Australian Critical Care (2008) 21, 18—28

A critical care nurse’s guide to intra abdominal

hypertension and abdominal compartment
syndrome
Penny Spencer RN, BN, Postgraduate Diploma Critical Care, MNSc a,∗,
Leigh Kinsman RN, BN, HDepCert, MNSc, PhD Candidate b,
Kim Fuzzard RN, CCCert, MNStud, GradCertClinEd(Nurs) c

a ANUM Critical Care Unit, Bendigo Health, P.O. Box 126, Bendigo, Vic 3552, Australia
b School of Rural Health, Monash University, Bendigo, Australia
c Bendigo Health, Bendigo, Australia

Received 15 June 2007 ; received in revised form 23 October 2007; accepted 30 October 2007

KEYWORDS Summary Abdominal compartment syndrome (ACS) is a life-threatening syndrome

Intra abdominal that is increasing in incidence amongst critically ill patients. A 2005 survey of critical
pressure; care nurses revealed that there were recognised knowledge deficits of ACS amongst
Intra abdominal surveyed nurses. The purpose of this review is to inform critical care nurses about
hypertension; ACS and its antecedent, intra abdominal hypertension (IAH). Detection techniques,
Abdominal compartment causes, clinical manifestations and pathophysiology of IAH and ACS will be outlined
and medical and nursing management will be reviewed.
syndrome;
The incidence of ACS is reported to be up to 35% in the intensive care population
Critical care;
with reduced survival when compared to other intensive care patients. Physiological
Nursing care
changes that occur with ACS include compromise to the cardiovascular, respiratory,
renal and neurological systems and development of metabolic acidosis. Management
may incorporate percutaneous drainage of ascitic fluid, use of muscle relaxants,
prone positioning and surgical intervention to open, decompress and gradually close
the abdomen. Throughout this care the critical care nurse should ensure accurate
monitoring of organ function, assessment for recurrence of ACS as well as the amount
and type of drainage, appropriate wound management and provision of physical and
psychosocial support of the patient. These aspects of care have the potential to
impact significantly on patient outcome.
Crown Copyright © 2007 Published by Elsevier Australia (a division of Reed
International Books Australia Pty Ltd) on behalf of Australian College of Critical
Care Nurses Ltd. All rights reserved.

∗ Corresponding author. Tel.: +61 3 5454 7927; fax: +61 3 5454 7931.
E-mail address: aphjs@homail.com (P. Spencer).

1036-7314/$ — see front matter. Crown Copyright © 2007 Published by Elsevier Australia (a division of Reed International Books Australia Pty Ltd) on behalf of Australian College of Critical Care Nurses Ltd. All rights reserved.

doi:10.1016/j.aucc.2007.10.005
A critical care nurse’s guide to IAH and ACS
Background
Abdominal compartment syndrome (ACS) is diag-
nosed when there is a sustained intra abdominal
hypertension (IAH) of >20 mmHg with single or
multiple organ dysfunction that was not previ-
ously present.1 Mortality and morbidity rates are
extremely high when patients develop ACS, and
recognition and treatment are time critical.2,3
While the cause of IAH can vary and the degree
of organ dysfunction can differ from patient to
patient, it is the effect of decreasing blood flow
and increasing pressure on abdominal organs and
surrounding organs that creates the end organ dys-
function which defines ACS. ACS is characterised by
a silent physiological derangement and can easily
be overlooked or misinterpreted. While the patient
with ACS remains undiagnosed or untreated their
risk of death is high.4
Critical care nurses at the bedside need to be
knowledgeable and vigilant in the care of patients
that are considered high-risk for ACS. Regular
assessments of intra abdominal pressure (IAP) and
organ function allow critical care nurses to antici-
pate and be prepared for appropriate intervention.
A 2005 survey of Australian critical care nurses
(n = 582) revealed that the majority of nurses sur-
veyed (n = 356; 61.2%) perceived their knowledge of
ACS to be minimal or nil.1 The survey also revealed
a significant knowledge deficit in regard to clinical
manifestations of ACS and patient groups at risk.5,6
This paper seeks to inform critical care nurses of the
existence of IAH and ACS, to outline the patients
at risk, the means of diagnosing ACS and to give
an overview of the management of these complex
patients.
Intra abdominal pressure
Normal values of IAP are considered to be close to
atmospheric pressure, represented as 0—5 mmHg.
Consensus definitions propose IAH as an IAP greater
than 12 mmHg,1,7,8 but there is much debate in
the literature regarding the point at which IAH
becomes pathological. Cheatham et al.9 state the
range in which definitive treatment is needed is
20—25 mmHg as there is a high incidence of mor-
tality associated with patients with an IAP of
>25 mmHg.8 However, whilst many patients are
reported to have profound clinical derangement
with an IAP of 20 mmHg others are asymp-
tomatic. Individual physiology and co-morbidities
may impact on the patient’s tolerance of IAH.10
This makes a global IAP threshold difficult to
apply.8,9
19
Incidence of intra abdominal
hypertension and abdominal
compartment syndrome
There are varying reports of the incidence of IAH
in medical and surgical ICU patients, with ranges of
20—32% in ICU populations.11—13 The actual rate of
progression to ACS is not clear and ACS is variously
reported to occur in 5—35% of the ICU population.13
This may reflect varying levels of detection rather
than incidence.
ACS is believed to be increasingly prevalent
amongst ICU patients today, for two main reasons.
Firstly, critically ill patients are now supported
with improved techniques and equipment in inten-
sive care settings long enough for ACS to develop
and warrant treatment.11,14 Secondly, increas-
ing knowledge of ACS has aided in increased
recognition.11
Measuring intra abdominal pressure
In the past it has been suggested that clinical
abdominal assessment of IAP including monitor-
ing for distended abdomen would reliably identify
IAH,15,16 however, this method has been found to be
erroneous.17 Kirkpatrick et al.17 conducted a study
comparing the sensitivity of abdominal assessment
with bladder pressure measurement in 42 adult ICU
patients. Each patient had a physical assessment
of the abdomen and simultaneous bladder pressure
measurement. The levels of IAP were considered
abnormal if they exceeded 15 mmHg. The study
demonstrated the sensitivity of abdominal assess-
ment in diagnosing IAH was considered to be too
low at 40%. Sugrue et al. conducted a similar study
which supported the findings of Kirkpatrick (sensi-
tivity 60%).18 Therefore, from both these studies
the validity of the abdominal assessment alone in
determining IAH now appears to be in serious doubt.
Intra abdominal pressure can be measured by
many methods via direct or indirect means. Direct
measurements involve using an intra peritoneal
cannula or measuring inferior vena cava pressures
via a femoral venous line. There is a close correla-
tion between the IAP and inferior vena cava (IVC)
pressure.19 Other indirect measurements involve
intra gastric and rectal pressure methods. With
use of an intra gastric tube, water is instilled into
the stomach and the pressure within the abdomi-
nal compartment measured within the stomach via
the use of a manometer or pressure transducer and
monitor. The rectal pressure measurement can be
achieved with the use of a tube that sits 10 cm
above the anal verge.19 The pressure measurement
20 P. Spencer et al.

Figure 1 Description of the procedure to measure IAP via the bladder8,10,19 .

is again achieved with the use of a manometer or
monitoring equipment. Due to difficulties of acces-
sibility, reproducibility and iatrogenic risks, these
methods are not regarded as the current best prac-
tice.
The bladder pressure method is described as
the gold standard and is the most reliable mea-
surement of IAP via indirect means.4,11,14,16,20—23
With the use of a manometer or monitoring equip-
ment a pressure measurement can be achieved to
establish a reflection of IAP. It is reliable, sim-
ple and widely accepted.2,4,19,21,23 The bladder is
considered as an excellent vehicle for reflecting
the IAP as it acts as a passive reservoir when its
volume is less than 100 ml. (Refer to Fig. 1 for
a description of bladder pressure measurement.)

Figure 2 Example of an algorithm for IAP monitoring and frequency10 .

A critical care nurse’s guide to IAH and ACS
The volume of fluid instilled is important, as larger
volumes have been identified as impairing the read-
ing due to reflex bladder muscle contraction.12,21
A few minutes of equilibrium time is also needed
before the reading is taken, as sudden instillation
of fluid can cause bladder contraction and impair
the measurement.24 This is particularly relevant in
patients who have an indwelling urinary catheter
or have been anuric, resulting in the bladder being
empty for a period of time. The instillation volumes
suggested throughout the literature range from 50
to 100 ml. Some authors stipulate an exact volume
between these ranges. Again, consistency between
measurements by using a fixed volume of fluid that
is instilled into the bladder is important in accu-
rately assessing the trend of IAP. Fusco et al.21
concluded 50 ml instillation of normal saline into
the bladder improved accuracy in measuring ele-
vated IAPs. The World Society for the Abdominal
Compartment Syndrome (WSACS) now recommend
no more that 25 ml of fluid to be instilled into the
bladder.8 More studies are required to ensure that
IAP measurement via the bladder is evidence based
and standardised.
Patient positioning impacts on IAP, therefore
it is important for reliability and reproducibil-
ity of the measurement, that patient variables
be replicated. Head of bed elevation significantly
increases the IAP reading,10 therefore a supine
and horizontal position during measurement is
most likely to provide reproducible and comparable
readings.13
The ideal level of the pressure transducer during
measurement has been identified in the litera-
ture as either on the symphysis pubis or the mid
axillary line. The mid axillary line is favoured
as the symphysis pubis site can be problem-
atic in consistently attaining the same point of
measurement with an expanding abdomen.10,13,19
Due to variation through the respiratory cycle,
the measurement should be taken at end expi-
ration, and pain and abdominal wall tensing
should be minimised to achieve the most accurate
reflection of IAP. A standardised bladder pres-
sure measurement technique is provided in Fig. 1,
whilst an example of measurement is provided in
Fig. 2.
There is a growing demand for continuous
IAP measurement via the gastric and bladder
route. This may address the pitfall of intermit-
tent measurements that provide only a snapshot
of the physiological state. Investigations into
IAP measurements show great variation over
time,7,25 hence continuous measurement may pro-
vide more reliable information of the patient’s
condition.
21
Diagnosis of intra abdominal
hypertension and abdominal
compartment syndrome
ACS is diagnosed when there is a sustained IAH of
>20 mmHg with single or multiple organ dysfunction
that was not previously present.1 The detection of
organ dysfunction is discussed later in the section
on clinical manifestations.
To aid diagnosis and direct treatment for ACS
the concept of abdominal perfusion pressure (APP)
needs to be understood.9,26 APP is considered as
a sensitive measure in determining the perfusion
of abdominal organs and the likelihood of organ
dysfunction.9 A similar concept to cerebral per-
fusion pressure (CPP), APP can be calculated by
subtracting the IAP from the mean arterial pres-
sure (MAP) as follows: APP = MAP − IAP. Adequate
perfusion is believed to be attained with an APP
greater than 50—60 mmHg.8,10 It has been postu-
lated that patients with sustained IAH may tolerate
a higher IAP because their MAP remains high allow-
ing for an APP of greater than 50—60 mmHg.8,9
Cheatham et al.9 suggest that a patient with IAH
who is unable to maintain an APP greater than
50 mmHg has an indication for definitive treatment.
Abdominal perfusion pressure has also been consid-
ered to have a prognostic value as an independent
predictor of outcome with poor outcome seen in
patients unable to sustain an APP > 60 mmHg by
day 3.8,10,13
Causes of intra abdominal hypertension
and abdominal compartment syndrome
Primary abdominal compartment syndrome
Primary ACS results from direct injury within the
abdomen and pelvic region (e.g., blunt or penetrat-
ing trauma, ruptured abdominal aortic aneurysm
or laparotomy).1 A direct injury to the abdomen
creates an opportunity for haemorrhage and tissue
injury. The initial bleed causes hypo-perfusion to
the tissues and the accumulating blood clots within
the abdomen initiate IAH.27 Cellular hypoxia results
and as reperfusion occurs with active resuscitation,
tissue injury promotes tissue oedema. This is known
as reperfusion syndrome and it increases the vol-
ume and pressure in the abdomen, adding to the
already rising IAP.2,27,28
A strategy to control abdominal haemorrhage
is damage control laparotomy. This development
in trauma surgery is primarily aimed at gain-
ing quick control of bleeding organs or vessels.
This involves applying direct pressure by pack-
22
ing the patient’s abdomen with surgical packs.
The abdomen is closed partially or completely
and the patient is transferred to ICU for resus-
citation and stabilisation, with a plan to re-open
later.2,27,29,30 However, it is apparent that this pro-
cedure puts patients at particular risk of primary
ACS.4 Packs are space occupying and create an
increased abdominal pressure.2 Also, the bowel has
a potential for becoming oedematous due to exten-
sive handling or injury, worsening the IAH.14,27 If the
abdomen is closed under tension the risk of ACS is
further increased as the abdominal wall has little
to no compliance.14 Since the introduction of dam-
age control laparotomy more people are surviving
extensive abdominal trauma,30 however, the inci-
dence of ACS has increased.2,4 Usually, the patient
will return to the operating theatre for removal of
packs once stabilised.29 If the patient’s condition
is complicated with ACS the abdominal pressure
needs to be released immediately to prevent the
sequelae.31
Other causes of primary ACS are pancreatitis or
peritonitis where the inflammatory response sets
up capillary leakage resulting in the swelling of
tissue and increased IAP. Otherwise, any abdomi-
nal surgery or trauma can contribute to IAH and
ACS.4,23,32
Chronic ACS is another subgroup of primary ACS
that has been described as an increasing pressure
over a long period of time and is caused by chronic
conditions such as ascites, pregnancy and morbid
obesity. Patients in this sub-group remain at risk of
developing acute ACS.33
Secondary abdominal compartment
syndrome
Secondary ACS develops without direct abdominal
injuries or conditions.2 Secondary ACS can be seen
in patients with severe shock and who have required
massive fluid loading due to haemorrhage, sepsis,
capillary leak, or major burns.1,3,27 The abdominal
pressures rise due to fluid shifts from the vascu-
lar space into the interstitial space, resulting in
problematic tissue and bowel oedema and fluid
accumulation in and around the abdomen.34
Massive fluid loading perpetuates the tissue
oedema and caution needs to be implemented with
these high-risk groups. Judicious use of resusci-
tation fluid and the use of vasopressors earlier
in resuscitation may help minimise the tissue
swelling.4,10
Patient groups without abdominal injury are
potentially at higher risk of being unrecognised pri-
marily because of the lack of an abdominal wound
P. Spencer et al.
to draw the clinician’s attention to the patient’s
tense abdomen.2 If the critical care nurse is aware
of the high-risk patient groups, suspicion and vig-
ilance may be pivotal in the recognition of the
clinical manifestations and early intervention. This
highlights the importance of establishing and track-
ing the IAP early in patients considered to be at risk
of ACS.
Patients at risk of abdominal compartment
syndrome
The lack of identification of patients at risk of ACS
is still considered by many as an obstacle in detect-
ing or monitoring the progression of ACS. Late
recognition associated with high mortality deems
it essential to have strategies that optimise patient
risk assessment and early recognition of impending
or established ACS.2
Patients that have had a laparotomy, massive
fluid loading, paralytic ileus, pneumoperitoneum,
haemoperitoneum, traumatic injury or abdominal
infection should create a degree of suspicion of
IAH and ACS. Indications for IAP monitoring include
abdominal surgery, traumatic injuries, distended
abdomen with ACS signs and symptoms such as olig-
uria, hypoxia, hypotension, unexplained acidosis,
mesenteric ischaemia and/or elevated intra cranial
pressure (ICP).1 Monitoring of IAP should be con-
sidered for patients that have temporary closure
with abdominal packs and received large volumes
of resuscitation fluids for septic or hypovolaemic
shock.1 There needs to be vigilance in assessment
of the patient’s IAP and organ function to optimise
early recognition.
Mortality from abdominal compartment
syndrome
The specific risk of death from ACS can be dif-
ficult to distinguish from other causes, although
it is obvious that there is a higher mortality if
the condition remains untreated.4 A multi-centre,
prospective, epidemiological study was conducted
in 2005 (n = 265) looking at the incidence and
prognosis of IAH and ACS.13 The incidence of IAH
was described as 32.1% (n = 85) with 12.9% (n = 11)
detected as having ACS. Patients with IAH (IAP > 12
mmHg) on admission had reduced 30 days survival
compared with those with no IAH (62% vs. 79%),
but this was not statistically significant. Further-
more, mortality rates for patients with IAH were
found to be significantly worse when standardised
and grouped using APACHE II scores (p < 0.05).13
A critical care nurse’s guide to IAH and ACS 23

The role of the critical care nurse throughout
this process of risk assessment and identification
of signs and symptoms of ACS is pivotal. Identifying
those patient groups that are considered high-risk
is a crucial step in identifying ACS.35 Screening
patients on admission against the risk factors asso-
ciated with IAH and ACS can help determine the
need for IAP measurement (Fig. 2).10 The critical
care nurse above all needs to be knowledgeable
about the signs and symptoms of ACS, its impact
on the physiological state of patients and possess
knowledge of management options. This exper-
tise may assist nurses in contributing to improved
patient outcomes.15,35
Pathophysiology and clinical
manifestations of abdominal
compartment syndrome
This review will outline the pathophysiology
and clinical manifestations of ACS. Fig. 3 sum-
marises the complex effects of ACS on the body
systems.

Figure 3 Summary of physiological impact on body systems and clinical manifestations of abdominal compartment
syndrome13,43 .
24
In ACS, restriction of the cellular blood supply
interrupts aerobic metabolism forcing the cells into
an anaerobic state. Lactic acidosis is a result of this
metabolism and is often seen in the patient with
developing intra abdominal hypertension.36 An un-
resolving serum lactate has been a useful indicator
of cellular perfusion. It has been described as a slow
marker, however, it is actually measurable early in
the sequelae.36
Carbon dioxide (CO2 ) levels continue to rise as
compression of the vasculature prevents removal of
the CO2 . This further increases acidity at a cellular
level, particularly in the gut and can be identi-
fied using gastric tonometry.37 The gut has been
described as the ‘‘canary’’ organ38 as it shows
clinical signs of hypo-perfusion before any other
organ, probably as a result of a lack of the auto-
regulatory properties present in the brain, kidney
and heart.38 Systemic acidosis will result as more
vascular disturbance and organ dysfunction occurs.
Having measurable evidence of this early sign of
ACS may prompt and support further investigation
into IAP.
As the pressure rises in the abdomen the car-
diovascular system is affected early. The pressure
on the inferior vena cava results in impedance
of the venous return. Pooling of the blood in the
peripheral circulation occurs as congestion builds
in the large veins due to the impeded pathway
through the abdomen. As the diaphragm is pushed
up by the expanding volume of the abdomen, the
heart and the pulmonary veins are compressed
causing increased pulmonary vascular resistance
and impaired right ventricular systolic function.
The congested heart often produces an elevated
central venous pressure and pulmonary capillary
wedge pressure. This is not a reflection of the
patient’s fluid status but rather an indicator of
the rising intra thoracic pressure and systemic vas-
cular resistance.2,7,13,14,39 The increasing thoracic
pressures also manifests as increasing peak airway
and plateau pressures that can be measured in a
mechanically ventilated patient. These pressures
are seen to rise early in the process of ACS (IAP
15 mmHg) and continue to rise as IAP increases.16
A decline in cardiac output is an early charac-
teristic of ACS, as well as an escalating heart
rate, in an attempt to compensate for reduced
stroke volume.7,39 Eventually cardiac contractil-
ity decreases and hypotension becomes apparent
after the compensatory mechanisms begin to fail.4
Hypotension is considered a late sign.40
Increasing thoracic pressures are representative
of the imposing abdominal compartment pressure.
This impairs the lungs’ oxygen exchange, as the
compressed lung is unable to expand. Alveoli con-
P. Spencer et al.
tinue to collapse as the pressure increases resulting
in decreased oxygen uptake within the blood.14
Hypoxaemia is noted early and augmentation of
oxygen delivery will benefit these patients. As the
lungs become more compressed and inefficient in
exchanging oxygen, other support such as positive
end expiratory pressure (PEEP) will be of benefit.
It has been suggested that the PEEP implemented
should equal or be greater than 12 cmH2 0 to aid in
lung recruitment,23 while overcoming the effects
of IAH. The fine balance remains achieving the best
PEEP without over inflation of the well-aerated lung
regions.7 If the patient is spontaneously breathing,
increasing respiratory rate and work of breathing
become apparent along with a decline in tidal vol-
umes. These changes occur early in ACS.41
Abdominal organs experience impaired blood
flow when the IAP has reached 15 mmHg.23 Direct
pressure on the renal parenchyma causes a
decrease in renal perfusion and glomerular filtra-
tion rate, resulting in oliguria and eventually anuria
if IAH persists. It is also thought that the compres-
sion of the renal veins decreases renal blood flow
and a decline in glomerular filtration rate (GFR)
leading to oliguria.23 Patients can maintain urine
output of 0.5 ml/kg/h up until IAP of 25 mmHg,
therefore, renal compromise and anuria are late
signs of ACS.42
The lack of vascular supply to the kidney creates
tissue ischaemia. This causes increased water and
sodium retention due to the activation of the renin-
angiotensin system contributing to the oliguria. If
prolonged this leads to acute tubular necrosis and
renal failure.2,14,35 If early decompression occurs,
renal dysfunction quickly improves. However, pro-
longed compression will cause irreversible renal
damage. Improvement in both urine output and car-
diac output post-decompression is considered an
indicator of patient outcome.2,27
Intestinal swelling adds to the already expand-
ing volume within the abdomen. The impaired
intestinal perfusion that results from IAH produces
anaerobic cellular metabolism, acidosis, and free
radical production.23 Hypo-perfusion also causes a
decline in gastric mucosa thickness which allows for
an easy passage for microorganisms and toxins from
the bowel to enter the systemic circulation.7,14,38
Bacterial translocation occurs as microorganisms
and toxins from the intestinal wall move and enter
the mesenteric lymph nodes, which are thought to
be the initial source of sepsis, and the initiation of
systemic inflammatory response syndrome (SIRS) is
triggered.14,43 Sustained IAH will lead to ischaemic
gut tissue becoming necrotic.
Central Nervous System manifestations are
indicative of poor venous outflow from the brain
A critical care nurse’s guide to IAH and ACS
due to raised IAP causing subsequent venous con-
gestion which, results in a reduction in cerebral
perfusion pressure.7,14 This may potentate brain
injury with symptoms of agitation, confusion, and
finally coma. During this decline in conscious state,
abnormal pupillary response will be evident.43
Unfortunately sedation may mask the neurological
effects of ACS and vigilance is required in assessing
conscious state, sedation scores and pupil activity.
Congestion in the femoral venous system occurs
with IAH as the returning blood flow is impeded.
Stasis of the venous circulation creates the opportu-
nity for blood clot formation, which can potentially
complicate the patient’s outcome if dislodged.23
The peripheries are cool, capillary refill is impaired,
the skin becomes mottled and eventually cyan-
otic and pitting oedema to the limbs develops.
Abdominal wall perfusion diminishes and the mot-
tled cyanotic skin becomes at risk of breakdown
around a laparotomy site.7,16
Management of abdominal compartment
syndrome
Medical management
Medical management of ACS has been more suc-
cessful in reducing IAP in the patient group that
has no abdominal injuries. Insertion of percuta-
neous drains has allowed for removal of ascitic fluid
creating a reduction in volume and pressure. Fluid
restriction and caution with crystalloid infusion
are conservative measures undertaken that limit
IAP.2,44 Endogastric tubes allow for gastric drainage
and enemas are used to decompress the bowel.
Muscle relaxants have also been used to reduce
abdominal muscle tone, increasing compliance and
reducing IAP.15 Prone positioning in the patient
with a closed abdomen has been used to reduce
the effect of IAH on the vena cava facilitating
venous return by redistributing the direct weight
and pressure from the organs off the IVC.7,44 These
measures are temporary means of reducing the
effects of ACS by reducing the IAP until the oedema
or fluid collection subsides. These measures are
useful, however, only surgical intervention is con-
sidered the definitive treatment.2,4,14,22,23,27,45
Surgical management
The general consensus is that the decompressive
laparotomy (also known as a ceiliotomy) is the most
effective treatment for ACS.2,4,14,22,23,27,45 There is
not an absolute critical IAP that triggers a laparo-
tomy as there is variation between patient groups of
25
Figure 4 The midline incision approach is the most com-
mon used.
the IAP that is tolerated and leads to ACS. However,
it is essential to activate appropriate intervention
when the clinical signs of organ failure are present
with concurrent IAH.45,46
Abdominal decompression is a surgical technique
aimed to open the abdomen to reduce the pressure
within the abdominal cavity. The most common sur-
gical approach is a midline incision (Fig. 4). The
abdominal muscle fascia is usually left open and
alternative dressing closure such as polypropylene
mesh is sutured to the abdominal fascia to give the
visceral layer more expansion.
Immediately after decompression, it is antici-
pated there will be restoration of organ function.27
If irreversible or refractory shock is present, then
decompression will be futile. Even if some parame-
ters improve with decompression the cardiac index
and urine output are the prognostic indicators. If
they fail to improve, patient outcome is anticipated
to be very poor.27
In order to prevent the sequelae of ACS occurring
patients that are considered high-risk can be man-
aged prophylactically with open fascias to prevent
the development of IAH and subsequent ACS.9,47,48
Use of prosthetic abdominal closure such as mesh,
sterile drape silos or Bogotá bags are being consid-
ered for patients that have oedematous bowel and
packs in situ to control haemorrhage.2,14,45
Staggered closure of the wound can be a possi-
bility if the wound cannot be closed initially. This
can take place over days to weeks with the muscle
fascia, subcutaneous tissue and skin of the wound
can be gradually reduced, and eventually closed.
Polypropylene mesh can be used to help facilitate
complete abdominal closure.16 For optimal timing
of closure, IAH needs to have subsided. The mesh
can then be removed and the muscle layer can be
closed at this point.16 If IAH remains and the muscle
layer is unable to be closed, there is likely to be a
26
prolonged delay in closure. The wound is often skin
grafted and will be surgically managed as a hernia
repair 6—12 months later.49
Nursing management
Reference to the nursing care specific to patients
with ACS is scarce within the literature. Specific
nursing management for patients with ACS involves
assessing for organ dysfunction, wound manage-
ment, assessing wound drainage and fluid output.
Ongoing risk assessment for recurrence of ACS
needs to be vigilant and ongoing. Psychosocial
impact needs to be assessed and monitored.50
Organ function
Caring for patients with ACS requires intensive
nursing care which involves continuous assess-
ment, modification of treatment and reassessment.
There is often a high input of technological and
pharmacological support to treat patients with
ACS. The critical care nurse’s expertise requires
advanced assessment, interpretation, interven-
tion and titration of treatments to support the
failing organ systems.50,51 Patient care may ben-
efit from nurses having knowledge of ACS and
the physiological impact it has on the patient
in order to anticipate and detect failing organ
systems.14,35
Wound management
Post-decompression the nursing challenges involve
maintenance of the complex dressings and numer-
ous drainage systems, including negative pressure
dressings or vacuum-assisted closure (VAC) systems
that evacuate and prevent fluid re-accumulation
within the abdomen16,49 (Fig. 5). The wound needs
to be assessed for infection and vascular supply.16
Assessment for dressing integrity is essential to
ensure the negative pressure is intact. A break
in the dressing causing a loss of negative pres-
sure will impact on the effectiveness of the VAC
dressing to evacuate the fluid. Fluid accumulation
will create dressing leaks, small occlusive dress-
ings may be used to patch the drape,16 however, an
entire occlusive dressing change may be the most
effective intervention if the leaks are extensive.
Manufacturer recommendations include maintain-
ing the suction settings within −50 to −200 mmHg
administered continuously or intermittently.52 This
P. Spencer et al.
Figure 5 Depicts the complex negative pressure dress-
ing that prevents re-accumulation of fluid.
can be achieved with wall suction or VAC suction
devices.
Assessment of wound drainage
Assessment of the nature and volume of fluid com-
ing from the wound needs to be noted, looking
for changes in the fluid being evacuated from
the abdomen.16 The entire dressing needs to be
changed every 48 h52 as thereafter granulation tis-
sue becomes embedded in the foam and can impede
and cause pain during the VAC sponge removal.47
Assessment for recurrent ACS
There is still a risk of the patient develop-
ing recurrent ACS post-decompression laparotomy,
even with the open muscle fascia52 as the pros-
thetic wound closure and occlusive dressing can
act as an abdominal layer and decrease abdomi-
nal compliance. Therefore, ongoing postoperative
IAP assessment is important in identifying any
trends that may signal the need for further
treatment.14,53
Patient impact
The process of healing is often slow, as it may be
complicated by intra abdominal abscess and fis-
tula formation leading to long hospitalisation.49
This highlights the economic and social effects ACS
has on the patient, their family and on the hos-
pital system. There is a documented decline in
quality of life during the extensive rehabilitation
process that follows. Once closure of the wound has
been achieved and the patient has completed the
A critical care nurse’s guide to IAH and ACS
rehabilitation process, survivors regain the same
perception of physical and mental health to that
of the general population.54
Conclusion
Technology and diagnostic capabilities have been
developed and refined to optimise the care and
treatment of critically ill patients. This has bought
with it a new set of challenges as critically ill
patients survive longer and new complications
unfold. ACS is considered such a complication
that is potentially reversible. A lower tolerance
for IAH1,45 and a growing trend to manage high-
risk patients with open abdomens contribute to
improved survival from ACS. It is essential to diag-
nose and intervene early with these patients as
without early intervention the risk of death is
extremely high. The critical care nurse is well sit-
uated to detect subtle signs or changes in the
patient’s clinical state that may prompt early
investigation into the IAP. Abdominal Compartment
Syndrome is a clinical syndrome that can easily be
misinterpreted and unless there is a high index of
suspicion may be overlooked and contribute to dev-
astating patient outcomes.
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