Intra-Abdominal Hypertension (IAH)

Abdominal Compartment

Syndrome (ACS)

&

By: Tim Wolfe, MDEmail: twolfe@wolfetory.com

What was their intra-abdominal pressure?

• 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?

Case: Septic child5 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 ER67 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hemodynamic compromise.• Pathology shows malignant effusion – pancreatic CA.• Care withdrawn at later time and allowed to expire.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 patient77 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.

DefinitionsWCACS, 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

Capillary leak

Tissue Edema (Including bowel wall and mesentery)

Intra-abdominal hypertension

Fluid resuscitation

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

MucosalBreakdown

(Multi-System Organ Failure)

Bacterial translocation

Acidosis

Decreased O2 delivery

Anaerobic metabolism

Capillary leak

Free radical formation

IAH / ACS affects outcomePoints:• 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 FoleyAssembled 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.orghttp://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