Abdominal compartment syndrome
Neil Berry
Simon Fletcher
Key points
Intra-abdominal
hypertension is common,
but the diagnosis may be
overlooked in the typical
intensive care patient.
Mortality for untreated
intra-abdominal
hypertension and abdominal
compartment syndrome is
high.
Presentation is commonly a
multi-system phenomenon
of abdominal distension,
renal, respiratory, and
circulatory compromise.
Physical examination has a
low sensitivity and
specificity for diagnosing
intra-abdominal
hypertension and therefore
intra-abdominal pressure
measurements should be
taken as soon as the
diagnosis is considered.
Maintenance of an
abdominal perfusion
pressure of .60 mm Hg by
fluid resuscitation and
vasoactive drugs is
associated with better
outcomes.
Surgical decompression is
effective, but should be
used in conjunction with
non-surgical management.
Neil Berry
Specialist Registrar
Norfolk and Norwich Hospital, Norwich
Norfolk, UK
Simon Fletcher
Consultant
Norfolk and Norwich Hospital
Norwich, Norfolk, UK
Tel: +44 (0)1603 287074
Fax: +44 (0)1603 287751
E-mail: simon.fletcher@nnuh.nhs.uk
(for correspondence)
110
Abdominal hypertension and abdominal com-
partment syndrome represent a spectrum of
severity of a disorder that carries a significant
morbidity and mortality. The diagnosis is often
not made until irreversible damage has
occurred. Mortality from untreated abdominal
compartment syndrome lies close to 100%.
In 2004, the World Society of Abdominal
Compartment Syndrome was founded and has
since published guidelines on diagnosis, meas-
urement, and treatment of intra-abdominal
hypertension and abdominal compartment
syndrome. These consensus guidelines were
created in 2004 and revised in 2009.
Definitions and incidence
Compartment syndrome occurs when a fixed
compartment defined by myofascial layers,
bone, or both becomes subjected to increasing
pressures, leading to vascular compromise and
ischaemia. This is most commonly associated
with limb trauma but is also well recognized as
occurring within the abdominal cavity.1
Normal intra-abdominal pressure in the
typical critically ill, intensive care patient is
5–7 mm Hg, but this is not static, varying
with respiration; increasing on inspiration and
decreasing on expiration. Many other factors
have an influence. The intra-abdominal pressure
is dependent on the volume of intra-abdominal
contents, for example, visceral volume,
tumours, the pathological presence of fluid
(blood, ascites, pus), and general visceral
oedema. Pathological conditions may also affect
the compliance of the abdominal wall, for
example, burns, oedema, or prolonged prone
positioning. Positive inspiratory and expiratory
pressures used in mechanical ventilation will in-
directly increase intra-abdominal pressure.
Intra-abdominal hypertension is defined as a
sustained intra-abdominal pressure of .12 mm
Hg, and abdominal compartment syndrome
occurs at a pressure .20 mm Hg in association
with new organ dysfunction.2 Intra-abdominal
hypertension is graded as follows: Grade
doi:10.1093/bjaceaccp/mks006
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& The Author [2012]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.
All rights reserved. For Permissions, please email: journals.permissions@oup.com
Matrix reference 1A03,2C03
1¼12 –15 mm Hg; Grade 2¼16–20 mm Hg;
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Grade 3¼21 –25 mm Hg; and Grade 4 .25
mm Hg.
Intra-abdominal hypertension is analogous to
raised intra-cerebral pressure in the head-injured
patient. Just as an adequate cerebral perfusion
pressure is critical in maintaining cerebral oxy-
genation, within the abdomen, an adequate ab-
dominal perfusion pressure must be maintained
for normal organ function. The abdominal per-
fusion pressure is calculated as the mean arterial
pressure minus the intra-abdominal pressure. It
is recommended that the abdominal perfusion
pressure should be maintained above 60 mm Hg
and this has been shown to correlate with
improved outcomes. Multiple regression ana-
lysis has shown that abdominal perfusion pres-
sure, as a resuscitation endpoint is superior to
other endpoints such as arterial pH, base deficit,
lactate, and urine output.3
Acute abdominal compartment syndrome
can be categorized into primary, where the
pathology lies within the abdomino-pelvic
cavity, or secondary, where the cause lies
outside of this region, for example, extra-
abdominal sepsis or fluid overload. A chronic
form of abdominal compartment syndrome is
also recognized in association with peritoneal
dialysis or chronic ascites. Intra-abdominal
hypertension may occur when the
intra-abdominal pressure is artificially raised by
external compression for a prolonged period of
time, for example, prolonged prone positioning
for spinal surgery with insufficient provision
for abdominal movement.
The incidence of intra-abdominal hyperten-
sion and abdominal compartment syndrome
varies, but studies have suggested that when
associated with septic shock, it may be as high
as 85% and 30%, respectively.4 In acute pan-
creatitis, 40 –70% of patients are thought to
develop intra-abdominal hypertension and 10 –
50% abdominal compartment syndrome.5
Incidence post-laparotomy is very variable,
from low with elective surgery to considerable
after emergency procedures.
Advance Access publication 8 March, 2012

Clinical presentation
The presentation of acute abdominal compartment syndrome is
varied, but commonly abdominal pain and distension are present
associated with hypoxia, hypercarbia, and oliguria due to respira-
tory and renal physiological changes. Physical examination has a
low sensitivity of around 40 –60%.6 Without timely intervention,
regardless of cause, a progressive increase in intra-abdominal
pressure, leading to multi-organ failure and ultimately death, is the
likely occurrence.
Diagnosis and measurement of
intra-abdominal pressure
The mainstay of diagnosis relies on early clinical suspicion of
raised intra-abdominal pressure in any patient with associated risk
factors. The World Society of Abdominal Compartment Syndrome
suggests that any patient with two or more risk factors is at high
enough risk to warrant intra-abdominal pressure monitoring.
Risk factors for abdominal compartment syndrome2
1. Diminished abdominal wall compliance
† Acute respiratory failure, especially with elevated
intrathoracic pressure
† Abdominal surgery with subjectively tight primary
closure
† Major trauma/burns
† Prone positioning, head of bed elevated .308
† High BMI, central obesity
2. Increased intra-luminal contents
† Gastroparesis
† Ileus
† Colonic pseudo-obstruction
3. Increased abdominal contents
† Haemoperitoneum/pneumoperitoneum
† Ascites/liver dysfunction
4. Capillary leak/fluid resuscitation
† Acidosis ( pH ,7.2)
† Hypotension
† Hypothermia (core temperature ,338C)
† Polytransfusion (.10 units of blood/24 h)
† Coagulopathy ( platelets ,55 000 mm23, prothrombin
time .15 s, partial thromboplastin time .2 times
normal, or international standardized ratio .1.5)
† Massive fluid resuscitation (.5 litre/24 h)
† Pancreatitis
† Oliguria
† Sepsis
† Major trauma/burns
† Damage control laparotomy
There are several methods of measuring intra-abdominal pressure,
broadly categorized as direct or indirect. Direct measurement
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Abdominal compartment syndrome
involves introducing a needle/line, connected to a pressure trans-
ducer, directly into the peritoneum; however, this is rarely done as
indirect methods give acceptable results with a much lower risk of
iatrogenic injury. Indirect measurement can be performed via the
intra-gastric, intra-uterine, rectal, or intra-vesical routes, the latter
of which is most commonly used.
To measure intra-abdominal pressure via the intra-vesical route,
a simple Foley catheter is connected via a three-way tap to a pres-
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sure transducer (Fig. 1). Several purpose-built devices are available
on the market, but these are more expensive with no proven in-
crease in accuracy. To measure via an intra-vesical catheter, the
patient should be catheterized and residual urine allowed to drain.
The catheter is then clamped distal to the point of pressure meas-
urement. The patient should be in the supine position for measure-
ment as intra-abdominal pressure is increased by 2 mm Hg for
every 208 of head-up tilt. A pressure transducer is connected to the
catheter and is zeroed at the iliac crest in the mid-axillary line. No
greater than 25 ml of saline is then instilled into the bladder (1 ml
kg21 if ,20 kg2) and 30–60 s allowed to elapse (to permit de-
trusor relaxation before the measurement is made). The measure-
ment should be made at the end of expiration and in the absence
of active abdominal muscle contraction. Measurement can be taken
at regular intervals (most units measure 4–6 hourly)7 and treat-
ment directed as necessary. Continuous measurement is more chal-
lenging via the intra-vesical route as the catheter must be clamped
at the time of measurement.
Pathophysiology and physiological effects
An increase in intra-abdominal pressure leads to multisystem
dysfunction (Fig. 2).
Cardiovascular system
Pressure within the abdominal cavity is directly transmitted to the
abdominal vasculature. Compression of the venous system leads to
venous occlusion and a reduction in preload, while arterial com-
pression leads to reduced arterial compliance and an increased
afterload. This combination leads to a decrease in cardiac output
and, often, abdominal perfusion pressure. Cardiac output may be
further compromised by an increase in intra-thoracic pressure due
to diaphragmatic splinting and elevation. The heart and great
vessels are both compressed and distorted thereby reducing
compliance and contractility. The combination of increasing
intra-abdominal pressure (with untreated pathology) and decreasing
cardiac output may rapidly result in catastrophic intra-abdominal
ischaemic injury and inevitable death.
Respiratory system
Not surprisingly, basal collapse/atelectasis, increasing V/Q mis-
match, and decreased pulmonary and chest wall compliance are a
feature of this condition. In combination, these factors lead to
increasing hypoxia and hypercarbia. In mechanically ventilated
111
Abdominal compartment syndrome

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Fig 1 Transvesical method for measuring intra-abdominal pressure. Reproduced with permission from Mullens W, Abrahams Z, Skouri HN, et al. Elevated
intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol 2008; 51: 300 –6.
&American College of Cardiology Foundation.

patients, increased inspiratory pressures and PEEP will further If PTP¼IAP, then
compromise venous return and cardiovascular function.
Treatment of intra-abdominal hypertension has been associated FG ¼ ðMAP  IAPÞ  IAP
with reduced ventilatory days in several studies.8 ¼ MAP  2IAP

where MAP is the mean arterial pressure and IAP the

Renal system
Renal function is at particular risk (Fig. 3). The increase in
intra-abdominal pressure and a subsequent decrease in cardiac
output are reflected in renal blood flow. Reduced renal blood flow,
however, is not the sole cause of renal dysfunction. The
intra-abdominal pressure is also transmitted to the renal outflow
tract. As pressure increases within the tubular system, this is inevit-
ably transmitted back to the glomeruli reducing the filtration gradi-
ent (FG).
The FG is the pressure difference between the abdominal perfu-
sion pressure and the proximal tubular pressure (PTP). If
intra-abdominal pressure increases above normal PTP (15– 18 mm
Hg) then there is increased resistance to filtration and decreased
urine output:
FG ¼ ðMAP  IAPÞ  PTP
intra-abdominal pressure.
It can be seen that when abdominal pressure is elevated, the
intra-abdominal pressure acts in two independent ways on the renal
system, both deleterious to renal function. Hormonal effects from
activation of the renin/angiotensin system and increased antidiure-
tic hormone have a further adverse effect.
Central nervous system
Intra-abdominal hypertension has been shown to elevate intra-
cranial pressure. Elevated intra-thoracic pressure inhibits venous
return with a consequent increase in intra-cranial pressure.
Associated hypercarbia, and any consequent cerebral vasodilata-
tion, may have an additive effect.
Several studies in patients with traumatic brain injury and
raised intracranial pressure have shown the benefit on intra-cerebral

112 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 12 Number 3 2012

Fig 2 Pathophysiological effects of raised intra-abdominal pressure.
pressure of lowering intra-abdominal pressure. Intra-abdominal
hypertension has been found to be an independent risk factor for
secondary brain injury in the brain-injured patient.9
Gastrointestinal system
The gastrointestinal system is particularly vulnerable to insult
in critically ill patients, and this is compounded when
intra-abdominal pressure is raised. The decrease in gut perfusion,
due to blood redistribution as part of the response to critical
illness, is exacerbated by a pressure-induced reduction in abdomin-
al perfusion pressure and increased venous obstruction leading to
bowel wall oedema. A critical decrease in bowel wall oxygen de-
livery may result, leading to bowel ischaemia, loss of cellular in-
tegrity, and translocation of bacteria into the systemic circulation
resulting in sepsis. Healing of bowel anastamosis and abdominal
wounds is impaired leading to anastomotic and wound breakdown.
Hepatic blood flow within the hepatic artery, vein, and portal
system is also adversely affected, leading to mitochondrial dys-
function and eventually liver dysfunction and failure. This normal-
ly presents as failure of clotting factor and protein synthesis,
increased susceptibility to infection, and encephalopathy. Lactic
acid clearance is compromised, making it less useful as a marker
of resuscitation and drug metabolism may also be affected, so
careful consideration to drug pharmacokinetics and dynamics is
needed.
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Abdominal compartment syndrome
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Management
Non-surgical management
The World Society of Abdominal Compartment Syndrome sug-
gests that any patient with two or more risk factors should have
their intra-abdominal pressure monitored and a proactive approach
to intervention followed. Initial management can be separated into
treatment regimes aimed at lowering intra-abdominal pressure and
those aimed at organ support. (See Appendix.)
Lowering intra-abdominal pressure
Simple measures such as supine positioning and passing a nasogas-
tric tube to decompress the stomach will have moderate effects on
reducing intra-abdominal pressure; however, the former increases
the risk of aspiration and therefore risks and benefits need to be
carefully considered.
Enemas, flatus tubes, aperients, and pro-kinetic agents may all
be of some benefit. Some centres advocate endoscopic or percutan-
eous decompression of the gastrointestinal tract, aimed at lowering
intra-abdominal pressure by draining gas or fluid.
Coughing, straining, and ventilator dyssynchrony all increase
intra-abdominal pressure, and for this reason, adequate sedation is
essential and a period of muscular paralysis may be beneficial.
Complications of sedation such as reduced cardiac output need to
be considered.
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Abdominal compartment syndrome
Fig 3 Effect of intra-abdominal pressure on renal function.
Organ support
One of the key aims in management is to optimize cardiac output.
As described earlier, cardiovascular compromise due to the
increased intra-abdominal pressure is much more marked in the
hypovolaemic under-resuscitated patient. Initial fluid resuscitation
should be aimed at restoring normovolaemia.
Central venous pressure measurement and pulmonary artery
wedge pressures may be misleading as a guide to fluid replacement
as they may be falsely elevated due to the intra-thoracic pressure
increase; however, trends and response to fluid challenges may be
of benefit. Markers such as stroke volume variation that are inde-
pendent of intra-thoracic pressure may be useful guides to fluid
resuscitation.
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Fluid overload, as already indicated, may in itself be detrimental, so
a balance must be sought. If a patient is fluid replete but the ‘target’ ab-
dominal perfusion pressure of 60 mm Hg has not been reached then
inotropic or vasopressor therapy should be commenced. There is no
clear evidence as to which inotrope or vasopressor should be started as
first line, but therapy should be tailored to the individual patient.
Renal replacement therapy may be necessary and should be
considered in all patients with clinical and biochemical signs of
renal dysfunction. It may be appropriate to initiate early replace-
ment rather than persist with large volume fluid resuscitation, with
an increased incidence of secondary abdominal compartment syn-
drome.7 Lung protective strategies as for treatment of adult respira-
tory distress syndrome should be used.

Enteral feeding should be continued in all patients if possible
to maintain gut integrity, as the feed volume does not contribute
significantly to intra-abdominal pressure; however, many patients
may have primary or secondary gastrointestinal failure and there-
fore feed will not be absorbed. Four-hourly gastric aspiration via a
nasogastric tube will give a guide to feed absorption. Where
gastrointestinal failure is evident, parenteral nutrition may be indi-
cated. As timing here remains controversial, local guidelines
should be observed.
Careful consideration is needed with respect to drug pharmaco-
kinetics as altered hepatic blood flow may lead to a deterioration
in hepatic function and therefore drug handling.
The combination of venous stasis and a sick, immobile patient
significantly increases the incidence of venous thrombosis, there-
fore thrombo-prophylactic measures should be taken in all patients.
Surgical management
Surgical intervention, the decompression of the abdomen by way
of laparotomy (the ‘open abdomen’), has been shown to improve
mortality in patients with abdominal compartment syndrome. In
the strict sense, the abdomen is not left open to the air as this
would lead to drying and desiccation of the bowel; instead a
plastic membrane or Bogota bag is stitched to the wound edges
allowing increased intra-abdominal space and therefore a decrease
in intra-abdominal pressure. After laparotomy, the abdominal
cavity is simply a larger closed compartment and further increases
in volume may still result in an increase in intra-abdominal pres-
sure, therefore pressure monitoring should be continued. In one
study, 25% of patients, who had a laparotomy for trauma and had
initial temporary closure with a Bogota bag, developed secondary
intra-abdominal hypertension.10
Subcutaneous release of the linea alba, leaving the skin and
peritoneum intact, has been shown to reduce intra-abdominal pres-
sure in patients with intra-abdominal hypertension secondary to
acute pancreatitis.11
The timing of surgical decompression is important. In patients
thought to be at high risk of abdominal compartment syndrome at
the time of any intra-abdominal procedure, then temporary closure
with a Bogota bag should be a primary event. In others who have
developed abdominal compartment syndrome, and where non-
surgical methods have failed, decompression should be performed
as an emergency procedure.
The abdomen should only be closed when the risk of continu-
ing intra-abdominal hypertension has passed, on average 5 days
after decompression. Vacuum dressings have been used with good
results to aid wound closure when surgical closure is not possible.
Anaesthesia for abdominal decompression
These patients are critically ill and anaesthetic management should
reflect this. There are four key concerns specifically related to
patients with abdominal compartment syndrome.
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Abdominal compartment syndrome
Pharmacokinetics/dynamics
Patients with abdominal compartment syndrome may be more sen-
sitive to the cardiac depressant effects of induction agents due to
liver dysfunction, altered drug handling, altered volume of distribu-
tion, and hypovolaemia. A reduced dose of drug and careful induc-
tion with invasive monitoring is required.
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Sudden decrease in intra-thoracic pressure
As the abdomen is opened, the intra-abdominal pressure rapidly
equilibrates with atmospheric pressure. There is a consequent de-
crease in the intra-thoracic pressure. A dramatic increase in respira-
tory compliance may occur, with the potential of ‘over ventilation’
and damage to lung parenchyma due to barotrauma and volu-
trauma. Therefore, close attention to airway pressures/tidal
volumes should be paid.
Sudden decrease in systemic vascular resistance
On opening the abdomen, afterload will fall as may cardiac output
and arterial pressure. This may be profound, resulting in sudden
cardiac arrest. Further fluid loading and/or vasopressors may be
required, and resuscitation drugs and equipment should be close at
hand.
Reperfusion injury
Finally, on opening the abdomen, previously ischaemic areas of
bowel and viscera may once again be perfused, leading to a sys-
temic reperfusion insult with potential of myocardial depression,
arrhythmias, and, on occasion, cardiac arrest.
With all of these patients, senior anaesthetic staff should be
available and extreme care and vigilance should be taken at induc-
tion of anaesthesia and on opening of the abdomen. Resuscitation
drugs and equipment should be immediately available.
Declaration of interest
None declared.
References
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2. World society of abdominal compartment syndrome. 2004. Available
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Abdominal compartment syndrome is common in medical intensive care
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2007; 22: 294 –9
115
Abdominal compartment syndrome
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hypertension on the central nervous system: current insights and clinical
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recommendations, is it all in the head? Acta Clin Belg Suppl 2007; 1:
89–97
10. Gracias VH, Braslow B, Johnson J et al. Abdominal
compartment syndrome in the open abdomen. Arch Surg 2002; 137:
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Please see multiple choice questions 5 –8.
 Abdominal compartment syndrome

Appendix
Intra-abdominal hypertension/abdominal compartment syndrome management algorithm. Reproduced with permission from the World
Society of the Abdominal Compartment Syndrome (WSACS).

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