Abdominal Compartment Syndrome

By
Sharra Way - Bingham, RN


? What it is ?
A disease process that dramatically increases
organ failure and death for medical and surgical
ICU patients
Abdominal Compartment syndrome occurs as a result of the
accumulation of fluid in the abdominal space from trauma
or surgical procedures, or the increasing of abdominal
contents due to tissue edema from an inflammatory
process or massive fluid resuscitation or from tumor
growth

As this pressure increases within the abdomen capillary
perfusion is compromised and tissue ischemia and/or
death occurs

If undetected or untreated multi-organ failure and patient
death may ensue


Objectives
Differentiate between intra-abdominal
hypertension (IAH) and abdominal compartment
syndrome (ACS)
Identify patient populations at risk for
IAH/ACS
Understand the pathophysiological process of
IAH/ACS
Discuss appropriate procedures for assessment
of abdominal pressure
Objectives
Anticipate clinical considerations for
management of IAH/ACS
What is a normal intra-abdominal
pressure
or
IAP

This is the pressure within the abdominal cavity
5 7 mmHg is normal in a critically ill adult
Intra abdominal Hypertension
IAH
Defined as sustained or repeatedly elevated
abdominal pressure

>12 and is graded
Grades of IAH
Grade I 12 15 mmHg
Grade II 16 20 mmHg
Grade III 21 25 mmHg
Grade IV >25 (ACS)
IAH
Sustained pressure, >12 that has significant
effects on abdominal organs and cardiac output
with subsequent dysfunction of both abdominal
and extra-abdominal organs
Understanding Abdominal Compartment Syndrome
APP Abdominal perfusion pressure
MAP Mean arterial pressure
IAP Intra-abdominal pressure
APP = MAP IAP
A critical IAP that leads to organ failure is
variable by patient & a single threshold cannot
be applied globally to all patients
APP is superior to IAP, arterial pH, base deficit
& lactate in predicting organ failure & patient
outcomes

Definition of ACS
A sustained IAP > 20 mmHg (with or without an
APP of <60 mmHg) that is associated with new
organ dysfunction/failure
Adverse physiological effects caused by massive
interstitial and retroperitoneal swelling which
leads to organ or multi-organ failure
Historically IAPs as high as 40 mmHg had been
acceptable; therefore, most clinicians are
concerned when IAP reaches 20 25 mmHg
Abdominal Compartment Syndrome
Primary ACS associated with injury or disease
in abdomen/pelvis requiring early surgical or
interventional radiological screening
Secondary ACS is from conditions not
originating in the abdomen/pelvis
Recurrent ACS is the redevelopment of ACS
following previous surgical or medical treatment
of primary or secondary ACS
Common Causes of ACS
Primary causes
Abdominal trauma with
bleeding
Pancreatitis
Ruptured abdominal aortic
aneurysm
Retroperitoneal hematoma
Obstructions/ileus
Pneumoperitoneum
Abcesses
Visceral edema


Common Causes
Secondary Causes
Acute respiratory distress
syndrome
Major trauma or burns
Massive fluid resuscitation
Hypothermia <33 degrees
Celsius
Acidosis with pH < 7.2
Hypotension
Massive blood transfusion > 10
units
Coagulopathy
Sepsis

Common Causes
Chronic Causes
Obesity
Liver failure with ascities
Malignancies

Ischemia
Inflammatory
response
Capillary leak
Tissue Edema
(Including bowel wall and mesentery)
Intra-abdominal hypertension
Fluid resuscitation
Physiologic Insult/Critical Illness
Pathophysiological Consequences
of ACS
Cardiovascular
Reduced Cardiac Output
Compression of the
inferior vena cava and
portal vein
Reduced blood return to
the heart
Afterload increased from
mechanical compression of
vascular beds and
vasoconstriction
Pathophysiology
Cardiovascular
Reduced Stroke volume
Tachycardia
Increased pressure on
great vessels making
hemodynamic monitoring
challenging with falsely
elevated and misguiding
pressures
Increased risk for
thromboembolic events
secondary to venous stasis
Pathophysiology
Pulmonary
Reduced lung compliance
secondary to diaphragmatic
elevation leads to
Hypoventilation and
ventilation-perfusion
mismatch
Increased work of
breathing
Hypoxia and hypercarbia
Mechanical ventilation
often required
Pathophysiology
Respiratory
Increased peak airway
secondary to decreased
lung compliance
Increased risk of
barotrauma


Pathophysiology
Renal
Increased IAH leads to
decreased renal blood flow
and decreased glomerular
filtration
Oliguria may be observed
with IAP of 15 - 20
An IAP of >30 leads to
anuria
Increase of antidiuretic
hormone and activation of
renin-angiotensin-
aldosterone system
Increased water retention
Pathophysiology
Abdominal Visceral
Reduced blood flow which
leads to
Intestinal ischemia
Decreased blood flow to all
abdominal organs
Pathophysiology
Central Nervous System
Increased thoracic and
central venous pressure
leads to
Decreased cerebral outflow
of blood
Increased intracranial
pressure which leads to
decreased cerebral
perfusion pressure


Measuring Intra-Abdominal Pressure
Importance of accurate measurement
Physical examination yields low levels of
detection of IAH/ACS
Early detection and intervention reduces
morbidity and mortality.
Diagnosis is dependent on frequent and accurate
measurement of IAP (watching trends)
Cost effective, safe and accurate
Assessment Guidelines
New ICU admission
Evidence of clinical deterioration
Pt has two risk factors for IAH/ACS
Decreased abdominal wall compliance
Increased intra-luminal contents
ileus, gastroparesis, obstruction
Increased abdominal contents
Pneumoperitoneum, hemoperitoneum, ascities, liver
dysfunction
Capillary Leak/fluid resuscitation

IAH/ACS Assessment algorithm from

World Society of Abdominal Compartment
Syndrome (WSACS)

www.wsacs.org

Excellent references
Types of Measurements
Direct Pressure via intraperitoneal catheters
Indirect Pressure
Gastric Measure
IVC
Rectal
Urinary bladder pressure Gold Standard
Urinary Bladder Pressure
Most technically reliable
Correlate closely with pressures measured directly
in the abdominal cavity
Reliably reproducible
Transduced through a Foley catheter
Intermittent Monitoring
Open Systems
Closed Systems
Equipment needed for open measurement
Disposable transducer
12 pressure monitoring
tubing
4-way stopcock
Red dead-ender
60 cc, lure-lock syringe,
sterile
Sterile normal saline
Clamp, non-sterile
Level

Procedure for open, intermittent monitoring
Collect and gather all
supplies
Attach stopcock to end of
sterile transducer
Important to maintain
sterile technique to avoid
contamination and
potential infectious
process
Procedure for open, intermittent monitoring
Attach pressure tubing to
the remaining end of the
transducer
Procedure for open, intermittent monitoring
Fill 60 cc syringe with 40
cc of sterile normal saline
Attach syringe to side
port of the stopcock
Flush stopcock, pressure
tubing and transducer
with the normal saline
ensuring all air is removed
Procedure for open, intermittent monitoring
Clamp the urinary drain tubing distal to the sampling port
Cleanse the sampling port with alcohol
Using sterile technique attach the pressure tubing to the
LuerLok connecting sampling port of the urinary catheter
Procedure for open, intermittent monitoring
Instill 25 cc of sterile normal saline into urinary
catheter via the sampling port (Larger vol. of NS can result in
falsely elevated IAP measurements)
Briefly release the clamp to allow fluid from the bladder
to fill tubing and reclaim
Read the IAP as a mean pressure at end expiration 30
60 seconds after instillation.
Perform with patient supine
Notify MD for sustained IAP greater than 12 mmHg
unless otherwise ordered.
Disadvantages with open, intermittent monitoring
Collecting a number of items
Correct assembly
Risk of infection every time system is accessed

Closed Monitoring
AbViser, Wolfe Tory Medical, SLC, UT
Pre-assembled kit
Adapts to Foley catheter and any transducer
Reduces risk of infection
Readily available, easily assessable data
Measuring Bladder Pressure
Position patient flat & supine
Read Mean pressure
End Expiration
Management Considerations
Early detection via frequent monitoring of at risk
patients
Screen for IAH/ACS in new ICU admissions with
new or progressive organ failure
Look for trends of increasing abdominal pressures
Preserve organ perfusion and treat clinical
conditions with grades I & II
Management Considerations
Early surgical consultations for at risk patients
Early intervention for ACS or Grade III
Anticipate emergent surgical interventions to
prevent tissue damage/death

Management Considerations
Anticipate patient to return with an alternative
surgical closure or open abdomen.
The abdominal contents will not be sutured into
the abdominal cavity
Alternative closures vary from surgeon to
surgeon
Examples:
The Bogata Bag A 3 L IV bag, open and
sterilized and applied to the abdominal opening

Management Considerations
KCI Vac Pac
Sponge overlies abd.
Dressing/contents
Attached to
continuous suction
canister
Covered over with
occlusive dressing
Management Considerations
Ioban Dressing
An occlusive dressing
with iodine
impregnation
Surgical towels will
overlie abdominal
contents with JP
drains Ioban
overlies abdomen
Another Excellent Reference,

IAH/ACS Management Algorithm from
WSACS

www.wsacs.org
Conclusion
Know the difference between IAH and ACS
IAH = Abdominal pressure >12 and graded via severity
ACS = Abdominal pressures > 20 25

Identify At risk patient populations
abdominal trauma/major burns
Pancreatitis
Ruptured AAA
abdominal obstructions/ischemia
ect.
Conclusion
Understand the pathophysiology
Ischemia/inflammation inflammatory response
capillary leak + fluid resuscitation = tissue edema in an
uncompromising cavity = ACS = tissue/cell death = bad

Perform an accurate assessment of abdominal pressure
using Abdominal bladder pressure monitoring via Foley
catheter or AbViser Wolfe Torey Medical

Anticipate patient interventions/outcomes
Support/educate family
Case Study - 63 Y.O. male pt with pancreatitis is admitted
to the ICU. Pt has history of gallbladder disease, COPD
and ETOH abuse. He has been without ETOH reportedly
for approximately 24 hrs. VS upon admission are T 38.0,
HR 130, BP 90/62, MAP 61, RR 30 34 & O2 sat of 91%
on 100% NRB, wt approximately 125 kg. His breathing is
labored and he has c/o SOB. He is also mildly agitated &
resistive to O2 therapy with Bi-Pap. His lung sounds are
diminished bilaterally. Denies recent increase in cough.
His abdomen is firm and distended. States unknown last
BM but + for N/V.
He has a Foley catheter in place with
approximately 100 cc of dark, amber urine in the
collection chamber. Lab values show H&H of
10.2/31.0, wbc 20, K 5.0, Na 142, Foley was
placed approximately 4 hours ago in the ED. His
peripheral arterial pulses are weak and thready
and his BLE show signs of PVD. He is currently
receiving bolus # 3 of NS.

Does this patient need IAP monitoring?

Is he at risk?

What could you use as a reference if you were
unsure?

After consulting with your attending MD, it is
decided that a baseline ABP reading would be
appropriate for this patient. Your initial ABP is
15mmHg.




Does this value represent intra-abdominal
hypertension or abdominal compartment
syndrome?

What is his APP based on his MAP and IAP?




What grade would you give this value?

Why is this patient at risk?

How would you proceed?

After reporting the findings to the resident,
serial ABP readings are ordered Q6 HR. His SBP
continues to remain low with a map consistently <
65 & his respiratory status continues to
deteriorate. The resident also orders another
fluid bolus.

With what you have learned about IAH /ACS
management, what clinical suggestions could you
collaborate on to advocate for your patient?


After collaboration with the medical team the decision is
made to intubate as his O2 sats continue to drop and RR
rate cont. to increase. After intubation and appropriate
sedation, the patient continues to have an increasingly
firm abdomen, increased HR and decreased SBP and map
<60 despite added norepinephrine. He is also now vented
with a respiratory rate of 24 30 and has become
increasingly agitated. His urine output for the last 2
hours is 30 ml. You repeat the ABP prior to the 4 hr
interval and you notice that his ABP value has risen to 20
after two separate measurements. What could you
expect at this point?

Bibliography
Cheatham, M. et al. (2007). Results from the
International Conference of Experts on intra-
abdominal hypertension and abdominal
compartment syndrome. II. Recommendations.
Intensive Care Med. 33:951 962.

Hunter, J.D. (2008). Abdominal Compartment
syndrome: An under diagnosed contributory
factor to morbidity and mortality in the
critically ill. Postgrad Med J. 84:293-298.


www.abdominalcompartmentsyndrome.org

The World Society of Abdominal Compartment
Syndrome, www.wsacs.org