intra-abdominal hypertension (iah) abdominal compartment syndrome (acs) & by: tim wolfe, md...
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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hemodynamic compromise.• Pathology shows malignant effusion – pancreatic CA.• Care withdrawn at later time and allowed to expire.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
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