact
on end-organ function within and outside the
cavity can be devastating. Abdominal compart-
ment syndrome (ACS) is not a disease, and as
such it can have many causes and can deve l o p
within many disease processes. It is only re c e n t-
ly that ACS has re c e i ved increased attention.
The development of intra-abdominal hypert e n-
sion (IAH) and ACS are of tremendous impor-
tance in the care of critically ill, surgical and
or other proprietary information of the Publisher.
animal and human data suggest that the adve r s e
effects of elevated IAP can occur at lower levels
(10 mmHg) than previously thought and eve n
b e f o re the development of clinically ove rt ACS.
In analogy to acute respiratory distress syndro m e
(ARDS), the authors suggest the terms acute
intestinal distress syndrome (AIDS) or acute
intestinal permeability syndrome (AIPS). This
re v i ewwill provide a concise overv i ew of the epi-
demiologic data, etiology, diagnosis, IAP meas-
u rement, organ dysfunction, pre vention and
t reatment options related to AC S .

trauma patients. The impact of increased intra- Historical background

abdominal pressure (IAP) on end organ func-
tion and especially the heart can no longer be
ignored. IAH is a graded phenomenon that can
be acute or chronic, primary or secondary, and
localised or generalized in nature. ACS, on the
contrary, is not graded, but is instead consid-
ered an ‘all or nothing’ phenomenon. Recent
As Schein recently summarized, the effects of
e l e vated IAP have been known since 1863, when
Ma rey of Paris highlighted that “the effects that
respiration produces on the thorax are the inve r s e
of those present in the abdomen”. 1 It was not
until 1911 that Emerson showed in dogs that

Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA 657

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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

MALBRAIN ACUTE INTESTINAL DISTRESS SYNDROME

This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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TABLE I.—Consensus definitions.

Definition 1 IAP is the steady-state pressure concealed within the abdominal cavity

Definition 2 APP=MAP–IAP

Definition 3 FG=GFP–PTP=MAP–2 * IAP

Definition 4 IAP should be expressed in mmHg and measured at end-expiration in the complete supine position after
ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the mid-
axillary line

Definition 5 The reference standard for intermittent IAP measurement is via the bladder with a maximal instillation volume
of 25 mL of sterile saline

Definition 6 Normal IAP is approximately 5-7 mmHg in critically ill adults

Definition 7 IAH is defined by a sustained or repeated pathologic elevation of IAP 12 mmHg

Definition 8 IAH is graded as follows:

— Grade I: IAP 12-15 mmHg
— Grade II: IAP 16-20 mmHg
— Grade III: IAP 21-25 mmHg
— Grade IV: IAP >25 mmHg

Definition 9 ACS is defined as a sustained IAP >20 mmHg (with or without an APP <60 mmHg) that is associated with new
organ dysfunction/failure

Definition 10 Primary ACS is a condition associated with injury or disease in the abdomino-pelvic region that frequently
requires early surgical or interventional radiological intervention

Definition 11 Secondary ACS refers to conditions that do not originate from the abdomino-pelvic region

Definition 12 Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment
of primary or secondary ACS

IAP: intra-abdominal pressure; APP: abdominal perfusion pressure; MAP: mean arterial pressure; FG: filtration gradient; GFP: glomerular filtra-
tion pressure; PTP: proximal tubular pre s s u re; IAH: intra-abdominal hypertension; ACS: abdominal compartment syndrome. [Adapted from Malbrain
et al.3].

e l e vated IAP increases systemic vascular resist- Definitions

ance (SVR) and can cause death from card i a c
f a i l u reeven before the development of asphyxia.
The term ACS was first used by Fietsam et al. in
the late 1980s to describe the pathophysiologic
alterations resulting from IAH secondary to aor-
tic aneurysm surgery: “ In four patients that
re c e i ved more than 25 L of fluid resuscitation
increased IAP developed after aneurysm repair.
or other proprietary information of the Publisher.
The World Society on Abdominal Compart-
ment Sy n d rome (WSACS – www.wsacs.org) was
founded in 2004 to serve as a peer-re v i ewed foru m
and educational re s o u rce for all healthcare providers
and industry members who have an interest in IAH
and ACS. The first consensus definitions report of
the WSACS was recently published.3 Table I sum-
marizes these consensus definitions.

It was manifested by increased ve n t i l a t o ry pre s-

s u re, increased central venous pre s s u re, and
decreased urinary output. This set of findings
constitutes an ACS caused by massive interstitial
and re t roperitoneal swelling [...]. Opening the
abdominal incision was associated with dramat-
ic improvements [...]”.2 Hence the first definition
of ACS was finally coined.
Recognition of ACS
Clinical awareness
Despite recently increased coverage of this
topic in the medical literature, ACS still appears
to be under-re c o g n i zed. The results of several

658 MINERVA ANESTESIOLOGICA November 2008

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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
ACUTE INTESTINAL DISTRESS SYNDROME
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(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
surveys on physicians’ knowledge of IAH and
ACS have recently been published.4 These sur-
veys show that there is still a general lack of clin-
ical awareness, and many intensive care units
( I C Us) never measure IAP. No consensus exists
on optimal timing of measurement or decom-
p ression. In a recent editorial, Iva t u ry stated
that:5 “ One potential exegesis of this widespre a d
under-appreciation of these syndromes may be
related to our rapidly evolving understanding of
their pathophysiologies. Our knowledge is no
longer restricted to experimentally sound (isolat-
ed IAH) concepts, but is elevated to a true clin-
ical phenomenon (IAH as a “s e c o n d - h i t” after
ischemia-reperfusion)”.
Etiology
ACS can be diagnosed when there is increased
IAP with evidence of end-organ dysfunction.
Although multiple causes of acute cardiopul-
monary, renal, hepatosplanchnic or neuro l o g i c
deterioration exist in the ICU, it is particularly
important that we recognize IAP as an independ-
ent risk factor for organ function deterioration.
Many conditions have been re p o rted in associa-
tion with IAH/ACS and can be classified into four
categories (Table II). 6, 7 Massive volume resuscita-
tion after a “first hit” for any reason (burns, pan-
creatitis, hemorrhagic shock, etc.) can lead to
increased IAP, particularly postoperatively or in a
septic patient. The “second hit” probably results
from ‘capillary leak’, shock with ischemia-re p e r-
fusion injury and cytokine release combined with
massive increases in total extracellular vo l u m e .8
This clinical evolution has some analogy with
ARDS. There f o re, we would like to use the terms
AIDS or, as suggested by others, AIPS to describe
this condition. An algorithm for the assessment
of IAH is proposed in Figure 1.9
or other proprietary information of the Publisher.
Diagnosis
Clinical and radiologic examination
The abdominal perimeter or girth cannot be
used as a surrogate for IAP, and clinical IAP esti-
mation is also far from accurate with a sensitivity
and positive predictive value of around 40-60%.10,
11 Radiologic investigations with plain radiogra-
Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA
MALBRAIN
TABLE II.—Risk factors for the development of IAH and ACS.
A. Related to diminished abdominal wall compliance
— Mechanical ventilation, especially fighting with the ve n t i-
lator and the use of accessory muscles
— Use of positive end expiratory pre s s u re(PEEP) or the pre s e n-
ce of auto-PEEP
— Basal pleuropneumonia
— High body mass index
— Pneumoperitoneum
— Abdominal (vascular) surgery, especially with tight abdomi-
nal closures
— Pneumatic anti-shock garments
— Prone and other body positioning
— Abdominal wall bleeding or rectus sheath haematomas
— C o r rection of large hernias, gastroschisis or omphalocoele
— Burns with abdominal eschars
B. Related to increased intra-abdominal contents
— Gastroparesis
— Gastric distention
— Ileus
— Volvulus
— Colonic pseudo-obstruction
— Abdominal tumour
— Retroperitoneal/ abdominal wall haematoma
— Enteral feeding
— Intra-abdominal or retroperitoneal tumour
— Damage control laparotomy
C. Related to abdominal collections of fluid, air or blood
— Liver dysfunction with ascites
— Abdominal infection (pancreatitis, peritonitis, abscess, etc.)
— Haemoperitoneum
— Pneumoperitoneum
— Laparoscopy with excessive inflation pressures
— Major trauma
— Peritoneal dialysis
D. Related to capillary leakage and fluid resuscitation
— Acidosis* (pH below 7.2)
— Hypothermia* (core temperature below 33°C)
— Coagulopathy* (platelet count below 50 000/mm3 OR an
a c t i vated partial thromboplastin time (APTT) more than 2
times normal OR a prothrombin time (PTT) below 50% OR
an international standardised ratio (INR) more than 1.5)
— Polytransfusion / trauma (> 10 units of packed red cells / 24
hours)
— Sepsis (as defined by the American – European Consensus
Conference definitions)
— Severe sepsis or bacteraemia
— Septic shock
— Ma s s i ve fluid resuscitation (> 5 L of colloid or >10 L of cry-
stalloid / 24 hours with capillary leak and positive fluid balan-
ce)
— Major burns
*The combination of acidosis, hypothermia and coagulopathy has
been advanced in the literature as the “deadly triad”.6, 7
phy of the chest or abdomen, abdominal ultra-
sound or CT scans are also not sensitive to
increased IAP.
659
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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
MALBRAIN
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
Patient meets ONE of the following criteria
and has at least ONE risk factor for IAH:
1. new Intensive Care Unit admission
2.evidence of clinical deterioration
Measure patient’s IAP to establish baseline pressure
IAP measurement should be:
1. expressed in mmHg (1 mmHg=1,36 cm H2 O)
2. measured at end-expiration
3. performed in the supine position
4. zeroed at the level of the mid-axillary line
5. performed with an instillation volume of on >25 mL
of saline (for bladder technique)
6. Measured 30-60 s after instillation to allow bladder
detrusor muscle relaxation (for bladder technique)
Sustained IAP
YES ≥12 mmHg? NO
Patient does not
Patient has IAH have IAH
Observe patient
Proceed to IAH/ACS Recheck IAP if patient
management algorithm
deteriorates clinically
Fi g u re 1.—Intra-abdominal pre s s u re assessment algorithm. IAH: intra-abdominal hypertension; ACS: abdominal compartment
s y n d rome; IAP: intra-abdominal pre s s u re; [Adapted from Cheatham et al.9].
MEASUREMENT OF INTRA- ABDOMINAL PRESSURE
Since the abdomen and its contents can be con-
s i d e red as re l a t i vely non-compre s s i ve and fluid in
character in addition to behaving in accord a n c e
with Pascal’s law, the IAP measured at one point
may be assumed to re p resent the IAP thro u g h o u t
the abdomen.12, 13 IAP increases with inspiration
(diaphragmatic contraction) and decreases with
or other proprietary information of the Publisher.
expiration (diaphragmatic relaxation).
In the strictest sense, the normal IAP ranges
from 0 to 5 mmHg.14 C e rtain physiologic condi-
tions such as morbid obesity,15, 16 ovarian tumors,
cirrhosis or pregnancy may howe ver be associated
with chronic IAP elevations of 10-15 mmHg to
which patients can adapt without significant patho-
660 MINERVA ANESTESIOLOGICA
ACUTE INTESTINAL DISTRESS SYNDROME
Risk factors for IAH/ACS
• Acidosis (pH <7.2)
• Hypothemia (core temperature <33°C)
• Polytransfusion (>10 U of blood/24 h)
• Coagulopathy (platelets <55 000/mm3OR)
activated partial thromboplastin time
(APTT) >2 times normal OR international
standardised ratio (INR) >1.5
• Sepsis (American-European Consensus
Conference definitions)
• Bacteraemia
• Intra-abdominal infection/anscess
• Peritonitis
• Liver dysfunction/cirrhosis with ascites
• Mechanical ventilation
• Use of positive end expiratory pressure
(PEEP) or the presence of auto-PEEP
• Pneumonia
• Abdominal surgery
• Massive fluid resuscitation (>5 L/24 h)
• Gastroparesis/gastric distention/ileus
•Volvulus
• Haemoperitoneum/pneumoperitoneum
• Major burns
• Major trauma
• High body mass index (>30 kg/m2)
• Intra-abdominal or retroperitoneal
tumours
• Prone positioning
• Massive incisional hernia repair
• Acute pancreatitis
• Distended abdomen
• Damage control laparotomy
• Laparoscopy with elevated inflation
pressures
• Peritoneal dialysis
physiology. In contrast, children commonly show
low IAP values.17 The clinical importance of IAP
must therefore be assessed in view of the baseline
steady-state IAP for the individual patient.
IAP can be directly measured with an intraperi-
toneal catheter attached to a pressure transducer.
During CO2-insufflation in laparoscopic surgery
IAP is measured directly via the Verres needle.
Different indirect methods for estimating IAP
a re used clinically because direct measurements
are considered to be too inva s i ve.12, 18 These tech-
niques include rectal, uteral, gastric, inferior ve n a
caval and urinary bladder pressure measurement.
Only gastric and bladder pressures are used clini-
cally. Over the years, bladder pressure has advanced
as the gold-standard indirect method and meas-
November 2008
 MINERVA MEDICA COPYRIGHT®
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
ACUTE INTESTINAL DISTRESS SYNDROME
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TABLE III.—Neurologic effects related to IAP.
Intracranial pressure ↑
Cerebral perfusion pressure ↓
Cerebral blood flow ↓
Jugular bulb saturation ↓
Cerebral venous outflow ↓
Cerebrovascular resistance ↑
Idiopathic intracranial hypertension in morbid obesity
Pseudotumor cerebri in morbid obesity
Neurologic effects reversed after bariatric surgery or weight loss
Neurologic deterioration during laparoscopy
TABLE IV.—Cardiovascular effects related to IAP*.
Diaphragm elevation ↑
Pleural and intrathoracic pressure ↑
Difficult preload assessment
Pulmonary artery occlusion pressure ↑
Central venous pressure ↑
Transmural filling pressure =ÿ
Intra thoracic blood volume index =ÿ
Global end-diastolic blood volume index =ÿ
Right ventricular end-diastolic volume =ÿ
Right, global and left ventricular ejection fraction =ÿ
Extra vascular lung water =⁄
Stroke volume variation ⁄
Pulse pressure variation ⁄
Systolic pressure variation ⁄
Inferior vena cava flow ↓
Venous return ↓
Left ventricular compliance and contractility ↓
Downward Starling curve shift to the right
Cardiac output ↓
Systemic vascular resistance ↑
Mean arterial pressure ⁄ =ÿ
Pulmonary artery pressure ↑
Pulmonary vascular resistance ↑
Heart rate ⁄ =
Lower extremity hydrostatic venous pressure ↑
Venous stasis, edema, ulcers ↑
Venous thrombosis ↑
Pulmonary embolism# ↑
Mixed venous oxygen saturation ↓
Central venous oxygen saturation ↓
*Cardiovascular effects are exacerbated in case of hypovolemia, hemor-
rhage, ischemia, auto-PEEP or high PEEP ventilation; #upon decom-
pression.
or other proprietary information of the Publisher.
u rement kits have become available including the
FoleyManometer (Holtech Medical, Kopenhagen,
Denmark) and AbViser-valve (Wolfe Tory Medical,
Salt Lake City, UT, USA). The bladder technique
has achieved the most widespread adoption world-
wide due to its simplicity and minimal cost.12, 13
Howe ve r, considerable variation is noted betwe e n
Vol. 74 - No. 11
MALBRAIN
TABLE V.—Cardiovascular effects related to IAP*.
Diaphragm elevation ↑
Intrathoracic pressure ↑
Pleural pressure ↑
Functional residual capacity (FRC) ↓
All lung volumes (TLC, TV,…) ↓ (~restrictive disease)
Extrinsic compression lung parenchyma* ↑
Auto-PEEP ↑
Compression atelectasis ↑
Peak airway pressure ↑ (volume controlled MV)
Mean airway pressure ↑
Plateau airway pressure ↑
Pulmonary vascular resistance ↑
Alveolar barotrauma =↑
Alveolar volutrauma =↑
Dynamic compliance ↓
Static respiratory system compliance ↓
Static chest wall compliance ↓↓
Static lung compliance =
Upper inflection point on PV curve ↓
Lower inflection point on PV curve ↑
Hypercarbia - pCO2 retention ↑
PaO2 ↓ and PaO2/FiO2 ↓
Alveolar oxygen tension ↓
Oxygen transport ↓
Dead-space ventilation ↑
Intrapulmonary shunt ↑
Ventilation perfusion mismatch ↑
Ventilation diffusion mismatch ↑↑
Oxygen consumption ↑
Metabolic cost and work of breathing ↑
Alveolar edema ↑
Extra vascular lung water (EVLW) =⁄
Prolonged ventilation
Difficult weaning
Activated lung neutrophils ↑
Pulmonary inflammatory infiltration ↑
Pulmonary infection rate ↑
*Parenchymal compression is exacerbated in case of hemorrhagic shock
or hypotension.
the different techniques used, and recent data sug-
gest that minimal volumes (10-25 ml) should be
instilled in the bladder for priming.19-21
CONTINUOUS INTRA-ABDOMINAL PRESSURE MEAS-
UREMENT
IAP can also be measured via a balloon-tipped
stomach catheter that recently became available
(Spiegelberg, Hamburg, Germany and Pulsion
Medical Systems, Munich, Germany). 13 This
avoids the problems associated with the creation of
a hyd rostatic fluid column and allows continuous
IAP measurement.
Several other methods for continuous IAP meas-
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

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TABLE VI.—Hepatic effects related to IAP. TABLE VIII.—Gastrointestinal effects related to IAP.

Hepatic arterial flow ↓ Abdominal perfusion pressure ↓

Portal venous blood flow ↓ Superior mesenteric artery blood flow ↓
Portocollateral flow ↑ Celiac blood flow ↓
Lactate clearance ↓ Blood flow to intra-abdominal organs ↓
Systemic lactate ↑ Mesenteric vein compression ↑
Glucose metabolism ↓ Abdominal venous hypertension ↑
Serum glucose levels ↑=↓ Mucosal blood flow ↓
Mitochondrial function ↓ Intestinal mucosal perfusion* ↓
Cytochrome p450 function ↓ Intramucosal pHi (gastric tonometry) ↓
Toxic metabolites medication ↑ Regional CO2 ↑
Indocyanine green Plasma disappearance rate (ICG-PDR) ↓ CO2-gap ↑
Success enteral feeding ↓
Gastric residuals ↑
Gastric dilatation ↑
TABLE VII.—Renal effects related to IAP. Paralytic or mechanic ileus ↑
Intestinal permeability ↑
Renal parenchymal compression ↑ Intestinal edema ↑
Renal perfusion pressure ↓ Bacterial translocation ↑
Filtration gradient ↓ Multiple organ failure ↑
Renal arterial blood flow ↓ Visceral swelling ↑
Renal venous blood flow ↓ Intra-abdominal pressure ↑
Renal vein compression ↑ Bowel ischemia ↑
Renal venous (back) pressure ↑ Lactic acidosis ↑
Tubular dysfunction ↑ Gastro-intestinal ulcer (re)bleeding ↑
Glomerular perfusion ↓ Variceal wall stress ↑
Glomerular filtration rate ↓ Variceal (re)bleeding ↑
Diuresis (oliguria to anuria) ↓ Peritoneal adhesions ↑
Prerenal azotemia* ↓ Necrotising enterocolitis (NEC) in children ↑
Urine sodium and chlorine ↑
Renal vascular resistance ↑ *A reduction in intestinal mucosal perfusion has been demonstrated
by gastric and rectal tonometry, laser doppler flow probes, intravital video
Corticomedullar shunting in renal plasma flow ↑ microscopy, Orthogonal Polarization Spectral (OPS) imaging, Sidestream
Effective renal plasma flow ↓ Da rk Field (SDF) imaging and indocyanine green clearance.
Compression ureters ↑
Anti-diuretic hormone ↑
Renin, angiotensin aldosterone ↑
Sympathic nervous system stimulation ↑
TABLE IX.—Effects of IAP on abdominal wall and endocrine
Arterial vasoconstriction ↑
system.
Systemic hypertension in chronic IAH (obese) ↑
Adrenal blood flow = Abdominal wall compliance ↓
Abdominal wall complications in CAPD ↑ Abdominal wall complications in CAPD ↑
Rectus sheath blood flow ↓
*Unresponsive to volume expansion to a normal CO, dopaminergic
agents or loop diuretics. Abdominal wall ischemia ↑
Abdominal wall edema ↑
Wound complications (dehiscence, herniation, necrotising fascii-
tis) ↑
Wound Infections ↑
u rement via the stomach, peritoneal cavity (using Incisional hernia ↑
air-chamber or piezo resistive membranes) and Antidiuretic hormone ↑
bladder have been validated.18, 22-24 Although these Renin, angiotensin, aldosterone ↑
Release pro-inflammatory cytokines
techniques seem promising, further clinical valida- (IL-1β, TNF-α, IL-6) ↑
or other proprietary information of the Publisher.

tion is necessary before their general use can be Relative adrenal insufficiency =
recommended.

ABDOMINAL PERFUSION PRESSURE MEASUREMENT s u re (MAP) minus intracranial pressure (ICP),

Analogous to the widely accepted and clinical- abdominal perfusion pre s s u re (APP), calculated
ly utilized concept of cerebral perfusion pressure as MAP minus IAP, has been proposed as a more
(CPP), which is calculated as mean arterial pres- accurate predictor of visceral perfusion and a poten-

662 MINERVA ANESTESIOLOGICA November 2008

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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

ACUTE INTESTINAL DISTRESS SYNDROME MALBRAIN

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IAP

Vascular compression Diaphragm elevation Organ compression

Pleural + intrathoracic Renin

Inferior vena cava flow Cardiac compression pressure Aldosterone

CVP P™ PAOP
EDV

Venous Cardiac preload Cardiac contractility Systemic afterload

stasis
DVT
PE

MAP CO

Figure 2.—Card i ovascular effects of intra-abdominal hypertension. APP: abdominal perfusion pressure; CO: cardiac output; CVP:
central venous pre s s u re; DVT: deep vein thrombosis; EDV: end diastolic APP
volume; IAP: intra-abdominal pre s s u re; MAP: mean
arterial pre s s u re; PAOP: pulmonary art e ry occlusion pre s s u re; PE: pulmonary embolism; P™: transmural pre s s u re .

tial endpoint for resuscitation:25-28 APP = MAP – — RPP = MAP – IAP

IAP.
With respect to both arterial inflow (MAP) and
restrictions to venous outflow (IAP), APP is statis-
tically superior to either parameter alone in predict-
ing patient survival from IAH and ACS.28 A tar-
get APP of at least 60 mmHg has been demon-
strated to correlate with improved survival from
IAH and ACS.
RENAL PERFUSION PRESSURE AND FILTRATION GRA-
DIENT MEASUREMENT
El e vated IAP significantly decreases renal art e ry
blood flow and compresses the renal vein, leading
or other proprietary information of the Publisher.
— FG = GFP – PTP = (MAP – IAP) – IAP =
MAP – 2*IAP
w h e re GFP is the glomerular filtration pressure
and PTP the proximal tubular pressure.
Thus, changes in IAP affect renal function and
urine production more than changes in MAP. It is
therefore not surprising that decreased renal func-
tion as evidenced by oliguria is one of the first vis-
ible signs of IAH.
Pathophysiologic implications
IAH affects multiple organ systems in a grad-

to renal dysfunction and failure.29 Oliguria deve l-
ops at an IAP of 15 mmHg and anuria at 30
mmHg in the presence of normovolemia and at
lower levels of IAP in patients with hypovolemia
or sepsis.30, 31 Renal perfusion pre s s u re (RPP) and
renal filtration gradient (FG) have been pro p o s e d
as key factors in the development of IAP-induced
renal failure and are defined as
ed fashion. In order to fully understand the clin-
ical presentation and management of IAH dis-
o rders, the pathophysiology of each organ sys-
tem must be considered separately.8 It is beyo n d
the scope of this re v i ew to discuss in depth the
pathophysiologic implications of raised IAP on
end-organ function within and outside the
abdominal cavity.32, 33

Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA 663

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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
MALBRAIN
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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Tables III-IX schematically list the different
effects on organ function.
Neurologic function
Acute IAH causes increased ICP due to aug-
mentation of pleural pre s s u re. CPP decreases due
to functional obstruction of cerebral venous out-
f l ow caused by increased intrathoracic pre s s u re
(ITP), which in turn is due to cephalad displace-
ment of the diaphragm in combination with the
reduction of systemic blood pressure by decreased
p reload and cardiac output (CO). Cerebral blood
flow and jugular bulb saturation also decrease.
Table III shows the neurologic effects of IAH.
The effects of IAP on the central nervous system
(CNS) have not been extensively studied to date
and remain a challenging area for laboratory and
clinical investigators.27, 34-40
Cardiovascular function
Pleural pre s s u re and ITP also increase due to
cephalad movement of the diaphragm. This results
in difficult preload assessment because tradition-
al filling pressures are erroneously increased. When
IAP rises above 10 mmHg, CO drops because of
i n c reased afterload as well as decreased pre l o a d
and left ventricular compliance (Figure 2). SVR
increases due to mechanical compression of va s c u-
lar beds, and preload is reduced by decreased stroke
volume and venous return.41-44 Mean arterial blood
pressure may initially rise due to shunting of blood
away from the abdominal cavity, but there a f t e r
normalizes or decreases.28, 45
Table IV shows the card i ovascular effects of
IAH.
Pulmonary function
Interactions between the abdominal and tho-
racic compartments pose a specific challenge to
or other proprietary information of the Publisher.
ICU physicians.46 Both compartments are linked
via the diaphragm and on average a 50% (range:
25-80%) transmission of IAP to the ITP has been
noted in previous animal and human studies.44
Patients with primary ACS often develop second-
ary ARDS and require a different ventilatorystrat-
egy as well as more specific treatment than patients
with primary ARDS.47, 48 The major problem lies
664 MINERVA ANESTESIOLOGICA
ACUTE INTESTINAL DISTRESS SYNDROME
in the reduction of functional residual capacity,
which together with alterations caused by second-
a ry ARDS leads to so-called “baby-lungs”. Table V
shows the pulmonary effects of IAH.
Hepatic function
The liver appears to be particularly susceptible
to injury in the presence of elevated IAP. Animal
and human studies have shown impairment of
hepatic cell function and liver perfusion even with
an only moderately elevated IAP of 10 mmHg.49, 50
Furthermore, acute liver failure, decompensated
chronic liver disease and liver transplantation are
frequently complicated by IAH and ACS.51, 52 Table
VI schematically shows the hepatic effects of IAH.
Renal function
IAH has been associated with renal impairment
for over 150 years,1 but a clinically recognized rela-
tionship was only recently found.53, 54 An incre a s-
ing number of large clinical studies have found
that IAH (15 mmHg) is independently associat-
ed with renal impairment and increased mortali-
ty.55, 56 The etiology of these changes is not we l l
established but may be multifactorial and include
reduced renal perfusion, reduced CO, incre a s e d
SVR and altered expression of humeral and neu-
rogenic factors. Table VII schematically shows the
renal effects of IAH.
Gastrointestinal function
IAH has profound effects on splanchnic organs,
causing diminished perfusion, mucosal acidosis and
setting the stage for multiple organ failure (MOF).57
The pathologic changes are more pronounced after
sequential insults of ischemia-reperfusion and IAH.
IAH and ACS may serve as the second insult in the
two-hit phenomenon of multiple-organ dysfunc-
tion syndro m e .58, 59 Recent clinical studies have
demonstrated a temporal relationship between ACS
and subsequent MOF.57, 60, 61 In animals, ACS pro-
vokes cytokine release and neutrophil migration,
resulting in remote organ failure. In humans, ACS
results in splanchnic hypoperfusion that may occur
in the absence of hypotension or decreased CO.
This ischemic and re p e rfusion injury to the gut
serves as the second insult in a two-hit model of
November 2008
 MINERVA MEDICA COPYRIGHT®
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
ACUTE INTESTINAL DISTRESS SYNDROME
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MOF where the lymph flow conducts gut-derived
pro-inflammatorycytokines to remote organs. Table
VIII schematically shows the gastrointestinal effects
of IAH.
Abdominal wall and endocrine function
Increased IAP has been shown to reduce abdom-
inal wall blood flow by direct compressive effects
leading to local ischemia and edema,62 which in
turn can decrease abdominal wall compliance and
exacerbate IAH.63 Abdominal wall muscle and fas-
cial ischemia may contribute to infectious and
non-infectious wound complications (e . g., dehis-
cence, herniation, necrotizing fasciitis) often seen
in this patient population. Table IX schematical-
ly shows the effects of IAH on abdominal wall and
endocrine function.
Importance of intra-abdominal pressure in
other clinical conditions
Abdominal compartment syndrome in pediatric
patients
Omphalocele and gastroschisis we re the first
clinical conditions to be closely associated with
increased IAP;64, 65 pediatric surgeons we re the
first to deal with defects of the abdominal wall
and the consequences of their closure .66 Se ve r a l
series from the last decade document the mani-
festations of elevated IAP in children undergoing
such repairs, the beneficial effects of monitoring
IAP and the role of elevated IAP in the increased
incidence of necrotizing enterocolitis. These stud-
ies make it clear that special attention should be
paid to IAP in children.
Abdominal compartment syndrome in burn patients
Patients with large burns ( 50% or with associ-
ated inhalation injury) are at risk for IAH.67 Patients
or other proprietary information of the Publisher.
with burns over 70% of their total body surface
a rea are at risk for ACS, particularly if they have a
concurrent inhalation injury. The development of
IAH and ACS is related to the volume of crystalloid
fluid infused during burn resuscitation and does
not require abdominal injury, operation or even the
presence of abdominal wall burn eschar.67-73
However, these patients have very large burns in
Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA
MALBRAIN
addition to often seve re inhalation injuries and
frequently die later from complications unre l a t-
ed to ACS.
Abdominal compartment syndrome in haematolog-
ical patients
Recent studies have alluded to the increased
incidence and consequences of IAH in haemato-
logical patients,74 the causes of which include:
— growth factor-induced capillary leak syn-
drome with concomitant large volume fluid re s u s-
citation and third space sequestration;
— chemotherapy-induced ileus, colonic pseu-
do-obstruction (Ogilvie’s syndrome), mucositis
or gastroenteritis;
— sepsis and infectious complications aggravat-
ing intestinal and capillary permeability;
— extramedullary hematopoiesis as seen with
chronic myeloid leukemia that results in
hepatosplenomegaly, chronic IAH and chro n i c
(irreversible) pulmonary hypertension;
— veno-occlusive disease seen after stem cell
transplantation that may be triggered by or relat-
ed to increased IAP.
Abdominal compartment syndrome in morbidly obese
patients
Recent studies show that obese patients have
higher baseline IAP values.75 As with IAH in the
critically ill, elevated IAP in morbidly obese
patients can have far-reaching effects on end organ
function. Disease processes common in morbid-
ly obese patients such as obesity hypoventilation
syndrome, pseudotumor cerebri, gastroesophageal
reflux and stress urinary incontinence are now
thought to be caused by increased IAP occurring
concurrently with elevated body mass index.16, 76,
77 Furthermore, increased incidence of poor fascial
healing and incisional hernia have been related to
IAH-mediated reductions in rectus sheath and
abdominal wall blood flow.
Clinical management
The management of patients with IAH is based
on three principles:78, 79
— specific procedures to reduce IAP and the
consequences of ACS;
665
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

MALBRAIN ACUTE INTESTINAL DISTRESS SYNDROME

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Patient with IAH NO

Initiate medical treatment

options to reduce IAP

Perform serial Discontinue

IAP IAP
IAP ≥20 mmHg measurements IAP ≥12 mmHg measurements
with organ failure NO every 4 hours YES Observe patients
consistently?
while patient for clinical
is critically ill deterioration

YES
Medical treatment options
to reduce IAP
Patient has ACS
1. Improve abdominal wall compliance
Sedation
Pharmacologic paralysis
Supine body positioning
Secondary or 2. Evacuate intra-luminal contents YES
Primary ACS NO recurrent ACS Nasogastric decompression
Rectal decompression
Gastro-/colo-procinectic agents
YES 3. Evacuate abdominal fluid collections
Paracentesis
Percutaneous abscess/hematoma
Perform/revise Have drainage
abdominal all medical 4. Correct positive fluid balance
decompression treatment Diuretics
with temporary YES
abdominal options Colloids
closure failed? Hemodialysis/ultrafiltration

NO

Continue medical treatment IAP <12 mmHg

options to reduce IAP NO consistently?

NO Perform serial IAP

measurement every 4 h
while patient is critically ill

Resuscitate with crystalloid/ NO

colloid/vasoactive agents to
maintain APP ≥60 mmHg
Consider
or other proprietary information of the Publisher.

abdominal
closure
Can APP (if open)
≥60 mmHg be IAP <20 mmHg guided by
YES YES IAP and APP
maintained? consistently?
measurement

Figure 3.—Intra-abdominal hypertension algorithm. IAH: intra-abdominal hypertension; IAP: intra-abdominal pressure; ACS: abdom-
inal compartment syndrome [Adapted from Cheatham et al.9].

666 MINERVA ANESTESIOLOGICA November 2008

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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
ACUTE INTESTINAL DISTRESS SYNDROME
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
— general support (intensive care) of the crit-
ically ill patient;
— optimization after surgical decompression in
an attempt to counteract some of the specific
adverse effects associated with decompression.
Medical treatment
Be f o re surgical decompression is considere d ,
less inva s i vemedical treatment options should be
exhausted. Di f f e rent medical treatment proce-
dures have been suggested to decrease IAP 26 and
are based on five different mechanisms:
— i m p rovement of abdominal wall compli-
ance;
— evacuation of intraluminal contents;
— evacuation of abdominal fluid;
— correction of capillary leak and positive flu-
id balance;
— specific treatments.
An algorithm for the clinical management of
IAH and ACS is proposed in Figure 3, while Table
X gives an ove rv i ew of the different medical tre a t-
ment options.
IMPROVEMENT OF ABDOMINAL WALL COMPLIANCE
The relationship between abdominal contents
and IAP is not linear but exponential. In septic
patients, abdominal wall compliance changes over
time and is dependent on baseline IAP. Sedation
can help to control IAH by increasing abdominal
wall compliance. Decreased IAP after curarization
is a long-established phenomenon in the operat-
ing theatre.27, 80-83 Fentanyl, however, may acute-
ly increase IAP by stimulation of active phasic
expiratory activity.84 In obese patients, weight loss
results in decreased IAP.85 Body positioning and the
use of skin pressure decreasing interfaces can also
reduce IAP. 86-88 A percutaneous procedure for
i n c reasing abdominal capacity/compliance and
d e c reasing IAP based on the principles of abdom-
or other proprietary information of the Publisher.
inal wall component separation was recently val-
idated in a porcine ACS model.89 In burn patients,
a similar procedure also had beneficial effects.73
EVACUATION OF INTRA-LUMINAL CONTENTS
Ileus is common in most critically ill patients.
No n - i n va s i ve evacuation of abdominal contents
Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA
MALBRAIN
TABLE X.—Medical treatment options for IAH and ACS.
1. Improvement of abdominal wall compliance
— Sedation
— Pain relief (not fentanyl)
— Neuromuscular blockade
— Body positioning
— Negative fluid balance
— Skin pressure decreasing interfaces
— Weight loss
— Percutaneous abdominal wall component separation
2. Evacuation of intraluminal contents
— Gastric tube and suctioning
— Ga s t ro p rokinetics (erythromycin, cisapride, metocloprami-
de)
— Rectal tube and enemas
— Colonoprokinetics (neostygmine, prostygmine bolus or infu-
sion)
— Endoscopic decompression of large bowel
— Colostomy
— Ileostomy
3. Evacuation of peri-intestinal and abdominal fluids
— Ascites evacuation
— CT- or US-guided aspiration of abscess
— CT- or US-guided aspiration of hematoma
— Percutaneous drainage of (blood) collections
4. Correction of capillary leak and positive fluid balance
— Albumin in combination with diuretics (furosemide)
— Correction of capillary leak (antibiotics, source control)
— Colloids instead of cristalloids
— Dobutamine (not dopamine)
— Dialysis or CVVH with ultrafiltration
— Ascorbinic acid in burn patients
5. Specific therapeutic interventions
— Continuous negative abdominal pressure (CNAP)
— Negative external abdominal pressure (NEXAP)
— Targeted abdominal perfusion pressure (APP)
— (experimental: Octreotide and melatonin in ACS)
should be attempted by gastric tube placement
and suctioning, rectal tubes, enemas and possibly
endoscopic decompre s s i o n .90-93 These pro c e d u res
can be performed in conjunction with adminis-
tration of gastro- and or colonoprokinetics such
as erythromycin (200 mg i.v. every 6 h), metoclo-
pramide (10 mg i.v. every 8 h), and neostygmine
or prostygmine (2 mg diluted in up to 50 m giv-
en slowly by i.v. infusion).94-99
EVAC UATION OF ABDOMINAL FLUID COLLECTIONS
Drainage of tense ascites may result in decreased
IAP.100-104 In patients with liver cirrhosis and
667
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

MALBRAIN ACUTE INTESTINAL DISTRESS SYNDROME

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Figure 4.—Different techniques for temporary abdominal closure in patients with abdominal compartment syndrome. A) Moist gauze
used to be the preferred method of covering the abdomen, but this is no longer used as it carries a substantial risk of creating intes-
or other proprietary information of the Publisher.

tinal fistulas . Improved solutions are now available. B) “Bogota bag”: a plastic sheet is cut from a sterile 3L irrigation bag, and sewn
to the skin or fascia. This system is inexpensive and offers the advantage that the bowel and abdominal contents can be easily inspect-
ed and accessed, but fluid losses are difficult to control, generating a challenge to the nursing staff. C) Towel clip closure is often used
as an initial method of TAC after damage control surgery because of the speed of closure. After re-exploration, it can be replaced by
one of the following techniques. D) Re m ovable prosthetic materials. These we re used initially for open abdomen treatment of intra-
abdominal sepsis, and can be used for TAC in other circumstances as well. Examples include zippers, Wittman patch (which uses a
Velcro closure system), etc. E) Vacuum assisted fascial closure (VAFC) systems. Di f f e rent packing techniques that use suction or
vacuum to control the fluid draining from the open abdomen have been described (the vacuum pack technique and modified sand-
wich vacuum pack technique, or Vacuum Assisted Closure system). These are simple solutions for the management of open abdomen
and provide easy control and quantification of fluid losses. F) Home-made VAC systems. Different “home-made” VAC techniques
for TAC have been developed over the years with good results, some using scrub sponges over silicone sheaths.

668 MINERVA ANESTESIOLOGICA November 2008

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not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo,
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
ACUTE INTESTINAL DISTRESS SYNDROME
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
esophageal varices, paracentesis helps to decre a s e
variceal wall tension and the risk of rupture and bleed-
ing.105 Paracentesis is also the treatment of choice for
burn patients with secondary ACS.73, 106, 107 For
hematomas, blood collections and local abscesses,
CT-guided fine needle aspiration has recently been
described in the setting of IAH and ACS.
C ORRECTION OF C A PI L LARY L E A K AG E AND POSI-
TIVE FLUID BALANCE
In the initial phase, fluid loss should be compen-
sated in order to pre vent splanchnic hypoperf u-
sion.108-110 Low-dose infusion of dobutamine, but
not dopamine, also corrects the impairment of intes-
tinal mucosal perfusion by moderate increases in
intra-abdominal pre s s u re.111 ACS patients retain
large volumes of sodium and water that exacerbate
tissue edema and third spacing due to capillary leak-
age, thereby resulting in a vicious cycle of ongoing
IAH. In the early stages, diuretic therapy in combi-
nation with albumin can mobilize the edema, but
only if the patient is hemodynamically stable. In
some cases, it is preferable to give colloids or albu-
min instead of crystalloids.112, 113 In burn patients,
co-administration of ascorbinic acid results in
reduced fluid requirements.114, 115 Many patients,
h owe ve r, will develop anuria as renal blood flow is
reduced. In these cases, renal replacement therapy
with fluid removal by intermittent dialysis or CVVH
should not be delayed.116-118
SPECIFIC TREATMENTS
Recently the application of continuous nega-
t i ve abdominal pre s s u re using a cuirass has show n
decreased IAP and increased end-expiratory lung
volumes in animals and humans.36, 40, 119-121
In a manner similar to the targeting of CPP
(CPP=MAP–ICP) or coro n a ry perfusion pre s-
sure (CoPP) (CoPP = diastolic blood pre s s u re –
pulmonary artery occlusion pre s s u re), it may be
a p p ropriate to target APP, where APP=MAP–IAP,
or other proprietary information of the Publisher.
to a level that reduces the risk of worsened
splanchnic perfusion and subsequent organ dys-
function.25, 26, 44
Surgical decompression
Although decompression remains the only
definite management for ACS, the timing of this
Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA
MALBRAIN
procedure still remains controversial. During
the intervention, specific anesthetic challenges
need to be addressed, and after decompre s s i o n
the patient is at risk for ischemia reperfusion
i n j u ry, venous stasis and fatal pulmonary
embolism.122 Maintenance of adequate preload
and APP is the key to success. 25, 28, 110 Op e n
abdomen treatment (or laparostomy) was ini-
tially intended for patients with diffuse intra-
abdominal infections and often used in combi-
nation with a planned re - l a p a rotomy approach.
Due to the increased awareness of the deleteri-
ous effects of IAH, open abdomen treatment,
either prophylactic or therapeutic, is more com-
mon in the ICU.60, 123
Se veral methods for temporary abdominal clo-
sure are available and shown in Figure 4.
Conclusions
First suggested in 1863 by Ma re y, ACS is a
constellation of physiologic sequelae of increased
IAP that are also termed IAH. Recent observa-
tions suggest an increasing frequency in all patient
types, and IAH and ACS are independently asso-
ciated with mortality. Even chronic elevations of
IAP seem to affect various organ systems. Despite
its pre valence and importance, this syndrome is
still poorly re c o g n i zed and thus poorly tre a t e d
in some cases. The diagnosis relies largely on IAP
m e a s u rement, which is most often performed
t h rough a bladder catheter. The effects of IAH
on different organ systems have been described
concomitantly with therapeutic recommenda-
tions. In analogy to the presence of first and sec-
ond hit insults in ARDS pathophysiology, the
term AIDS has been suggested. The ultimate goal
of treatment is not only to decrease IAP, but also
to improve organ function and to decrease mor-
tality. Decompressive laparotomy is the only tre a t-
ment option thus far that has been shown to
a c h i e ve most of these goals. Howe ve r, some less
invasive techniques and medical treatment strate-
gies have shown promise in achieving IAP reduc-
tion as well as organ function improvement. A
complete management algorithm has been pro-
posed although treatment recommendations for
IAH are likely to change significantly as more
clinical data become ava i l a b l e .
669
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is
MALBRAIN
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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Received on March 26, 2008 - Accepted for publication on March 27, 2008.
Corresponding author: M. Malbrain, MD, PhD, Past President W S ACS, ICU Director, Intensive Care Unit, ZiekenhuisNetwerk Antwe r p e n ,
ZNA Stuivenberg, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium. E-mail: manu.malbrain@skynet.be0
or other proprietary information of the Publisher.
Vol. 74 - No. 11 MINERVA ANESTESIOLOGICA
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