ABDOMINAL

COMPARTMENT
SYNDROME

The silent killer!

DR.MD AHSANUL ABEDIN

Astt.Registrar,SU-II.CMCH
• Have you ever seen a critically ill patient
become progressively more swollen and
edematous after fluid resuscitation?
• Have any of your ICU patients developed
renal failure requiring dialysis?
• Have you ever seen a patient develop
multiple organ failure and die?

What was their intra-abdominal

pressure?
 Remember
• Trauma is not required for ACS to develop:
– Intra-abdominal hypertension and ACS occur in many
settings .
• IAP measurements are clinically useful: Help to
determine if IAH is contributing to organ dysfunction (i.e.
useful if normal or abnormal)
• Waiting for clinically obvious ACS to develop
before checking IAP changes urgent problem to
emergent one.
• Medical interventions are often all that is needed
• IAP monitoring will allow early detection and
early intervention for IAH before ACS develops.
 Definitions
WCACS, Antwerp Belgium 2007

• Intra-abdominal Pressure (IAP): Intrinsic pressure

within the abdominal cavity
• Abdominal perfusion Pressure (APP):Mean arterial
pressure- IAP
• Intra-abdominal Hypertension (IAH): A sustained IAP >
12 mm Hg (often causing occult ischemia) or APP <60
mm Hg without obvious organ failure

• Abdominal Compartment Syndrome (ACS): IAH > 20

mm Hg or APP <60 mm Hg with at least one
organ dysfunction or failure
Compartment Syndromes versus
Hypertension

• Abdominal compartment syndrome =

Emergent Surgical Disease.

• Intra-abdominal hypertension =
Urgent Medical Disease.
 What intra-abdominal pressures
are concerning?
Pressure (mm Hg) Interpretation
0-5 Normal
5-10 Common in most ICU patients
> 12-15(Grade I) Intra-abdominal hypertension
16-20 (Grade II) Dangerous IAH - begin non-
invasive interventions
>21-25 (Grade III) Impending abdominal compartment
>25(GradeIV ) syndrome- strongly consider
decompressive laparotomy
The IAH grades have been revised downward as the detrimental impact of
elevated IAP on end-organ function has been recognized WSACS.org
Physiologic Insult/Critical Illness
Ischemia Inflammatory (SIRS) response

Fluid resuscitation
Capillary leak

Tissue Edema
(Including bowel wall and mesentery)

Intra-abdominal hypertension
 Causes of Intra-abdominal
Pressure (IAP) Elevation
1. Major abdominal /
retroperitoneal problem
2. Ischemic insult / SIRS
requiring fluid
resuscitation with a
positive fluid balance of 5
or more liters within 24
hours – (10 lb weight gain)

Where does all that

fluid go?
The fluid goes Right Here!!
 How common – Shock with fluid
resuscitation
• Requeira, 2007: Intraabdominal hypertension in
patients with septic shock.
– 51% incidence of IAP > 20 mm Hg in septic shock

• Daugherty, 2007: Abdominal compartment syndrome

is common in medical intensive care unit patients
receiving large volume resuscitation.
– 85% of patients with 5 liters positive fluid balance had IAH
– 30% had IAP > 20 with organ failure (abdominal
compartment syndrome)
 TYPES OF ACS
Primary: Due to condition associated with injury or
disease in the abdominopelvic region requiring
emergent surgical or angioradiological
intervention.
Secondary:Due to condition outside abdomen.
Recurrent:Redevelopes following initial successful
medical & surgical treatment of either primary or
secondary ACS or following closure of
decompressive laparotmy.
 Causes of ACS
• Primary (ie, acute) :
– Penetrating trauma
– Intraperitoneal hemorrhage
– Pancreatitis
– External compressing forces, such as debris from
a motor vehicle collision or after a large structure
explosion
– Pelvic fracture
– Rupture of abdominal aortic aneurysm
– Perforated peptic ulcer
 Causes of ACS(contd..)
• Secondary:
– Large-volume resuscitation: The literature shows
significantly increased risk when more than 3 L are
infused.
– Large areas of full-thickness burns: In 2002, Hobson et
al demonstrated abdominal compartment syndrome
within 24 hours in burn patients who had received an
average of 237 mL/kg over a 12-hour period.2
– Penetrating or blunt trauma without identifiable injury
– Postoperative
– Packing and primary fascial closure, which increases
incidence
– Sepsis
• Chronic / Recurrent:
– Peritoneal dialysis
– Morbid obesity
– Cirrhosis
Intra-abdominal Hypertension
&
Abdominal Compartment
Syndrome
Physiologic Sequelae
Physiologic Sequelae
Cardiovascular:
• Increased intra-abdominal pressures causes:
– Compression of the vena cava with reduction in venous return
to the heart
– Elevated ITP with multiple negative cardiac effects
• The result:
– Decreased cardiac output increased SVR
– Increased cardiac workload
– Decreased tissue perfusion.
– Misleading elevations of CVP and PAWP
– Cardiac insufficiency Cardiac arrest
Ridings, et al 1995
Physiologic Sequelae
Pulmonary:
• Increased intra-abdominal pressures causes:
– Elevation of the diaphragms with reduction in lung volumes,
stiffening of thoracic cage, reduced alveolar inflation, increased
intersitial fluid (lymph obstruction)
• The result:
– Elevated intrathoracic pressure
– Increased peak pressures, Reduced tidal volumes
• Intersitial edema, Atelectasis, hypoxia, hypercarbia
– Ventilator Induced lung injury/Barotrauma
• Cytokine release – pro-inflammatory response
• ARDS
Physiologic Sequelae: Lung

Normal

ITV, ITP

IAH
ATX
 Physiologic Sequelae
Gastrointestinal:
• Increased intra-abdominal pressures causes:
– Compression /Congestion of mesenteric veins
&capillaries (capillary flow 25 mm arterial down to 15 mm
venous)
– Reduced cardiac output to the gut
The result:
– Decreased gut perfusion, increased gut edema and leak
– Ischemia, necrosis, cytokine release, neutrophil priming
– Bacterial translocation
– Development and perpetuation of SIRS
– Further increases in intra-abdominal pressure
IAP>15 mm Hg reduces portal venous flow by 30% &
hepatic arterial flow by 40%
 Physiologic Sequelae
Renal:
• Elevated intra-abdominal pressure causes:
– Compression of renal veins, parenchyma
– Reduced cardiac output to kidneys
The Result:
– Reduced blood flow to kidney
– Renal congestion and edema
– Decreased glomerular filtration rate (GFR)
– Renal failure, oliguria/anuria
 Physiologic sequelae
Abdominal Wall:
• Increased IAP causes decreased abdominal
wall blood flow& fascial ischaemia.
• Result:
Wound complication (dehiscence &
infection)
 Normal Abdominal CT
Normal kidney

   
Note that
abdomen is
oval, not
round                                                                      

Inferior Vena Cava

 Abdominal CT in ACS – Renal
compression Kidneys are
Pickhardt, AJR 1999
compressed,
Note that patient is
abdomen is anuric
round, not
oval

Retroperitoneal hemorrhage Flattened Inferior Vena Cava

 Physiologic Sequelae
Neuro:
• Elevated intra-abdominal pressure causes:
– Increases in intrathoracic pressure
– Increases in superior vena cava (SVC) pressure with reduction in
drainage of SVC into the thorax
The Result:
– Increased central venous pressure and IJ pressure
– Increased intracranial pressure
– Decreased cerebral perfusion pressure
– Cerebral edema, brain anoxia, brain injury
• Maryland Shock Trauma unit often decompresses abdomens in patients
with intractable intra-cranial hypertension
 Physiologic
Sequelae
Direct impact of IAP on
common pressure
measurements:
• IAP elevation causes
immediate increases in
ICP, IJP and CVP (also in
PAOP)

15 liter bag placed on abdomen

(Citerio 2001)
 IAH in neuro patients
Joseph 2004: Decompressive laparotomy to treat
intractable intracranial hypertension
• 17 patients with intractable ICP despite maximal therapy
(including decompressive craniectomy in 14)
– Mean ICP 30 mm Hg, Mean IAP 27 mm Hg
– All 17 underwent decompressive laparotomy
• 100% had drop in the ICP immediately or in few hours
– To mean of 17 mm Hg
• 11 had persistent reduction in ICP
– These 11 all survived and with “good neurologic outcome”
Ischemic Time and Cell survival
Aerobic
metabolism
Baseline cellular
oxygen requirement

Anaerobic
metabolism

Irreversible Cellular Apoptosis or necrosis

Rivers – Early goal directed therapy for sepsis lecture

 Circling the Drain

Intra-abdominal Pressure

Mucosal
Capillary leak Breakdown Decreased O2 delivery

Free radical formation (Multi-System Organ Failure) Anaerobic metabolism

Bacterial translocation,
Cellular Apoptosis,
Necrosis

Acidosis
 How common is this syndrome*?
Malbrain, Intensive Care Medicine (2004):
Abdominal Total MICU SICU
pressure: Prevalence prevalence prevalence
IAP > 12 58.8% 54.4% 65%
IAP > 15 28.9% 29.8% 27.5%
IAP > 20 8.2% 10.5% 5.0%
plus organ failure

*These data are for ALL ICU patients. MUCH higher if

you use a protocol to select high risk patients.
 CLINICAL PRESENTATION
SYMPTOMS: Varies depending upon the cause of ACS
• Abdominal pain
• Distended abdomen
• Difficulty breathing
• Decreased urine output
• Syncope
• Melena
• Nonsteroidal anti-inflammatory drug (NSAID) use
• Alcohol abuse
• Nausea and vomiting
• History of Pancreatitis.
SIGNS:
• Increased abdominal girth.
• Wheezes, rales, increased respiratory rate
• Cyanosis
• Wan appearance
 CLINICAL PRESENTATION
• Laboratory Studies
• Comprehensive metabolic panel (CMP)
• Complete blood cell count (CBC)
• Amylase and lipase assessment
• Prothrombin time (PT), activated partial
thromboplastin time (aPTT) if the patient is
heparinized
• Test for cardiac markers
• Urinalysis and urine drug screen
• Measurement of serum lactate levels.
• Arterial blood gas (ABG): This is a quick way to
measure the pH, lactate, and base deficit.
 CLINICAL PRESENTATION
• Imaging Studies
• Examine the abdominal series for evidence of free
air or bowel obstruction.
– Realize plain abdominal radiographic studies
are often useless in identifying abdominal
compartment syndrome.
• Abdominal CT scanning
• Abdominal ultrasonography
– An aortic aneurysm, particularly when large,
may be detected.
– Bowel gas or obesity makes performing the
study difficult.
• Other Tests
• Intraluminal bladder pressure measurement.
 How good is clinical judgment for
detecting elevated IAP?
Prospective, blinded trial - Staff
physician judgment

Results: < 50% of the time was

the clinician able to determine
when IAP was elevated.

“…findings suggest that more

routine measurements of
bladder pressure…”
Kirkpatrick, Can J Surg 2000
Intra-Abdominal Pressure
Monitoring
 Intra-Abdominal Pressure
Monitoring

“The reference standard for intermittent

IAP measurement is via the bladder with
a maximal instillation volume of 25 ml
sterile saline.”

WSACS.org
 “Home Made” Pressure
Transducer Technique
Home-made assembly:
– Transducer
– 2 stopcocks
– One 50 ml syringe,
– 1 tubing with saline bag
spike / luer connector
– 1 tubing with luer both
ends
– 1 needle / angiocath
– Clamp for Foley
Assembled sterilely, used in
proper fashion!
 “Home Made” Pressure
Transducer Technique
PROBLEMS:
• Home-made:
– No standardization - confidence problem with data
– Sterility issues
• Time consuming* – therefor its use is late and infrequent
due to the hassle factor (i.e. not monitoring - waiting for ACS)
• Data reproducibility errors - what are the costs /
morbidity of inaccurate or delayed information?
• Other: Needle stick, Recurrent penetration of sterile
system, Leaks, re-zeroing problems, failure to trend
 Fluid-Column Manometry
Problems:
Failure to pay extreme
attention to detail may lead
to errors
• Siphon effect leads to
false elevations
• Inadequate volume of
infusion will lead to
falsely low
measurements
CAUTI Risk - Need to infuse
urine back into patient
Sedrak 2002
 Bladder Pressure Monitoring:
How to do it
Commercially available devices :
– Foley Manometer – (Bladder manometer)
– CiMon (Gastric)
– Spiegelberg (Gastric)
– AbViser – (Bladder transduction)
– IAP monitor – (Bladder transduction)
Advantages – Simple, Standardized,
Reproducible, Time efficient, Sterile
 Common Questions: How much fluid
should be infused into bladder?

Non-compliant Compliant
bladder: Measured bladder:
pressure increases as Measured pressure
volumes exceed 50 ml of changes very little
infusion with higher
volumes of fluid
IAP
infusion
Measured
(mm Hg)

WSACS: Max
volume 25 ml,
1 ml/kg in
children.
Volume of infusion (ml)
 Common Question: How do I recognize
appropriate IAP transduction onto my
monitor?
Proper transduction
clues:
• Respiratory
variation noted
(subtle at low
pressures)
• Oscillation test
positive
• Reproducible over
several
measurements
Does IAH / ACS affect patient outcome?

Mixed Med-Surg
population
•IAH predicted mortality

IAH > 12 mortality 38.8%

No IAH - mortality: 22.2%

Malbrain, Crit Care Med, 2005

 Does IAH / ACS affect patient
outcome?
Al-Bahrani, 2008: Clinical relevance of intra-
abdominal hypertension in severe acute
pancreatitis.
18 cases of severe pancreatitis
• 7 (39%) cases with IAP < 15 mm Hg:
14 % mortality
Mean ICU LOS 4 days
• 11 (61%) cases with IAP > 15 (all over 20) mm Hg:

45 % mortality
Mean ICU LOS 21 days
 Does IAH intervention affect
patient outcome?
Ivatury, J Trauma, 1998: Intra-abdominal hypertension
after damage control surgery.
• 70 patients monitored for IAP > 18 mm Hg (25 cm H2O)
– 25 had facial closure at time of surgery:
• 52% developed IAP > 18 mm Hg
• 39% Died
– 45 cases had abdomen left “open”:
• 22% developed IAP > 18 mm Hg
• 10.6% Died
 Does IAH intervention affect
patient outcome?
Sun, 2006: Indwelling peritoneal catheter vs conservative
measures in fulminant acute pancreatitis.
• 110 cases of severe fulminant pancreatitis - RCT
– Control group: Routine ICU supportive care
– Study group: Routine ICU supportive care PLUS
• IAP monitoring (mean pressure 21 mm Hg on day 1)
• Indwelling peritoneal drain catheter (drain 1800 cc on day 1)
– Outcome:
• Control - 20.7% mortality, 28 day hospital LOS
• Study group - 10.0% mortality (p<0.01), 15 day LOS
 Does IAH intervention affect
patient outcome?
Cheatham 2007, Is the evolving management of IAH/ ACS
improving survival? Acta Clinica Belgica
• Introduced management protocol in 2005, compared before and
after data:
– Open abdomens decreased from 28% to 15% (medical
management)
– When they do open, they do it sooner (do not wait for ACS)
• Days to closure decreased from mean of 21 days to 6 days
• Successful closure during primary visit improved from 1/3 to 2/3
– Ventilator days decreased
– Length of stay decreased from 28 days to 18 days
– Survival improved from 51% to 72%
 Does IAH / ACS affect patient
outcome?
Points:
• IAH / ACS is common in the ICU environment (including yours).
• IAH and ACS increase morbidity, mortality and ICU length of stay.
• Early, protocol driven interventions improve outcomes without
increasing cost of care (shorter ICU and hospital LOS)
However:
• Clinical signs of IAH are unreliable and only show up late in the
clinical course …..SO
• Early monitoring (TRENDING) & detection of IAH with early
intervention is needed to obtain optimal outcomes.
Management of IAH
and ACS
 IAH/ACS Management
Relatively easy, bedside nursing control interventions
• Bed Position (Binders – NO!)
– Consider fully recumbent with reverse trendelenberg

• Sedation, Pain control

– Often all that is needed
• Fluids – enough but not too much
– Be aware of problems with hemodynamic data in the face of IAH
– Think about infusion volumes, concentrating some of the drips
• Abdominal perfusion pressure (>50- 60 mm Hg)
– Similar to Cerebral perfusion pressure
– APP = MAP-IAP
• NGT / Cathartics / Rectal tube / enemas
• Paralysis - Balance risk vs. benefit
IAH/ACS Management :
Positioning

Vasquez, 2007
IAH/ACS Management: Paralysis
IAP

UOP

De Waele, Crit Care Med 2003

 IAH/ACS Management: Colloids
O’Mara, 2005: Prospective randomized evaluation of IAP
with crystalloid and colloid resuscitation in burns
• 31 cases with >25% burn plus inhalation or >40% burn
without inhalation
– Randomized to saline vs plasma
• Results post resuscitation:
– Crystalloid IAP mean 26.5 mm Hg
– Plasma IAP mean 10.6 mm Hg
 IAH/ACS Management:
Hemofiltration
Oda, 2005: Management of IAH in patients with severe acute
pancreatitis using continuous hemofiltration.
• 17 cases of severe pancreatitis and IAH
– Treated with hemofiltration when IAP + 15 mm, PRIOR to
developing renal insufficiency (maintained adequate serum
oncotic pressure with albumin)
• Results:
– Interleukin (IL-6) cytokine levels cut in half
• Reduced vascular permeability and interstitial edema
– Mean IAP value dropped from 15 mm to less than 10 mm
– 16 of 17 patients discharged alive without complication
 IAH/ACS Management:
Paracentesis
Multiple case series reporting successful treatment
of IAH and ACS:
– Latenser 2002: Burn patient management
– Reckard 2005: Peripancreatic fluid filled mass
– Sharp 2002: Pediatric blunt trauma
– Etzion 2004: Malignant ascites therapy
– Sun 2006: Pancreatitis (prospective RCT)
• Cut deaths in half, cut hospital LOS by 13 days
 IAH/ACS Management
Decompressive Laparotomy:
• Err on the side of early vs late intervention
– Less bowel edema or cell damage, better chance
of early closure and early recovery.
• Be aware that delaying care until this
complication occurs is VERY expensive –
more expensive the longer you wait.
 IAH/ACS Management:
Decompressive Laparotomy

Rigid Abdomen in ACS

Post decompressive laparotomy
Decompressive Laparotomy
• Delay in
abdominal
decompression
may lead to
intestinal ischemia
• Decompress Early!
 Decompressive Laparotomy

Post-operative dressing Several days post-op

 No such thing as an “Open
Abdomen” in the ICU
• “Open Abdomen” Vac-pac dressing placed in OR.
Now 6 hours post-op:
– MAP=70 HR=114 IAP=24
– UOP < 30 cc/ hour, PIP = 60 cm H2O
– Lactate 6.5
– Abdominal dressing firm and bulging

• Vacuum pack is removed, replaced with silo:

– Dramatic bowel evisceration
– MAP=70 HR=96 IAP=12
– UOP >100 cc/ hour PIP = 30 cm H2O
 No such thing as an “Open
Abdomen” in the ICU
• 24 hours into ICU
stay:
– Worsened bowel
edema
– However:
• MAP = 79
• IAP = 12
• Lactate = 1.9
Note expansion of viscera
 Is IAP monitoring and intervention
cost effective?
• IAH is very common in fluid resuscitated patients
• IAH cannot be clinically detected
• IAH/ACS outcome is time dependent.
• Delayed detection/intervention consumes more
resources
• Delayed detection/intervention results in higher
mortality.
• Aggressive intervention leads to reduced costs with
better outcomes.
So……………….
 Is IAP monitoring and intervention
cost effective?
• The cost of monitoring intra-
abdominal pressure - early and
often - is far outweighed by the
savings in clinician time, organ
function, hospital days and lives
saved.
IAH monitoring and
intervention protocol
WSACS IAH/ACS
Guidelines

Assessment algorithm
WSACS IAH/ACS
Guidelines

Management algorithm
IAP monitoring
algorithm
• Entry criteria defined
in table
• Nurse is
empowered
to enter any patient
fulfilling these criteria
 IAP Monitoring & Intervention Protocol
IAP monitoring Q 2 hours for first
24-48 hours

IAP IAP 12 to 15 IAP 15-20 mm Hg IAP >20-25 mm Hg

consistently mm Hg with no evidence or evidence of
<12 mm Hg of organ dysfunction/ organ dysfunction/
•Careful fluid management ischemia (ACS) ischemia (ACS)
•Correct CVP for IAP
•Adjust bed position?
•Optimize APP?
Reduce IAP •Concentrate drips
•Sedate Medical Management
measurements
• Sedation/pain control
to Q4-6 hours
• Empty GI tract
for 24 hours
-Gastric suction, cathartics
-Rectal tube/enemas Surgical consult:
“Second Hit” pt. IAP remains • Neuromuscular blockade Consider Surgical
develops new <12 mm Hg • Colloids/diuretics Decompression
indication for IAP discontinue • Paracentesis/Percutaneous drain
monitoring monitoring • CVVH plus Colloids
 Final Thought
Do NOT wait for signs of ACS to be present
before you decide to check IAP
– By then the patient has one foot in the grave!
– You have lost your opportunity for medical therapy
– The costs of saving this patient are now HUGE

Monitor ALL high risk patients early and often:

– TREND IAP like a vital sign
– Intervene early, before critical pressure develops