INTRA-ABDOMINAL

HYPERTENSION (IAH) AND

Abdominal Compartment

Syndrome (ACS)

Dr Punit D. Ghetia

MD,IDCCM.

Consultant Intensivist Banker’s Heart Institute.

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 year / female child presenting with sepsis:

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 year/female presenting to ER with pleurisy, dyspnea

Hypotensive, agitated.

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.

Etzion, Am J EM 2004

CASE: ASPIRATION PATIENT

77 year male aspirated on general medicine floor. Transferred to MICU & intubated; hypotensive.

4.5 liters IVF overnight plus noradrenalin high dose

Anuric (35 ml urine in 8 hours).

IAP = 31 mm Hg.

USG-massively distended small and large bowel AND no free ascitic fluid.

Surgeon consulted for possible decompressivesurgery

Rx: NGT, Rectal Tube, oral cathartics

1 hour later: IAP 12 mm Hg, UOP 210 ml, noradrenaline 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, OR, ER).

IAP measurements are clinically useful: Help to determine if IAH is contributing to organ dysfunction

“Spot” IAP check results in delayed diagnosis SO TREND OF IAP IS ESSENTIAL and IAP monitoring will allow early detection and early intervention for IAH before ACS develops.

Waiting for clinically obvious ACS to develop before checking IAP worsen the problem.

DEFINITIONSWSACS*, ANTWERP BELGIUM 2007

*WORLD SOCIETY OF THE ABDOMINAL COMPARTMENT

SYNDROME

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 /ACSWSACS, 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

HISTORY:

Fietsam et al (1989) first to describe the

abdominal compartment syndrome (ACS) as the

collective effects of increased intra-abdominal

pressure (IAP) on the body.

Their description was in the setting of ruptured

abdominal aortic aneurysms.

Trauma literature now a major source of information.

In general, the trauma literature has recognized that

end organ dysfunction occurs in the presence of a

grossly distended and tense abdomen..So there was

“Open abdomen concept”.

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/4.5 kg

weight gain)

Cause are…..

CAUSES

Acidosis Hyperthermia transfusion

Coagulopathy Sepsis: intra or

extra abd

Bacteremia

pancreatitis Liver

dysfunction

Mechanical

ventilation

Pneumonia Abdominal

surgery (DCL)

Massive

resuscitation

Gastric or

colon dist’n

Hemo-

peritoneum

Burns and

trauma

obesity Abdominal

tumors

Prone

ventilation

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 progression 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

Increased intracranial pressure

Decreased cerebral perfusion pressure

Cerebral edema, brain anoxia, brain injury

Intra-abdominal

Pressure

Mucosal

Breakdown

(Multi Organ dysfunction

System)

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 (TRENDS OF PRESSURE READINGS) & detection of IAH with early intervention is needed to reduce these complications.

INDEX OF SUSPICION: In following Settings,

Ascites

Bowel distention: mechanical obstruction/ileus

Bowel edema: resuscitation or ischaemia

Retroperitoneal hematoma

Hemoperitoneum

Coagulopathy

Trauma

Abdominal packing after damage control

surgery

DIAGNOSIS: Index of suspicion

When any signs of intra-abdominal hypertension are present:

Abdominal distention

Refractory oliguria

Hypercarbia

Refractory hypoxemia

Increasing PIPs

Refractory hypotension

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 50 ml syringe,

1 tubing with saline bag spike / luerconnector

1 tubing with luer both ends

1 needle / angiocath

Clamp for Foley

Assembled sterilely in proper fashion

27

Method for Measuring the pressure

Insert a Foley catheter and clamp the tube distal

to the sample port

Instill 10-20 ml of saline into the bladder so as to

leave a continuous column of fluid from the

bladder to the sample port on the Foley

Insert a 18g catheter into the sample port and

connect to a CVP transducer

Level the transducer at the symphysis pubis Fusco et al J Trauma 2001

Guidelines for measurement by WSACS

Completely supine

Relaxed abdominal wall

mid-axillary line

25 mL saline into the bladder

“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

DIAGNOSIS;

Most papers suggest several measurements

during a 24 hr period: every 4 hrs

Repeat measurements are indicated by the

clinical appearance of the abdomen and on the

clinical situation (index of suspicion)

INTERPRETATION:

NORMAL IAP

3-15 mmHg

Obesity: higher (8 vs. 5 mmHg)

Age: no definite trend

Surgery: no definite trend

Comorbidities: trend to higher IAP with more

concurrent illnesses

Sanchez et al Am Surg Mar 2001

INTERPRETATION: As the pressure rises over 15 mmHg there

will be some evidence of hypoperfusion

Most will accept surgical decompression if the intra-abdominal pressure is over 20-25 mmHg.

More recent authors are advocating surgical decompression for IAP of 20-25 mmHg (Cheatham et al)

WSACS: suggests need for treatments above 12 mmHg

INTERPRETATION:….evidence

Decreased ACS with earlier decompression

Decreased mortality with earlier

decompression: ??? Need further study ..

More pronounced benefit with increasing age

MANAGEMENT OF IAH

AND ACS

Management:

Medical:

Maintain APP (Abdominal Perfusion Pressure) >60mmHg

Sedation / Analgesia

NMB

Supine positioning

NG / Colonic decompression

diuretics

ABDOMINAL PERFUSION PRESSURE

(APP)APP = MAP – IAP

APP :Abdominal Perfusion Pressure

MAP :MEAN ARTERIAL PRESSURE

IAP : INTRA ABDOMINAL PRESSURE

Abdominal perfusion pressure reflects actual gut

perfusion better than IAP alone

Optimizing APP to > 60 mm Hg should probably be

primary endpoint

Surgical:

Percutaneous tube drainage

Abdominal decompression

DECOMPRESSIVE LAPAROTOMY

• Delay in abdominal decompression

may lead to intestinal ischemia

• Decompress early!

TREATMENT: SURGICAL DECOMPRESSION /

DAMAGE CONTROL LAPAROTOMY

Surgical decompression involves opening

the abdominal wound and packing the

wound open or closing it with a plastic

dressing

Delayed closure can be done once the edema /

bleeding has resolved

Ascites can be drained percutaneously

DAMAGE CONTOL LAPAROTOMY:

Stone et al (1982)

Useful in Penetrating injuries to the abdomen

Try to Avoid hypothermia / acidosis / coagulopathy

Damage control surgery Involves:Rapid control of bleeding and contamination.Skin closure only or plastic tent closure.

WSACS

GUIDELINESCHEATHAM, ICM 2006

SUMMARY:

IAP – measureable / preventable / treatable

ACS – end organ dysfunction from untreated or undertreated elevated IAP

Measurement: simple technique with an 18 g needle through the Foley port and a CVP transducer

Damage control – the standard for avoiding or treating elevated IAP or ACS

Deompressive laparotomy:

Most studies show a significant decrease in the IAP

Overall benefit for oxygenation (PaO2/FiO2) and increased urine output

Still Mortality Rate remained high at 35%

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 they are at risk for ACS and

in such high risk group ,1 in 11 suffer full blown abdominal compartment syndrome

FOR MORE INFORMATION

IAH and ACS Educational Web sites:

www.abdominal-compartment-syndrome.org