Intra Abdominal Hypertension

Best Practice & Research Clinical Anaesthesiology 27 (2013) 249270
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Best Practice & Research Clinical

Anaesthesiology
journal homepage: www.elsevier.com/locate/bean
Intra-abdominal hypertension: Denitions,

monitoring, interpretation and management
Manu L.N.G. Malbrain a, *, Inneke E. De laet a, Jan J. De Waele b,
Andrew W. Kirkpatrick c
a
Intensive Care Unit, ZiekenhuisNetwerk Antwerpen, ZNA Stuivenberg, Lange Beeldekensstraat 267,
B-2060 Antwerpen, Belgium
Department of Critical Care Medicine, Ghent University Hospital and Ghent Medical School, Ghent, Belgium
c
Regional Trauma Services, EG 23 Foothills Medical Centre, Calgary, Alberta, Canada T2N 2T9
b
Keywords:
abdominal pressure
abdominal hypertension
denitions
management
monitoring
This review will describe the denitions on intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). In
order to understand these denitions the reader must be aware of
the interactions between intra-abdominal pressure (IAP) and
intra-abdominal volume (IAV), explaining why dramatic IAP increases can be observed in some patients related to anthropomorphic measurements, body positioning, use of positive pressure
ventilation, or relatively small accumulations of uid or blood. The
adverse effects related to increased IAP have been named IAH for
moderate cases and ACS for advanced cases. In order to improve
clinical communication as well as evaluation of the scientic
literature, the World Society for the Abdominal Compartment
Syndrome (WSACS) has published its rst guidelines and denitions in 2006. The denitions and guidelines have recently been
revised according to evidence based medicine and the Grading of
Recommendations Assessment, Development and Evaluation
(GRADE) methodology. This review will be based on the revised
guidelines. The standard method to measure IAP is via the bladder
and as experience with IAP measurement has evolved considerably, a number of tips and potential pitfalls are listed.
2013 Elsevier Ltd. All rights reserved.
* Corresponding author. Fax: 32 3 2177574.

E-mail address: manu.malbrain@skynet.be (M.L.N.G. Malbrain).
1521-6896/$ see front matter 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.bpa.2013.06.009
250
M.L.N.G. Malbrain et al. / Best Practice & Research Clinical Anaesthesiology 27 (2013) 249270
Introduction
Owing to its restricted capacity to expand, the peritoneal cavity is subject to raised internal pressures like any other anatomic compartment such as the head, the chest or the extremities [1]. Raised
intra-abdominal pressure (IAP) above 12 mmHg, dened asintra-abdominal hypertension (IAH), has
been increasingly recognized as a frequent complication resulting in morbidity and mortality among
critically ill patients admitted to the intensive care unit (ICU) [25]. These detrimental physiologic
effects of increased IAP have been recognized for decades in nearly all organ systems, including the
central nervous system and the cardiovascular, respiratory, renal, gastrointestinal, and hepatic systems.
When IAP is increased without new organ failure, the diagnosis of IAH is made; when new or progressive organ failure ensues this constitutes a formal diagnosis which is an end-stage manifestation of
severe IAH [2,6,7], IAH and abdominal compartment syndrome (ACS) can have many inciting causes
and can occur within many disease processes. Mortality of ACS approaches 100% when left untreated as
reported in a hallmark paper by Kron et al. who coined the term ACS and launched the modern revival
in recognizing this phenomenon in the 80s of the last century [8]. As ACS represents organ failure from
IAH, it still carries a high mortality despite decompression and correction of the underlying cause [9].
Recently, interest shifted from ACS to more moderate forms of IAH, which may prove to be more
susceptible to prevention and treatment. IAH is also more frequently seen in non-trauma surgical
patients and medical patients, mainly in those requiring massive uid resuscitation and presenting
with so-called secondary IAH [6].
These developments, including increased awareness among both the surgical and critical care
specialists [10,11], and the birth of the World Society of the Abdominal Compartment Syndrome
(WSACS, www.wsacs.org) in 2004 in Noosa, Australia [12] have led to more published material being
available to clinicians. The WSACS has published the rst consensus denitions in IAH and ACS in 2006
and the rst guidelines for diagnosis and management of IAH/ACS in 2007, together with recommendations for future research [1315]. Just recently an update of these recommendations was made
using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system
for clinical practice guidelines developers in order to provide consistency in identifying and rating the
quality of available evidence and strength of management suggestions and recommendations [16]. This
was performed utilizing a consensus committee process convened by the WSACS before, during and
after the 5th World Congress on Abdominal Compartment Syndrome held in Orlando, Florida in August
2011.
Denitions
The new and updated WSACS denitions regarding IAH and ACS are summarized in Table 1 and will
be discussed in detail hereafter [16,17]. Since the standard treatment for ACS is still decompressive
laparotomy (DL), which leaves the patient with an open abdomen (OA), a new classication for OA
(modied after Bjorck et al.) was also proposed by the WSACS [18]. Although the physiopathology of
raised IAP in children is quite similar to adults, cut-off values for denitions and IAP measurement
technique are somewhat different and those denitions that were amended for pediatric use are listed
in Table 2 but will not be discussed herein [19].
Denition 1: IAP is the steady-state pressure concealed within the abdominal cavity.
Since the abdominal compartment is dened by a combination of rigid (the spine, rib cage and
bony pelvis) and semi-rigid borders (the muscular abdominal wall, the diaphragm and the pelvic
muscles), it is vulnerable to the development of raised compartmental pressure (CP), just like any
other identiable compartment in the human body [20]. The IAP is directly affected by the volume of
the solid organs or hollow viscera, the presence of ascites, blood or other space-occupying lesions
(such as tumors or a gravid uterus), and the presence of conditions that limit expansion of the
abdominal wall (such as circular burn eschars, obesity, tight closure, velcro belt, prone positioning or
ascites) [14].
251
Table 1
Denitions regarding intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) according to the 2006
and 2013 WSACS guidelines update (Adapted from Malbrain et al. [14] and Kirkpatrick et al. [16]).
Def
2006 Denitions
IAP is the steady-state pressure

concealed within the abdominal cavity.
APP MAP IAP
FG GFP PTP MAP 2*IAP
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 midaxillary line.
The reference standard for intermittent
IAP measurement is via the bladder
with a maximal instillation volume of
25 mL of sterile saline.
Normal IAP is approximately 5
7 mmHg in critically ill adults.
IAH is dened by a sustained or
repeated pathologic elevation of
IAP 12 mmHg.
IAH is graded as follows:
Grade I: IAP 1215 mmHg
Grade II: IAP 1620 mmHg
Grade III: IAP 2125 mmHg
Grade IV: IAP > 25 mmHg
ACS is dened as a sustained

IAP 20 mmHg (with or without an
APP < 60 mmHg) that is associated with
new organ dysfunction/failure.
Primary ACS is a condition associated
with injury or disease in the abdominopelvic region that frequently requires
early surgical or interventional
radiological intervention.
Secondary ACS refers to conditions that
do not originate from the abdominopelvic region.
Recurrent ACS refers to the condition in
which ACS redevelops following
previous surgical or medical treatment
of primary or secondary ACS.
2
3
4
6
7
10
11
12
Def
2
3
5
6
10
11
12
13
14
2013 Denitions
IAP is the steady-state pressure
concealed within the abdominal cavity.
APP MAP IAP
REJECTED
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 midaxillary line.
The reference standard for intermittent
IAP measurements is via the bladder
with a maximal instillation volume of
25 mL of sterile saline.
IAP is approximately 57 mmHg and
around 10 mmHg in critically ill adults.
IAH is dened by a sustained or
repeated pathologic elevation of
IAP 12 mmHg.
IAH is graded as follows:
ACS is dened as a sustained
IAP 20 mmHg (with or without an
APP < 60 mmHg) that is associated with
new organ dysfunction/failure.
Primary ACS is a condition associated
with injury or disease in the abdominopelvic region that frequently requires
early surgical or interventional
radiological intervention.
Secondary ACS refers to conditions that
do not originate from the abdominopelvic region.
Recurrent ACS refers to the condition in
which ACS redevelops following
previous surgical or medical treatment
of primary or secondary ACS.
NEW: A poly-compartment syndrome
is a condition where two or more
anatomical compartments have
elevated compartmental pressures.
NEW: Abdominal compliance quanties
the ease of abdominal expansion, is
determined by the elasticity of the
abdominal wall and diaphragm, and is
expressed as the change in intraabdominal volume per change in intraabdominal pressure in L/mmHg.
NEW: An open abdomen (OA) is any
abdomen requiring a temporary
abdominal closure due to the skin and
fascia not being closed after
laparotomy. The technique of
temporary abdominal closure should be
explicitly described.
(continued on next page)
252
Table 1 (continued )
Def
2006 Denitions
Def
2013 Denitions
15
NEW: The open abdomen is classied

with the following grading system:
1 No xation
1A: clean, no xation
1B: contaminated, no xation
1C: enteric leak, no xation
2 Developing xation
2A: clean, developing xation
2B: contaminated, developing
xation
2C: entero-atmospheric/cutaneous
stula, developing xation
3 and 4 Frozen abdomen
3: frozen abdomen, no stula
4: frozen abdomen with enteroatmospheric/cutaneous stula
16
NEW: Lateralization of the abdominal

wall refers to the phenomenon
whereby the musculature and fascia of
the abdominal wall, most well seen by
the rectus abdominis muscles and their
enveloping fascia, move laterally away
from the midline with time.
ACS: abdominal compartment syndrome.

APP: abdominal perfusion pressure.
FG: ltration gradient.
GFP: glomerular ltration pressure.
IAH: intra-abdominal hypertension.
IAP: intra-abdominal pressure.
MAP: mean arterial pressure.
OA: open abdomen.
PTP: proximal tubular pressure.
Denition 2: abdominal perfusion pressure (APP) MAP IAP.

Analogous to cerebral perfusion pressure (CPP), APP has been proposed as a more accurate predictor
of visceral perfusion and as an endpoint for resuscitation. APP, by considering both arterial inow
(mean arterial pressure (MAP)) and restrictions to venous outow (IAP), is statistically superior to
either parameter alone in predicting patient survival from IAH/ACS [2,21]. Retrospective analysis
showed that APP was superior to other common resuscitation endpoints in patients with elevated IAP
including arterial pH, base decit, arterial lactate, and hourly urinary output [22]. It seems prudent to
maintain APP above 60 mmHg, although hard prospective evidence for this statement is still lacking.
Table 2
Denitions regarding IAP for pediatric use according to the 2013 WSACS guidelines update (Adapted from Kirkpatrick et al [16]).
IAP measurement
Normal IAP
IAH
ACS
The reference standard for intermittent IAP measurement in

children is via the bladder using 1 mL/kg as an instillation volume
and a minimal instillation volume of 3 mL and a maximum
installation volume of 25 mL of sterile saline.
IAP in critically ill children is approximately 410 mmHg.
IAH in children is dened by a sustained or repeated pathological
elevation in IAP > 10 mmHg.
ACS in children is dened as a sustained elevation in IAP of greater
than 10 mmHg associated with new or worsening organ dysfunction
that can be attributed to elevated IAP.
For those items not mentioned in Table 2, the denitions of Table 1 apply also to children.
253
Denition 3: 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 midaxillary line.
IAP measurements are essential to the diagnosis of IAH/ACS as physical examination is notoriously
poor in identifying elevated IAP [23,24]. Studies also showed that the abdominal perimeter does not
correlate well with true IAP [25]. Several key principles must be followed to ensure accurate and
reproducible measurements [26]. Early studies using water manometers reported their results in cm
H2O while subsequent studies using electronic pressure transducers reported IAP in mmHg
(1 mmHg 1.36 cm H2O). This led to confusion and difculty in comparing studies [27]. IAP varies with
respiration and is most consistently measured at end-expiration.
Denition 4: The reference standard for intermittent IAP measurement is via the bladder with a
maximal instillation volume of 25 mL of sterile saline.
For an IAP measurement, the residual urine from the bladder is completely drained and the bladder
catheter is blocked, followed by instillation of 25 mL sterile saline after which the IAP can be measured.
Fig. 1 shows a home-made system that can be used to measure IAP. Multiple studies have demonstrated
that, for the bladder technique, instillation of volumes in excess of 25 mL may articially increase IAP,
leading to potentially erroneous measurements and inappropriate therapy [2830]. Recent studies
have suggested that volumes as low as 25 mL are sufcient [31].
Denition 5: Normal IAP is approximately 57 mmHg and around 10 mmHg in critically ill adults.
Normal IAP ranges from sub-atmospheric to zero mmHg but values from 5 to 7 mmHg have also
been reported [32]. From a physiological point of view sub-atmospheric values do not make sense in
supine critically ill mechanically ventilated patients using the midaxillary line as a zero reference point
and may rather reect a measurement error [33]. Morbid obesity or pregnancy may be associated with
asymptomatic IAP elevations of up to 15 mmHg, which are seemingly well tolerated due to their
chronic nature and generally occult effects [33,34]. Such levels, occurring acutely, however, can have
signicant pathophysiologic impact upon organ perfusion and result in organ dysfunction and/or overt
ACS. Recent abdominal surgery, sepsis, organ failure, and need for mechanical ventilation are all
associated with elevated IAP [3539]. The clinical importance of any IAP measurement must always be
assessed in view of the baseline IAP for the individual patient. Table 3 lists some well-recognized risk
factors for IAH/ACS, and this is an area of active research by the WSACS.
Denition 6: IAH is dened by a sustained or repeated pathologic elevation of IAP 12 mmHg.
Pathological IAP is a continuum ranging from mild, asymptomatic elevations in IAP to marked elevations in IAP with severe consequences on virtually all organ systems in the body. The exact IAP that
denes IAH has long been a subject of debate, however the majority of animal studies show that
visceral organ perfusion begins to decrease at an IAP of 1015 mmHg [20]. It is at this level that cardiac,
renal, hepatic, and gastrointestinal perfusion becomes compromised to the point that anaerobic
metabolism may ensue followed by organ dysfunction and failure.
Denition 7: IAH is graded as follows:
Patients with prolonged untreated elevations in IAP commonly manifest inadequate perfusion and
subsequent organ failure. The more severe the degree of IAH, the more urgent is the need to reduce the
254
pressure (either medically or surgically). Grading systems help to improve communication and
improve clinical research.
Denition 8: ACS is dened as a sustained IAP > 20 mmHg (with or without an APP < 60 mmHg)
that is associated with new organ dysfunction/failure.
ACS is best remembered as the presence of signicant IAH with new onset organ failure. Failure to
recognize and appropriately treat ACS is often fatal whereas prevention and timely intervention are
associated with marked improvements in organ function and patient survival. In contrast to IAH, ACS is
not graded, but rather is considered an all or nothing phenomenon. There are three different types of
ACS, which are listed below under denitions 911.
Fig. 1. Modied method for intrabladder pressure monitoring as described by Malbrain. Set-up: (a) Wash hands and follow universal
antiseptic precautions. (b) A Foley catheter is sterile placed and the urinary drainage system connected. (c) Using a sterile eld and
gloves, the drainage tubing is cut (with sterile scissors) 40 cm after the culture aspiration port after disinfection. (d) A ramp with 3
stopcocks (e.g. Manifold set, Pvb Medizintechnik Gmbh, a SIMS Trademark, 85614 Kirchseeon, Germany, REF: 888-103-MA-11; or
any other manifold set or even 3 stopcocks connected together will do the job) is connected to a conical connection piece (e.g.
Conical Connector with female or male lock tting, B Braun, Melsungen, Germany, REF: 4896629 or 4438450) at each side with a
male/male adapter (e.g. Male to Male connector piece, Vygon, Ecouen, France, REF: 893.00 or 874.10). (e) The ramp is then inserted in
the drainage tubing. (f) A standard intravenous (IV) infusion set is connected to a bag of 500 mL of normal saline or D5W and
attached to the rst stopcock. (g) A 60-mL syringe is connected to the second stopcock and the third stopcock is connected to a
pressure transducer via rigid pressure tubing. (h) The system is ushed with normal saline. (i) The pressure transducer is xed at the
symphysis or the thigh. (j) Connect the transducer to the monitor via the special pressure module and ensure a normal waveform on
the scope. (k) Select a scale from 0 to 20 or 40 mmHg. Method of measurement: (a) If the patient is awake, explain the procedure. (b)
If the patient is sedated, ensure good sedation. (c) Place the patient in a complete supine position. (d) Zero the pressure module at
the midaxillary line of the patient at the level of the iliac crest (mark for future reference) by turning the proximal stopcock on to the
air and the transducer. (e) At rest the 3 stopcocks are turned off to the IV bag, the syringe and transducer giving an open way for
urine to ow into the urometer or drainage bag, said otherwise the 3 stopcocks are turned on to the patient. (f) To measure IBP, the
urinary drainage tubing is clamped distal to the ramp-device and the third stopcock is turned on to the transducer and the patient
and off to the drainage system. (g) The third stopcock also acts as a clamp. (h) The rst stopcock is turned off to the patient and
on to the IV infusion bag, the second stopcock is turned on to the IV bag and the 60-mL syringe (i) Aspirate 2025 mL of normal
saline from the IV bag into the syringe. (j) The rst stopcock is turned on to the patient and off to the IV bag and the 2025 mL of
normal saline is instilled in the bladder through the urinary catheter. (k) The rst and second stopcock are then turned on to the
patient, and thus turned off to IV tubing and the syringe. (l) The third stopcock already being turned on to the transducer and
patient allows then immediate IBP reading on the monitor. Adapted from Ref. [26] with permission.
255
Table 3
Risk factors for the development of IAH and/or ACS according to the WSACS (Adapted from Malbrain et al. [14]).
Risk factors
Agea
Increased APACHE-II or SOFA scorea
Acidemiaa
Hypothermiaa
Coagulopathy
Sepsis/bacteremiaa
Shock or hypotensiona
Mechanical ventilationa
PEEP > 10 cm H2O or the presence of auto-PEEPa
Pneumonia
Major burns
Major traumaa
Massive uid resuscitation or positive uid balancea
Polytransfusiona
Liver dysfunction/cirrhosis with ascites
Intra-abdominal infection/abscessa
Peritonitis
Abdominal surgerya
Hemoperitoneum/pneumoperitoneum or intra-peritoneal uid collectionsa
Gastroparesis/gastric distention/ileusa
Volvulus
Obesity or increased body mass indexa
Intra-abdominal or retroperitoneal tumors
Increased head of bed anglea
Prone positioninga
Massive incisional hernia repair
Acute pancreatitisa
Damage control laparotomy
Laparoscopy with excessive ination pressures
Peritoneal dialysis
Where APACHE-II indicates Acute Physiology and Chronic Health Evaluation-II; PEEP, positive end-expiratory
pressure; and SOFA, Sequential Organ Failure Assessment.
a
Indicates primary literature support.
Denition 9: Primary ACS is a condition associated with injury or disease in the abdomino-pelvic
region that frequently requires early surgical or radiological intervention.
Primary ACS is characterized by acute or subacute IAH of relatively brief duration occurring as a
result of intra-abdominal pathology such as abdominal trauma (and lesions to spleen or liver), ruptured
abdominal aortic aneurysm, hemoperitoneum, acute pancreatitis, secondary peritonitis, retroperitoneal hemorrhage, or liver transplantation. It is most commonly encountered in the traumatically
injured or post-operative surgical patient.
Denition 10: Secondary ACS refers to conditions that do not originate from the abdomino-pelvic
region.
Secondary ACS is characterized by subacute or chronic IAH that develops due to extra-abdominal
pathology such as sepsis, capillary leak, major burns, or other conditions requiring massive uid
resuscitation [4043]. It is most commonly encountered in the medical or burn patient and can be
considered iatrogenic related to excessive crystalloid resuscitation [44]. Secondary IAH can be
considered as a frequent iatrogenic and thus avoidable problem. Recent studies show a relative
decrease in secondary ACS compared to primary ACS due to increased awareness [45].
Denition 11: Recurrent ACS refers to the condition in which ACS redevelops following previous
surgical or medical treatment of primary or secondary ACS.
256
Recurrent ACS is a redevelopment of ACS symptoms following resolution of an earlier episode of

either primary or secondary ACS. It may occur despite the presence of an open abdomen or as a new
ACS episode following denitive closure of the abdominal cavity. Recurrent ACS (formerly termed
tertiary IAH/ACS) is associated with high morbidity and mortality [4648].
Denition 12: A poly-compartment syndrome is a condition where two or more anatomical
compartments have elevated compartmental pressures.
A compartment syndrome (CS) is dened as an increased pressure in a closed anatomic space which
threatens the viability of enclosed and surrounding tissue [14]. Within the body there are 4 major
compartments among many: the head, the chest, the abdomen and the extremities. Within each
compartment, a CS can affect individual organs and the CS can be associated with different causal
disease states. The abdominal compartment has unique topographic properties because it is upstream from the lower extremities and down-stream from the chest. Therefore, it may inuence the
pathophysiology of these compartments. Scalea et al. was the rst to introduce the term multiple CS
(MCS) in a study of 102 patients with increased IAP, intrathoracic (ITP), and intracranial pressure (ICP)
after severe brain injury [49]. He suggested that different compartments within the body are not
isolated and independent entities but instead are closely connected. Because the term multi or multiple
CS is nowadays mostly used in relation to multiple limb trauma with CS needing fasciotomy, the term
poly-compartment syndrome (PCS) was nally coined in 2007 in order to avoid further confusion
[1,50]. Because of the clinical importance of diverse aspects of PCS, further classication in the future
seems warranted. First, PCS can either be primary or secondary or a combination of both, in view of the
potential effect on organ function [42]. A primary CS is dened as a pathological rise of CP in a
compartment due to physical tissue or organ injury within the compartment (i.e. intracranial hematoma or limb fracture). In secondary CS, there is no primary injury in the affected compartment and
symptoms are solely based on pressure transmission from one compartment to another (i.e. ACS that
develops following a tension pneumothorax) [51]. Different conditions precipitate the occurrence of
PCS: severe burns, massive uid resuscitation, severe sepsis, or prolonged hypotension.
Denition 13: abdominal compliance is a measure of the ease of abdominal expansion, and is
determined by the elasticity of the abdominal wall and diaphragm and is expressed as a change in
intra-abdominal volume per change in intra-abdominal pressure.
The abdominal compliance quanties the ease of abdominal expansion and is determined by the
elasticity of the anterior and lateral abdominal wall and to a smaller degree the diaphragm, whereas the
more rigid spine and pelvis only minimally if at all affect abdominal elasticity. The abdominal compliance
changes with changes in abdominal volume. It can be expressed as the slope on a volumepressure curve
and the slope will depend on its position on the abdominal volumepressure curve as explained further.
Denition 14: an open abdomen is any abdomen requiring a temporary abdominal closure due to
the skin and fascia not being closed after laparotomy. In order to facilitate research in this
controversial eld, the technical details regarding the type of temporary closure should be
explicitly stated.
The open abdomen continues to be variably dened, even in contemporary reviews, and surveys
even among trauma surgeons reveals confusion as to exactly what anatomy constitutes an open
abdomen [52]. Surveys asking this simple question have noted surprising confusion and disagreement
in regards to skin closure without fascial closure, or visceral containment with mesh interposition
between fascia with or without skin or soft-tissue closure.
Denition 15: The open abdomen is classied with the following grading system.
Planning to successfully and safely close any open abdomen must begin immediately after the
abdomen is rst left open. Clinical studies performed in this eld should address abdominal closure
257
rates considering the indications for open abdominal management, and compare abdominal closure
problems of similar difculty. This requires an open abdomen classication systems, two of which have
been previously proposed, by Swan and Banwell [53] and Bjorck et al. [18]. The WSACS recognizes two
critical complications which should be considered in managing an open abdomen; namely xation of
the abdominal contents to the abdominal wall, and the development of entero-atmospheric stulae
(EAF). The classication of Bjorck was therefore amended to reect this hierarchy of challenges to the
patient and this is listed below.
1 No Fixation
1A: clean, no xation
1B: contaminated, no xation
1C: enteric leak, no xation
2 Developing Fixation
2A: clean, developing xation
2B: contaminated, developing xation
2C: entero-atmospheric/cutaneous stula, developing xation
3 and 4 Frozen Abdomen
3: frozen abdomen, no stula
4: frozen abdomen with entero-atmospheric/cutaneous stula
Denition 16: Lateralization of the abdominal wall refers to the phenomenon whereby the
musculature and fascia of the abdominal wall, most well seen by the rectus abdominis muscles and
their enveloping fascia, move laterally away from the midline with time.
There are many recognized complications of the open abdomen such as entero-atmospheric
stulae; heat, uid, and protein losses; catabolism; and increased nursing resources; among many
others. However, loss of domain, wherein the peritoneal contents no longer reside naturally within the
connes of the abdominal wall, may be an overlooked concern. Although not well studied or reported,
this phenomenon is increasingly being understood as both inuencing the degree of complexity
involved in abdominal wall reconstruction, and as an undesirable outcome that temporary abdominal
closures aim to avoid [54].
Pathophysiology of increased IAP
At normal physiological conditions with normal abdominal volumes, any additional predened
abdominal volume will only minimally increase IAP. However, when the abdominal volume is already
increased as in IAH grade III and above, the same abdominal volume will now signicantly increase IAP.
A reduced abdominal compliance implies that any change in volume increase will result in a greater
change in IAP, as found in patients with abdominal burn eschars, tight closure following abdominal
surgery, or generally in those with high grade IAH. A compliant abdomen, however, indicates greater
tolerance to changes in IAV as seen in the elderly patient with loss of elastic recoil of the abdominal
wall, women after childbirth, or in the obese after weight loss. Some studies also reported a decrease in
abdominal compliance with age [55,56]. Abdominal compliance should be expressed in L/mmHg. The
relation between pressure and volume can be expressed by the analysis of pressure volume (P/V)
curves. In analogy with the respiratory system the abdominal compliance (Cabd) is calculated by the
change in volume over the change in pressure DV/DP or thus:
Cabd DIAV=DIAP
ElastanceE 1=Cabd
The relation between abdominal volume and abdominal pressure is curvilinear with an initial linear
part followed by an exponential increase once a critical volume is reached. Fig. 2 shows abdominal P/V
curves in a patient with good and poor abdominal compliance. The Cabd can be estimated by looking at
258
60
IAP (mmHg)
50
40
30
IAP
20
IAV
10
IAP
0
0
10
Abdominal Volume (L)

Fig. 2. Pressurevolume curves of the abdominal compartment. Abdominal pressure volume curves in a patient with low abdominal
compliance (closed squares) and normal compliance (open circles). The compliance is respectively 133 mL/cm H2O versus 400 mL/
cm H2O for the same change in IAV from 4 to 6 L.
the changes in IAP during respiration: a low Cabd is characterized by large respiratory swings and this
could help to identify patients at risk for the detrimental effects associated with IAH or ACS (Fig. 3). The
observed respiratory variations are dependent on the respiratory setting and the tidal volume excursions (DIAV or DTV).
DIAP IAPei IAPee

DIAP DIAV=Cab
or Cab DIAV=DIAP
Cab DITV=DIAP
Epidemiology
As stated above, when intra-abdominal volume (IAV) increases, the compliant abdominal wall will
initially expand, keeping IAP constant over a relatively wide range of IAV [20]. However, when
abdominal wall expansion has reached its maximum, or when abdominal compliance is impaired by
internal (e.g. edema) or external (e.g. restrictive bandages or sutures) causes, any increase in IAV leads
to a rapid increase in IAP. Therefore, any condition associated with increased IAV, decreased abdominal
Fig. 3. Respiratory variations in abdominal pressure. Continuous intra-abdominal pressure (IAP) tracing obtained with CiMON
balloon tipped gastric catheter. Note the respiratory variations. Depending on the respiratory settings (tidal volume, respiratory rate,
inspiratory and the amount of positive end-expiratory pressure) the endinspiratory (IAPei) and end-expiratory (IAPee) values will
vary. The difference between IAPei and IAPee or DIAP is dependent on the respiratory settings, baseline IAP and Cab.
259
compliance or a combination of both, can lead to the development of IAH and/or ACS. The WSACS has
published a list of risk factors, which are partly supported by literature data and partially based on
physiopathological common sense [14]. A modied version of the WSACS risk factor list is presented in
Table 3, and work is continuing in this area.
The incidence of overt ACS, and specically primary ACS, seems to be decreasing, as concepts
like damage control surgery and prophylactic use of the OA have found their way into routine
surgical management of critical abdominal trauma or injury. Furthermore, damage control
resuscitation practices emphasizing enhanced ratios of plasma to red blood cells and moderate
crystalloid uids appears to be helping reduce the incidence of ACS after trauma [57]. However, if
not vigilant, aggressive uid resuscitation for sepsis, burns and trauma, can lead to an increased
incidence of IAH, and especially secondary IAH. Even very recently, incidences for IAH in the
critically ill have ranged from about 25% in the general ICU population [2] to up to about 7585% in
patients with septic shock [38,58]. This is a worrying situation since the mortality of secondary IAH
is even higher than that of primary IAH [45]. One of the most critical factors in the development of
secondary IAH seems to be the iatrogenic effect of massive uid resuscitation [44]. In some
populations e.g. post-operative patients after major abdominal surgery, a direct correlation between uid balance and IAP was found [59]. Better targeting of uid resuscitation and control over
uid balance currently offer the best hope for lowering the incidence of IAH in critically ill patients
[60].
The effect of IAH on organ function
IAH affects multiple-organ systems in a graded fashion. In order to better understand the clinical
presentation and management of IAH, one must understand the physiologic derangements within each
organ system separately [61]. It is beyond the scope of this review to discuss in depth the pathophysiologic implications of raised IAP on each end-organ function within and outside the abdominal
cavity, we refer to other publications covering these topics more extensively [6264].
Briey however, increased IAP leads to organ dysfunction of all abdominal organs due to
compromise of arterial blood ow, venous outow obstruction and impaired microcirculatory ow.
Kidney failure is the most often and consistently described organ failure associated with IAH, but
hepatic, adrenal and gastrointestinal dysfunction has also been reported repeatedly [20,65]. It is
especially important to note that IAH can lead to increased bacterial translocation lending truth to the
adagio the gut is the motor of sepsis [66].
Neurologic function
Acute IAH causes an increase in intracranial pressure (ICP) due to augmentation in pleural pressure
and impediment of venous return. The increased thoracic pressure leads to increased central venous
pressure (CVP), increased intrajugular pressure, impaired venous outow from the brain and increased
intracranial pressure (ICP). This association between IAP and ICP is important to consider when
treating patients with IAH at risk for brain injury [49]. The CPP will decrease due to a functional
obstruction of cerebral venous outow caused by the increased intrathoracic pressure (ITP) due to the
cranial displacement of the diaphragm in combination with a reduced systemic blood pressure as a
result of decreased preload and cardiac output (CO) [6774]. Cerebral blood ow and jugular bulb
saturation will decrease [75,76].
Cardiovascular function
The impact of IAH on the cardiovascular system is multifactorial. Cranial displacement of the diaphragm leads to direct compression of the heart and decreased contractility, while compression of the
systemic arterial circulation causes increased afterload, and decreased venous return from the lower
half of the body due to compression of the inferior vena cava. All these changes usually lead to
decreased cardiac output, which may temporarily be augmented by uid loading (although this in turn
can lead to further increased IAP) [77]. When IAP rises above 10 mmHg cardiac output (CO) drops
260
[7881]. Mean arterial blood pressure may initially rise due to shunting of blood away from the
abdominal cavity but thereafter normalizes or decreases [82,83]. Within this respect volumetric preload monitoring may be superior to the use of traditional barometric lling pressures [77]. This is
related to the abdominothoracic pressure transmission [1,20]. When IAP is increased, the diaphragm is
displaced upward and part of the IAP increase is transmitted to the thorax. This leads to an increase in
all intrathoracically measured pressures (such as CVP and pulmonary artery occlusion pressure (PAOP))
if transmural pressures are not considered [1].
Pulmonary function
The interactions between the abdominal and the thoracic compartment pose a specic challenge to
the ICU physician [84]. Both compartments are linked via the diaphragm as stated above and on
average a 50% (range 2580%) transmission of IAP to the ITP has been noted in previous animal and
human studies [1,81,85,86]. Patients with primary ACS will often develop a secondary acute respiratory
distress syndrome (ARDS) and will require a different ventilatory strategy and more specic treatment
than a patient with primary ARDS [87,88]. ACS results in a reduction of the functional residual capacity
(FRC).
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
only moderately elevated IAP of 10 mmHg [89,90]. Furthermore acute liver failure, decompensated
chronic liver disease and liver transplantation are frequently complicated by IAH and the ACS
[91,92].
Renal function
Elevated IAP signicantly decreases renal artery blood ow and compresses the renal vein
leading to renal dysfunction and failure [93]. Oliguria develops at an IAP of 15 mmHg and anuria at
25 mmHg in the presence of normovolemia and at lower levels of IAP in the patient with hypovolemia or sepsis [94,95] It should not be surprising, therefore, that decreased renal function, as
evidenced by development of oliguria, is one of the rst visible signs of IAH. An increasing number
of large clinical studies have identied that IAH (15 mmHg) is independently associated with
renal impairment and increased mortality [35,9698]. The etiology of these changes is not entirely
well established, however it may be multifactorial: reduced renal perfusion, reduced
cardiac output, increased systemic vascular resistance and alterations in humeral and neurogenic
factors.
Gastrointestinal function
Intra-abdominal hypertension has profound effects on splanchnic organs, causing diminished
perfusion and mucosal acidosis, setting the stage for multiple-organ failure [99]. The pathologic
changes are more pronounced after sequential insults of ischemia-reperfusion and IAH. It appears that
IAH and ACS may serve as the second insult in the two-hit phenomenon of the causation of multipleorgan dysfunction syndrome [41,99102].
Abdominal wall and endocrine function
Increased IAP has been shown to reduce abdominal wall blood ow by direct, compressive effects
leading to local ischemia and edema [103]. This can decrease abdominal wall compliance and exacerbate IAH [104]. Abdominal wall muscle and fascial ischemia may contribute to infectious and noninfectious wound complications (e.g., dehiscence, herniation, necrotizing fasciitis) often seen in this
patient population.
261
IAP monitoring
Since clinical examination has proven to be unreliable, accurate and reproducible IAP measurement
is crucial in the management of patients with IAH and ACS [24]. Although the IAP can easily be
measured at the bedside with simple tools, care should be taken to avoid common pitfalls. Theoretically, IAP can be measured intermittently or continuously, directly in the peritoneal cavity or indirectly
through hollow viscera, most frequently the bladder or the stomach [26]. The WSACS recommends
routine measurement of IAP through the bladder in critically ill or injured patients when any known
risk factor for IAH/ACS is present [14,16]. The level of evidence for this recommendation is low, but
since adverse effects are not reported and unlikely to occur and the information obtained has the
potential to inuence patient care, it was retained as a strong recommendation in the 2013 consensus
conference [16].
Currently, the most adopted form of IAP monitoring involves intermittent IAP measurement
through the bladder every 46 h using no more than 25 mL of instillation volume (Fig. 1), starting when
at least one risk factor (Table 3) for IAH is present, until the risk factor(s) are resolved and IAP has
remained normal for 2448 h [66]. Gastric IAP measurement techniques are mainly used when the
bladder is not available for catheterization, a localized increase in pelvic pressure is suspected (e.g. due
to a pelvic hematoma), or monitoring of the upper abdominal compartment is deemed useful (e.g. in
severe acute pancreatitis or after liver surgery) [105].
Some points need to be taken into account regarding IAP measurement
Zero reference level. Most of the techniques to monitor IAP use uid lled systems
for pressure transduction. Correct calibration of the transducer is of paramount importance
for reliable IAP measurement. It is advisable to indicate the zero level on the patient at the
level of the midaxillary line and the transducer should be zeroed before each IAP
measurement
Positioning of the patient. The patient should be put in the supine position for IAP measurement.
Measuring IAP with the head of bed (HOB) elevated leads to higher values. In some patients, it may
be contraindicated to change the body position - in these cases IAP can be measured with the head
of bed elevated, but the classical thresholds for IAH and ACS will not apply.
The awake patient. In awake patients, IAP monitoring is challenging as spontaneous breathing as
well as abdominal muscle contractions (notably after abdominal surgical procedures) can inuence the IAP reading obtained. This can lead to falsely elevated values.
The chronic obstructive pulmonary disease (COPD) patient. In case of forced expiration or
increased abdominal muscle tension. The IAP at end-expiration will be falsely increased, thus
overestimating true IAP [106].
Intra-abdominal space-occupying lesions. The presence of intrapelvic mass lesions such as hematomas in patients with pelvic fractures or spontaneous hemorrhages in the rectus abdominis or
iliopsoas muscle may compress the bladder and lead to falsely elevated IAP values.
Gastric route. When measuring IAP via the stomach, it is important to consider temporary elevations due to the migrating motor complex. Intrathoracic position of the balloon can be excluded
from the analysis of the waveform. When looking at gastric pressure tracings one can also observe
cardiac rhythm artefacts.
Abviser Autovalve When using the Abviser kit with the Autovalve (ConvaTec Medical, USA), be
aware that the valve opens automatically after 60120 s, readings beyond that timepoint will
underestimate IAP.
Foleymanometer. When using the FoleyManometer (Holtech, Denmark), make sure that the
amount of uid in the tubing is adequate, in oliguric patients this may not be the case. Insufcient
volume may lead to underestimation of the IAP.
Obesity. Patients with higher body mass index (BMI) have chronically elevated IAP. This seems to
be tolerated better. Other thresholds for IAH and ACS may be applicable.
Children. Normal IAP is lower in children. Other thresholds for IAH and ACS apply as stated in the
WSACS consensus denitions.
262
Infusion volume (intravesicular measurement). Installation of volumes larger than 20 mL saline

carries an inherent risk of overestimation of IAP.
Chronic dialysis. In patients under chronic dialysis and anuria, bladder compliance may be
decreased so that instilling even a small amount into the bladder may overestimate IAP Although
these differences usually are small, they can be clinically signicant.
Infusion temperature (intravesical measurement). Avoid using cold uids as this may cause
bladder detrusor contraction and elevated intravesicular pressure measurements
Frequency of IAP measurement. IAP may rapidly change in critically ill patients, most importantly
in patients with primary IAH/ACS. When IAP is only measured once or twice a day, these changes
may go unnoticed or only diagnosed at a late stage. IAP measurement every 4 h or more frequently
in unstable patients is recommended.
Risk of urinary tract infection. Instillation of saline in the bladder has not been associated with
increased incidence of urinary tract infection [107,108].
Management of IAH/ACS
Since the modern revival of ACS as a real concern in critically ill or injured patients, surgery (DL) has
been considered the ultimate treatment. Initially, when overt primary ACS was the only clinical entity
considered, DL was even considered the only treatment option, even though outcomes were poor in
terms of mortality [109]. Over the years, as focus shifted toward earlier and more moderate stages of
increased IAP (mostly secondary IAH), more attention was diverted into looking for non-invasive
techniques to decrease IAP [110]. This has led to publication of a medical management algorithm by
the WSACS to be used at the bedside (Fig. 4) [111]. The management of patients with IAH is based on the
following 4 principles: 1) specic procedures to reduce IAP and the consequences of IAH/ACS; 2)
general support and medical management of the critically ill patient; 3) surgical decompression and 4)
optimization after surgical decompression.
Medical management
Keeping in mind the mechanisms through which IAH develops, it is evident that IAP can be
lowered by decreasing IAV, increasing abdominal compliance or combining both. The WSACS
medical management algorithm is essentially a collection of non-invasive techniques that were
proposed to reach these goals after small clinical studies or based on physiopathological rationale,
organized into ve major categories, reecting the columns of the algorithm [110]: 1) improvement of abdominal wall compliance; 2) evacuation of intraluminal contents; 3) evacuation of
abdominal free uid collections; 4) correction of capillary leak and positive uid balance; 5)
specic treatment to support end-organ function. This stepwise approach recognizes the contributions of: 1) excessive uid (especially crystalloid) administration on visceral edema and ascites
formation; 2) inadequate sedation and analgesia of abdominal and thoracic wall muscular tone; 3)
space-occupying lesions in the abdominal cavity (including the enterally nourished intestine and
gas lled colon); and 4) the role of myocardial contractility and its assessment by ow-based
volumetric monitoring in the genesis and management of IAH and the evolution of the ACS in
at-risk patients [112].
The algorithms efcacy is largely dependent on its users knowledge and experience. The evidence
supporting many of the techniques is low at best. The 2013 consensus statement made weak recommendations for using a protocol to avoid sustained IAH, using sedation and analgesia for pain and
anxiety relief in critically ill patients, brief trials of neuromuscular blockers for patients with IAH,
consideration of body position in patients with IAH, gastric or colonic decompression using tubes for
patients with gastric or colonic dilatation and IAH and the use of neostigmine for established refractory
colonic ileus in patients with IAH, all based on low quality and quantity of evidence [16]. A weak
recommendation was made to try to avoid a positive cumulative uid balance in critically ill patients
with, or at risk of, IAH, after the acute resuscitation has been completed and the inciting issues/source
control have been addressed [113]. The WSACS also suggested that an enhanced ratio of plasma/packed
263
Fig. 4. Medical management algorithm (www.wsacs.org).
red blood cells should be used for resuscitation of massive hemorrhage versus low or no attention to
plasma/packed red blood cell ratios [16]. Paracentesis or percutaneous catheter drainage (PCD) is
another minimally invasive procedure frequently advocated for treatment of IAH and evaluated by the
consensus conference [114]. The WSACS eventually made a weak recommendation to use PCD to
remove uid (in the setting of obvious intra-peritoneal uid) in those with IAH/ACS when this is
technically possible compared to doing nothing [16]. The WSACS also suggests that PCD be used to
remove uid (in the setting of obvious intra-peritoneal uid) in those with IAH/ACS when this is
technically possible compared to immediate DL, as this may alleviate the need for DL. Both
264
recommendations were again based on low quality evidence [16]. The WSACS consensus conference
was not able to make any recommendations on using APP as a resuscitation target, the use of diuretics
to mobilize uids, the use of renal replacement therapy (RRT) to mobilize uid or administration of
albumin to mobilize uids, due to lack of evidence [16].
Some of the measures described in the algorithm are not designed to decrease IAP, but to optimize
general ICU management of patients with IAH/ACS [115]. Especially hemodynamic management
should be adapted to the increased IAP in patients with IAH. To assess the true cardiac preload status,
the transmural CVP can be calculated as the CVP minus half the IAP (in view of the average
abdominothoracic index of transmission of 50%). An alternative strategy is to use volumetric monitoring, using parameters like left ventricular end-diastolic area index (LVEDAI) or right ventricular or
global end-diastolic volume index (RVEDVI or GEDVI), that have shown to be less affected by IAH [77].
Due to increased ITP, IAH can mimic a state of increased uid responsiveness with increases in stroke
volume variation and pressure variation [116]. Although uid loading can be used temporarily to
correct this state, it can also exacerbate IAH. In the setting of IAH therefore new thresholds of stroke
volume variation (SVV) and pulse pressure variation (PPV) need to be used to guide resuscitation [116]
and nally one must also bear in mind that IAH can lead to a false negative passive leg raising test
[117,118].
Since the abdominothoracic pressure transmission causes decreased chest wall compliance,
while lung compliance remains mostly constant [84,119] higher ventilation pressures (transpulmonary pressure plateau pressure minus half of IAP) will be required in the presence of IAH to
recruit the lungs. Furthermore, higher than normal positive end-expiratory pressure (PEEP) is recommended to preserve alveolar recruitment and some studies suggest to set the PEEP at the level of
IAP [120,121].
Surgical management
When the different options contained in the medical management algorithm have been
exhausted and the IAP is still critically elevated, surgery becomes unavoidable. Decompressive
laparotomy (DL) through a midline incision from xiphoid to symphysis is still the most standard
approach to abdominal decompression. Dramatic improvement in organ function and immediate
decrease in IAP after DL have been reported consistently. However, DL is associated with a high risk
of complications and mortality remains high and around 50% [109]. In order to address these issues
some less invasive surgical techniques were developed, most notably subcutaneous linea alba fasciotomy (SLAF) [122]. Performing a DL leaves the patient with an open abdomen and several
techniques have been suggested for temporary abdominal closure (TAC) [20]: 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 intestinal stulas. The Bogota bag is a plastic sheet cut from a sterile 3 L irrigation
bag, and sewn to the skin or fascia [123]. This system is cheap and offers the advantage that the
bowel and abdominal contents can be easily inspected and accessed, but uid losses are difcult to
control, which makes it a real challenge to the nursing staff. Towel clip closure is sometimes used as
an initial method of TAC after damage control surgery, because of the speed of closure. After reexploration, it can be replaced by other techniques, like removable prosthetic meshes that have
been used initially in open abdomen treatment for intra-abdominal sepsis, but can be used for TAC
in other circumstances as well. Examples are the zippers, Wittman patch (which uses a Velcro
closure system), etc. Recently, the use of negative pressure wound therapy (NPWT) has changed
open abdomen management signicantly [110]. NPWT offers easy control and quantication of uid
losses.
During the intervention specic anesthetic challenges need to be solved and after decompression
the patient is at risk for ischemia-reperfusion injury, venous stasis and fatal pulmonary embolism
[124]. Treatment with NPT dressings specically designed for use in the abdominal cavity seems to
cause less typical complications associated with TAC. There even seems to be an added effect that NPT
can successfully remove inammatory cytokines along with peritoneal uid from the peritoneal space,
leading to lower cytokine levels, both in peritoneal uid and in plasma [125] and maintaining adequate
preload and APP is the key to success [22,82,126]. Open abdomen treatment (or laparostomy) was
265
initially intended for patients with diffuse intra-abdominal infections, and often used in combination
with a planned relaparotomy approach. Due to the increased awareness of the deleterious effects of
intra-abdominal hypertension, open abdomen treatment, either prophylactic or therapeutic, is more
common in the ICU [41,127].
The WSACS 2013 consensus recommendations made a strong recommendation to use NPT in
critically ill patients with an open abdomen, based on low grade evidence [16]. It is important to note
that there is no evidence comparing various types of NPT (commercially available versus home-made,
different types of commercially available NPT dressings) while they may have signicantly different
outcomes.
Even though currently the evidence base for both surgical and medical management of IAH/ACS is
weak, Cheatham and Safcsak have shown that a global approach, including prophylactic use of the
open abdomen, early abdominal decompression, negative pressure therapy and the medical management algorithm, in the hands of experienced clinicians, can achieve better outcomes in terms of
primary closure rates, time to closure and even survival [110]. By using this approach secondary IAH/
ACS (being an iatrogenic and thus potentially avoidable condition) will probably cease to exist in the
near future [128].
Practice points
The abdomen is a closed anatomical space, with the abdominal contents being primarily uid
in character, hence following Pascals law that can be interpreted as stating that any change in
pressure applied at any given point of the uid is transmitted undiminished throughout the
uid so that IAP can be measured via different (in)direct routes.
The diagnosis of IAH/ACS relies on accurate IAP measurement. The current gold standard for
IAP measurement is intermittently every 46 h via the bladder, using no more than 25 mL of
instillation volume, in the complete supine position, using the midaxillary line as a zero
reference point.
IAP monitoring should be performed in all critically ill or injured patients exhibiting one or
more risk factors for the development of IAH and continued until risk factors are resolved and
IAP has remained normal for 2448 h.
The intra-abdominal volume (IAV) will exert a certain intra-abdominal pressure (IAP) on the
compartment walls that will be mainly determined by the compliance of the abdominal wall
(Cab) and the relation between IAV and IAP is curvilinear with an initial linear part followed
by an exponential increase once a critical volume is reached.
IAH and ACS cause organ dysfunction through direct compression of the heart, compression
of both arterial and venous perfusion of the abdominal organs and abdominothoracic
pressure transmission. All organ systems in the human body are affected by IAH induced
injury.
The WSACS medical management algorithm contains a number of minimally invasive techniques aimed at decreasing IAP and sustaining adequate systemic and regional perfusion,
which can be applied in a stepwise fashion until IAP is decreased. The current evidence to
support these techniques is rather low, but since there are no reports on adverse effects and
there is a possible therapeutic benet, some of them were retained as weak recommendations by the 2013 WSACS consensus guidelines.
Standard surgical treatment of established ACS not responding to non-invasive management
consists of DL via midline or transverse incision. Promising alternative surgical strategies like
subcutaneous linea alba fasciotomy (SLAF) are being developed to avoid the complications of
the open abdomen. Prophylactic OA treatment is currently only recommended for trauma
damage control surgery. Critically ill patients with an OA are preferentially treated with NPT.
266
Research agenda
Large epidemiologic studies are needed to validate the different risk factors that have been
associated with IAH and ACS in the past
The merits of continuous IAP monitoring need to be assessed as compared to intermittent IAP
monitoring
The impact of head of bed position on baseline IAP values needs to be put into relation to
morbidity and mortality
Future interventional studies should look at the impact of the medical management treatment algorithm on the incidence of ACS and subsequent morbidity and mortality
Randomized studies are needed to compare prophylactic open abdomen with active drainage
versus closed abdomen with passive drainage in patients with abdominal sepsis needing
surgical exploration
The relation between a positive cumulative uid balance and IAH needs to be assessed
prospectively
Acknowledgements
MLNG Malbrain is member of the medical advisory board of Pulsion Medical Systems (Munich,
Germany), a monitoring company. Parts of this article were based on the open access 2013 revised
consensus denitions paper, published under CC BY Licence, doi: 10.1007/s00134-013-2906-z [16]. For
further reading we refer to the full consensus denitions paper (http://www.ncbi.nlm.nih.gov/pmc/
articles/PMC3680657/) and online electronic supplemental material (http://link.springer.com/article/
10.1007/s00134-013-2906-z). Other parts were adapted from the recent book: Malbrain MLNG, De
Waele J: Core Critical Care Series: Intra-abdominal hypertension. Edited by Vuylsteke A. Cambridge:
(ISBN-13: 9780521149396) Cambridge University Press; 2013.
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Best Practice & Research Clinical Anaesthesiology 27 (2013) 249270

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Best Practice & Research Clinical

Intra-abdominal hypertension: Denitions,

* Corresponding author. Fax: 32 3 2177574.

IAP is the steady-state pressure

ACS is dened as a sustained

NEW: The open abdomen is classied

NEW: Lateralization of the abdominal

ACS: abdominal compartment syndrome.

Denition 2: abdominal perfusion pressure (APP) MAP IAP.

The reference standard for intermittent IAP measurement in

Recurrent ACS is a redevelopment of ACS symptoms following resolution of an earlier episode of

Abdominal Volume (L)

DIAP IAPei IAPee

Infusion volume (intravesicular measurement). Installation of volumes larger than 20 mL saline

Fig. 4. Medical management algorithm (www.wsacs.org).

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