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
Grade
Grade
Grade
I
II
III
IV
12 – 15 mmHg
16 – 20 mmHg
21 – 25 mmHg
>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
Physiologic Insult/Critical Illness
Ischemia
Inflammatory
response
Fluid resuscitation
Capillary leak
Tissue Edema
(Including bowel wall and mesentery)
Intra-abdominal hypertension
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-angiotensinaldosterone 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
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–
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–
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
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•
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 intraabdominal 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