INTRAABDOMINAL

HYPERTENTION &
ABDOMINAL
COMPARTMENT
Aditya Bhayusakti, M.D
SYNDROME

important values

Normal intra-abdominal pressure is 0 - 5 mmHg.

Pressures > 13 mmHg may be sufficient to restrict perfusion
to the organs of the gut.
If the abdominal compartment pressures is between 16-25
mmHg, hypervolemic volume expansion therapy can be used
to maintain the perfusion pressure gradient for the abdominal
organs.
When compartment pressures exceed 25 mmHg,
decompression surgery should be considered to prevent
organ damage. Pressure may rise rapidly with active
bleeding. Edema (which occurs with any ischemic insult) will
generally result in a later rise in the pressure (27 hours or
more post insult).

Classify IAH into 4 groups:

Hyperacute(sec,min):laughing,strain,coughing,sneez,physical activities)
Acute(couple H):trauma,hge
Subacute (couple days): most medical
cases.
Chronic: morbid obesity,intraabdominal
tumor,pregnancy.

Patients at risk for ACS

include:
trauma (blunt or open), as a result of the

accumulation of blood, fluid or edema.

gastrointestinal hemorrhage can also lead to
increased pressure in the abdominal compartment as
ischemic cells swell or fluids collect.

pancreatitis
pneumoperitoneum
neoplasm

syndrome may follow a ruptured

abdominal aortic aneurysm
intra-abdominal infection
Coagulopathies with abdominal
bleeding
cirrhosis, or
profound hypothermia

massive intra-abdominal
retroperitoneal hemorrhage,

severe gut edema

intestinal obstruction

ascites under pressure.

Patients who have undergone long surgical

procedures with intraoperative hypotension and
large fluid requirements are at significant risk,
particularly if the abdomen has been closed
under pressure in the OR.
External pressure from circumferential burns
about the abdomen, application of military antishock trousers (MAST), or even tight abdominal
restraint devices can cause tension within the
abdomen due to external forces and result in
ACS.2

Recently, awareness of the ACS has increased for 2

primary reasons.
First, the increased use of laparoscopy among general
surgeons has brought with it an appreciation of IAP as a
readily quantifiable entity.
Second, the more frequent use of planned repeat
laparotomy for trauma has allowed both surgeon and
intensivist to appreciate the beneficial effects of
abdominal decompression upon removal of packing or
evacuation of hematoma.

The Pathophysiology of IAH

IAP
VASCULAR
COMPRESSION
RVP

IVC
Flow

DIAPHRAGMATIC
ELEVATION

DIRECT ORGAN
COMPRESSION

Cardiac
Intrathoracic
compression
pressure

Cardiac preloadCardiac contractility Systemic afterload

PV pressure
Renal Vascular
Resistance
RENAL FAILURE

CARDIAC OUTPUT
Splanchnic
Vascular Resistance
ABDOMINAL WALL
ISCHAEMIA/OEDEMA

RESPIRATORY
FAILURE

ICP SPLANCHNIC
ISCHAEMIA

Compartment syndrome occurs when

the pressure within a closed
anatomic space increases to the
point where vascular tissue is
compromised with subsequent loss
of tissue viability and function. This
can occur within any closed body
cavity.

Increased IAP leads to decreased

MBF and to Bacterial translocation
(BT), which may contribute to later
septic complications and organ
failure.

IAH provokes the release of proinflammatory cytokines which may

serve as a second insult for the
induction of MOF.
production of interleukin-1b (IL1beta), interleukin-6 (IL-6), tumor
necrosis factor (TNF-alpha)

Anaesthetic Implications of ACS:

Pulmonary
Implications
Renal implications
Portosystemic
visceral
Implicatio
ns

Cardiovascul
ar
Implications

Central
nervous
system
Implications

Effects on CVS

As intraabdominal pressure increases above 10

mmHg, cardiac output declines, despite normal
arterial pressures.
Additionally, whole body oxygen consumption, pH,
and PO2 decrease.
Intraabdominal hypertension affects cardiac
function by pushing the hemidiaphragms upward,
thus transmitting the abdominal pressure to the
heart and its vessels.
This decreases preload and increases afterload on
the left ventricle and at the same time creates a
hemodynamic picture of low cardiac output and
high filling pressures.1,4

On the pulmonary system

The most commonly noted effects of IAH on the

pulmonary system are elevated peak inspiratory
pressures, decreases in Pao2 and increases in
Paco2 requiring the use of complete ventilatory
support to maintain adequate oxygenation and
ventilation.
Hypercarbia, hypoxemia, and acidosis are evident
when arterial blood gases are measured.6
Positive end-expiratory pressure has been shown
to exacerbate the cardiac and respiratory
consequences of IAH.

Pulmonary effects of increased

intra-abdominal pressure (2)

mechanical ventilation
often necessary
high peak airway
pressures ?barotrauma
high PEEP often
required further
compromising CO

Pulmonary effects of increased

intra-abdominal pressure (3)
Pressure on the IVC
predisposes to venous
stasis and increased
risk of
thromboembolism

Renal effects

include decreased renal plasma flow, glomerular filtration

rate, and glucose reabsorption. Oliguria also occurs, with
anuria noted in animal models when IAP reaches 30
mmHg.1 These effects occur without significant
decreases in blood pressure(mechanical,
RVR,compression of R veinoutflow obstuction
intraparenchymal pressureshunting of blood from R
cortex) .
Improvement of cardiac output does not improve renal
function, nor do renal blood flow and glomerular filtration
rate improve.
the placement of ureteral stents failed to improve renal
function.
Improvement in renal function occurred only after
abdominal decompression.7

These findings suggest that the effects of IAH

on renal function are related to compression of
the renal parenchyma itself and to
compression of renal vasculature and are not
related to decreased cardiac output. Other
mechanisms proposed include shunting of
blood away from the renal cortex into the
medulla, decreased renal arterial flow with a
concomitant increase in renal vascular
resistance, and the presence of high levels of
renin, aldosterone, and antidiuretic hormones.1

Experimental
Control

20
Aldosterone level
(ng/dl)

15
10
5
0
0

10

15

20

25

Fluids

IAP (mmHg above baseline)

Effect of increased intra-abdominal pressure on plasma
aldosterone. The increased levels are reduced by volume
expansion (J Trauma 1997;42:997-1003)

(ng/ml/hr)

Plasma renin activity

Experimental
Control

30
25
20
15
10
5
0
0

10

15

20

25

Fluids

IAP (mmHg above baseline)

Effect of increased intra-abdominal pressure on plasma
renin activity. The increased levels are reduced by volume
expansion (J Trauma 1997;42:997-1003)

IAH and Splanchnic Flow

Increases in IAP have adverse

effect on splanchnic flow
>15mmHgSMA blood flow
marked reduction in hepatic
artery and portal venous blood
flow
leads to mucosal acidosis and
oedema

Cycle of events created by

IAH on splanchnic circulation
Splanchnic
hypoperfusion
Hepatic
ischaemia

IAH

Gut mucosal acidosis

Bowel oedema

Coagulopathy
hypothermia

Unrelieved

acidosis
Intraabdominal
bleeding

?Free oxygen radicals

ACS

Distant organ damage

They measured mucosal and intestinal blood flow

and intramucosal pH (pHi) and found that
mesenteric and mucosal blood flow decreased when
IAP reached 20 mmHg, with intestinal mucosal flow
declining to 61% of baseline.

At an IAP of 40 mmHg, intestinal flow decreased to

28% of baseline.
The intestinal mucosa showed signs of a severe
degree of acidosis, measured by tonometer. These
changes in splanchnic blood flow occurred despite
maintenance of baseline cardiac output with volume
loading.

pp

IAP 25mmHg for

60 min
IAP 15mmHg for
60 min

Baseline
Bowel 5
TPO2
Axillary
TPO2

3
1
0

20

40

60

80

100

Effects of increasing IAP on bowel mucosal oxygen (tissue

partial pressure, TPO2) compared with systemic tissue
oxygenation in the axilla (J Trauma 1995;39:519-522)

blood flow to virtually every abdominal organ

decreased significantly. The only exception
was the adrenal gland; the reason this
organ is not affected is unknown ?

EFFECTS ON CNS

The rise in intra-abdominal pressure,

intrathoracic pressure leads to a rise in central
venous pressure which prevents adequate
venous drainage from the brain, leading to a rise
in intracranial pressure and worsening of
intracerebral oedema.

Intracranial Derangements
and IAH

IAH associated with

ICP

CPP

cerebral ischaemia
? Why?
may be due to
impairment of cerebral
venous outflow

increased intrathoracic pressure causing increased

resistance to cerebral venous return associated with
IAH( ?pseudotumor cerebri).
Volume expansion further increased ICP. Cerebral
perfusion pressure declined as ICP increased and
cardiac output declined.
Only abdominal decompression reversed effects of IAH.
The exact level of IAH that results in elevated ICP and
decreased CPP in the brain injured patient is unknown;

Abdominal compartment pressure

monitoring is done to help recognize life
threatening elevations in pressure before
ischemia or infarction of the abdominal
organs occurs. When a patient exhibits a
distended and taut abdomen, the
measurement of abdominal compartment
pressure can provide direction regarding
the need for decompressive surgery.

Measurement of I A P

Measurement of IAP
Direct

Indirect

Direct Monitoring

The most direct, accurate way to measure

intraabdominal pressure is through an
intraperitoneal catheter attached to a water
manometer or pressure transducer, the preferred
method in most experimental studies of IAH.1,6,15
Its use in the clinical situation is limited by the
potential complications, specifically the risk of
peritoneal contamination or bowel perforation.
Abdominal pressure measured during laparoscopy
is another example of direct measurement

Indirect Monitoring

Intraabdominal pressure may be indirectly measured

by measuring pressure within certain abdominal
organs.
The first indirect method described involves placement
of transfemoral catheters into the inferior vena cava.
The associated risks of this procedure include
infection and thrombus formation.
measurement of gastric pressure through gastrostomy
or nasogastric tubes
esophageal stethoscope catheter
urinary bladder pressure measurement.

Bladder Pressure
Monitoring

At intravesical volumes less than 100

mL, the bladder acts as a passive
reservoir, accurately reflecting
intraabdominal pressure within a range
of 5 to 70 mmHg.1,16 When bladder
volumes exceed 100 mL, the intrinsic
contraction of the bladder wall causes
bladder pressure to increase.

The basic technique of bladder pressure measurement is not

complicated. Fifty to 100 mL of sterile saline is injected into the
bladder through a Foley catheter while the tubing to the
drainage bag is clamped distal to the aspiration port.
The clamp is then opened to allow fluid to fill the tubing
proximal to the clamp and the tubing is then reclamped.
A 16-gauge needle attached to a water manometer or a pressure
transducer is then inserted into the aspiration port of the
catheter, zeroed to the level of the symphysis pubis, and the
intraabdominal pressure recorded.
Use of the pressure transducer attached to the bedside monitor
allows a pressure waveform to be printed. Slight variation will be
seen with the respiratory cycle.
Measurements should always be taken at end expiration
because the diaphragm is elevated at this point, and thoracic
pressure is less likely to influence the pressure reading

Patient positioning affects the accuracy of bladder

pressure measurements. Monitoring should occur
with the patient supine so that the weight of the
abdominal contents pressing on the bladder does
not falsely elevate the reading. Should the patient
be unable to remain supine, the position at which
the first measurement is taken should be noted and
subsequent measurements taken with the patient
in that position.2 Although the individual reading
may be inaccurate, trends in abdominal pressure
can still be assessed.

Others describe the use of a three-way Foley

catheter, with the saline injected into one of the
ports. Because three-way Foley catheters are not
routinely used, their use requires either identification
of the patient at risk before the catheter is inserted,
or replacement with a three-way catheter when the
need to measure IAP is identified. This increases
costs and the potential for infection. Burch et al.7
described a technique in which the drainage tubing
is clamped distal to the aspiration port and 50 mL of
saline is injected through the aspiration port of the
Foley catheter

Unfortunately, this procedure requires that the

closed urinary drainage system be opened
each time pressure is measured, placing the
patient at increased risk of infection.
Strict aseptic technique is essential. A sterile
towel should be placed under the Foley
catheter to maintain sterility.

In patients having a neurogenic

bladder or in those having a small
contracted bladder (e.g., after
radiotherapy), measurements may
be inaccurate.

It is also possible that bladder pressure

may not capture an elevation of the
abdominal compartment pressure if there
is a loculated area.
While abdominal compartment pressure
monitoring via the bladder may provide
valuable information regarding patients
with abdominal hypertension, abdominal
compartment syndrome should not be
ruled out in the presence of a normal
pressures if persistent clinical findings
exist

Grading system for ACS

Grade
Bladder pressure
(cm water)

Indication of
surgical
decompression

10-15

No evidence of
ACS

II

15-25

Based on patient
condition

III

25-35

Decompression
indicated

IV

>35

Immediate
decompression

Pressure

Grade

Management

10-15 mm Hg

maintain
normovolemia

16-25 mmHg

II

Hypervolemic
resuscitation

26-35 mmHg

III

decompression

> 35 mm Hg

IV

decompression
and reexploration

CT findings

CT findings common included tense infiltration of the

retroperitoneum out of proportion to peritoneal disease,
extrinsic compression of the inferior vena cava by retroperitoneal
hemorrhage or exudate, and massive abdominal distention with an
increased ratio of anteroposterior-to-transverse abdominal
diameter (positive round belly sign; ratio > .80; p < .001).
Direct renal compression or displacement, bowel wall thickening
with enhancement, and bilateral inguinal herniation were each
present in two of the four patients.
Radiologists should be aware of this life-threatening syndrome.
In the appropriate clinical setting, CT findings of increased
intraabdominal pressure should be swiftly communicated to other
physicians involved in treating the patient because the abdominal
compartment syndrome requires emergent surgical
decompression.

Central nervous system Implications

ICP
CPP

retinal capillaries rupture

Valsalva retinopathy

Sudden decrease of central vision

Management of ACS

Prevention
vs.
Formal Closure?

Management
Prevention Adequate resuscitation
Adequate ventilation

Identification
of patients at risk
Monitoring

Non-surgical
interventions

Paracentesis
Neuromuscular blockade
CNAP
Gut emptying
Octreotide

Prevention of ACS (2)

Open abdomen technique

Most commonly used open

abdomen techniques include
Bogota bag (25%)
absorbable mesh (17%)
Prolene mesh (14%)
silastic mesh (7%)
miscellaneous (28)%

Current opinion does

not support liberal use
of an open abdomen
technique to prevent
ACS

The Journal of Trauma, Infection and

Critical Care 1999;47 :509-511

An alternative technique is the 'vacuum-pack'

technique. Here the 3 litre bag is opened and placed
into the abdomen to protect the gut contents, under
the sheath. This has been referred to as the Bogota
bag, after the city in Colombia, South America, of its
inception.9
Two large calibre suction drains are placed over
this, and a large adherent steridrape placed over the
whole abdomen. The suction catheters are
connected to high-displacement suction to provide
control of fluid losses and create the 'vacuum-pack'
effect

The easiest method to control the open abdomen is

to use a silo-bag closure. A 3 litre plastic irrigation
bag is emptied and cut open so it lies flat. The
edges are trimmed and sutured to the skin, away
from the skin edges, using a continuous 1 silk
suture. It is useful to place a sterile absorbent drape
inside the abdomen to soak up some of the fluid and
ease control of the laparostomy.

Adverse Effects of Surgical

Decompression

Sudden release of the abdominal compartment

syndrome may lead to an ischaemia-reperfusion injury
The mechanism was postulated to be related to washout
of anaerobic metabolic products by reperfusion of the
previously underperfused splanchnic bed causing
acidosis, vasodilatation, cardiac dysfunction and arrest.
Prior to release the patient should be pre-loaded with
crystalloid solution. Mannitol and vasodilators such as
dobutamine or the phosphodiesterase inhibitors may
have a place here.

MEDICAL
DECOMPRESSION

The adverse cardiovascular and

pulmonary effects of intraabdominal hypertension [IAH]
were reversed with
pharmacological neuromuscular
blockade (NMB(

Management
Prevention Adequate resuscitation
Adequate ventilation

Identification
of patients at risk
Monitoring

Non-surgical
interventions

Paracentesis
Neuromuscular blockade
CNAP
Gut emptying
Octreotide

Prognosis

The death rate in patients with ACS is extremely high.

Several small series have reported death rates ranging from
42% to 71%.These high rates must be considered in the
context of the patients' underlying disease.
The majority of these patients are critically ill and are
admitted to the intensive care unit with severe intraabdominal sepsis, intra-abdominal injuries or after repair of
a ruptured abdominal aortic aneurysm.
Even with prompt recognition and abdominal
decompression, the frequency of multiple organ dysfunction
and death is high because of the severity of the initial
physiologic insult.

However, in the face of elevated IAP

and a clinical picture consistent with
ACS, the chance of survival is
extremely low without urgent
abdominal decompression.1

THANK YOU