Intra-Abdominal

Hypertension (IAH)

&
Abdominal
Compartment
Syndrome (ACS)
• 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?

 Case: Septic child
5 y.o. female presenting with septic syndrome
• Treatment: Fluids, antibiotics, vasopressors
• 24 hours into therapy develops worsening
hypotension, oliguria, hypoxemia, hypercarbia.
PIP rises from 20 to 40 cm
• IAP = 26 mm Hg decompressive
laparotomy
• Immediate resolution of renal, pulmonary and
hemodynamic compromise
• 7 days later abdomen closed. Alive and well
now.
DeCou, J Ped Surg 2000
 Case: Dyspnea in ER
67 y.o. female presenting to ER with pleurisy, dyspnea
• Hypotensive, agitated, H&P suggest liver dz
• IVF resuscitation, intubation, sedation
• Worsened over next 4-6 hours - Difficult to ventilate,
hypoxic/hypercarbic, hypotension, no UOP.
• IAP = 45 mm Hg, abdominal ultrasound showed tense
ascites paracentesis of 4500 cc fluid (IAP = 14)
• Immediate resolution of renal, pulmonary and
hemodynamic compromise.
• Pathology shows malignant effusion – pancreatic CA.
• Care withdrawn at later time and allowed to expire.

Etzion, Am J EM 2004
 Case: Aspiration patient
77 y.o. male aspirated on general medicine floor.
Transferred to MICU & intubated; hypotensive.
• 10 liters IVF overnight, Levophed 40 mcg/min.
• Anuric (35 ml urine in 8 hours).
• IAP = 31 mm Hg. KUB – massively distended
small and large bowel. U/S shows no free ascitic
fluid.
• Surgeon consulted for possible decompressive
surgery
• Rx: NGT, Rectal Tube, oral cathartics
• 1 hour later: IAP 12 mm Hg, UOP 210 ml,
norepinephrine discontinued.
Cheatham, WSACS 2006
 Case Points
• Trauma is not required for ACS to develop:
– Intra-abdominal hypertension and ACS occur in
many settings (PICU, MICU, SICU, CVICU, NCC,
OR, ER).
• IAP measurements are clinically useful: Help to
determine if IAH is contributing to organ
dysfunction (i.e. useful if normal or abnormal)
• “Spot” IAP check results in delayed diagnosis:
– Waiting for clinically obvious ACS to develop before
checking IAP changes urgent problem to emergent
one.
• 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
• Intra-abdominal Hypertension (IAH): An
IAP > 12 mm Hg (often causing occult
ischemia) without obvious organ failure
• Abdominal Compartment Syndrome
(ACS): IAH with at least one overt organ
failing
 Types of IAH /ACS
WCACS, Antwerp Belgium 2007

• Primary – Injury/disease of abdomino-

pelvic region, “surgical”

• Secondary – Sepsis, capillary leak, burns,

“medical”

• Recurrent – ACS develops despite

surgical intervention
 IAP Interpretation
Pressure (mm Hg) Interpretation
0-5 Normal

5-10 Common in most ICU patients

> 12 (Grade I) Intra-abdominal hypertension

16-20 (Grade II) Dangerous IAH - begin non-

invasive interventions

>21-25 (Grade III) Impending abdominal compartment

syndrome - strongly consider
decompressive laparotomy
Physiologic Insult/Critical Illness

Ischemia Inflammatory response

Fluid resuscitation
Capillary leak

Tissue Edema
(Including bowel wall and mesentery)

Intra-abdominal hypertension
 Causes of Intra-abdominal
Pressure (IAP) Elevation

• Major abdominal / retroperitoneal problem

• 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?

Intra-abdominal Hypertension
&
Abdominal Compartment
Syndrome
Physiologic Sequelae
 Physiologic Sequelae
Cardiac:
• Increased intra-abdominal pressures cause:
– Compression of vena cava with reduced venous
return
– Elevated intra-thoracic pressure with multiple
negative cardiac effects
• Result:
– Decreased cardiac output, increased SVR
– Increased cardiac workload
– Decreased tissue perfusion
– Misleading elevations of CVP and PAWP
– Cardiac insufficiency; cardiac arrest
 Physiologic Sequelae

Pulmonary:
• Increased intra-abdominal pressures causes:
– Elevated diaphragm, reduced lung volumes &
alveolar inflation, stiff thoracic cage,, increased
interstitial fluid
Result:
– Elevated intrathoracic pressure (which further
reduces venous return to heart, exacerbating
cardiac problems)
– Increased peak pressures, reduced tidal volumes
– Barotrauma - atelectasis, hypoxia, hypercarbia
– ARDS (indirect - extrapulmonary)
 Physiologic Sequelae

Gastrointestinal:
• Increased intra-abdominal pressures causes:
– Compression / Congestion of mesenteric veins and
capillaries
– Reduced cardiac output to the gut
The result:
– Decreased gut perfusion, increased gut edema and
leak
– Ischemia, necrosis
– Bacterial translocation
– Development and perpetuation of SIRS
– Further increases in intra-abdominal pressure
 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
• Mortality of renal failure in ICU is over 50% - DO NOT WAIT
for this to occur!
 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
 Circling the Drain

Intra-abdominal Pressure

Mucosal
Capillary leak Breakdown Decreased O2 delivery

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

Bacterial translocation

Acidosis
 IAH / ACS affects outcome
Points:
• IAH and ACS are common entities in the critical
care environment (including your own).
• IAH and ACS increase morbidity, mortality and ICU
length of stay…………
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 reduce these
complications.
Management of IAH and ACS
Abdominal Perfusion Pressure (APP)

APP = MAP – IAP

• Abdominal perfusion pressure reflects

actual gut perfusion better than IAP
alone

• Optimizing APP to > 60 mm Hg should

probably be primary endpoint
 IAH/ACS Management:
Decompressive Laparotomy
 Decompressive Laparotomy

• Delay in abdominal decompression

may lead to intestinal ischemia
• Decompress early!
Intra-Abdominal Pressure
Monitoring
 Intra-Abdominal Pressure
Monitoring
Bladder pressure monitoring through the
Foley catheter is:
– The current standard for monitoring
abdominal pressures (Consensus, World Congress
ACS Dec 2004)

– Comparable to direct intraperitoneal pressure

measurements, but is non-invasive (Fusco 2001,
Davis 2005, Risin 2006, Schachtrupp 2006)

– More reliable and reproducible than clinical

judgment (Kirkpatrick, CJS 2000; Sugrue World J Surg
2002)
 “Home Made” Pressure Transducer
Technique
Home-made assembly:
– Transducer
– 2 stopcocks
– 1 60 ml syringe,
– 1 tubing with saline
bag spike / luer
connector
– 1 tubing with luer both
ends
– 1 needle / angiocath
– Clamp for Foley
Assembled sterilely in
proper fashion
 “Home Made” Pressure Transducer
Technique
PROBLEMS:
• Home-made:
– No standardization
– Sterility issues
• Time consuming – therefore it is used infrequently
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
 Bladder Pressure Monitoring:
How to do it

Commercially available devices :

– Foley Manometer – (Bladder manometer)
– CiMon (Gastric)
– Spiegelberg (Gastric)
– AbViser – (Bladder transduction)

Advantages – Simple, standardized,

reproducible, time-efficient, sterile
AbViser Intra-Abdominal Pressure
Monitoring Kit
Closed system in-line with the Foley
catheter
• Once attached it is left in place during
entire time IAP is measured.
• 30 seconds to measure IAP
• Standardized measurement
• No reproducibility errors
 Intra-Abdominal Pressure
Monitoring
• How much fluid should be infused into
the bladder?
– The minimal amount of fluid required to obtain
a reliable IAP measurement.
– Too much fluid leads to bladder over
distention and bladder wall compliance issues
– Currently it appears that one never needs
more than 25 ml in an adult, less (10-20 ml) is
probably adequate
 WSACS
Guidelines
Cheatham, ICM 2006
 Final Thoughts
Do NOT wait for signs of ACS to check IAP
– By then the patient has one foot in the grave!
– You have lost your opportunity for medical
therapy
Monitor ALL high risk patients early and
often:
– TREND IAP like a vital sign
• 30-50+% of all ICU patients have some IAH and
are at risk for ACS
• 1 in 11 suffer full blown abdominal compartment
syndrome
 For More Information

IAH and ACS Educational Web sites:

www.abdominal-compartment-syndrome.org
http://www.wolfetory.com/education.html

Video to review concepts of monitor set-up:

http://www.wolfetory.com/abviser_autovalve.html
My email:
twolfe@wolfetory.com