Intra-Abdominal Hypertension (IAH)

1. Intra-Abdominal Hypertension (IAH) & Abdominal CompartmentSyndrome (ACS) By: Tim Wolfe, MD Email: twolfe@wolfetory.com

2. 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?

3. 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

4. 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 • Care withdrawn at later time and allowed to expire.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

5. 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

6. 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.

7. 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

8. Types of IAH /ACSWCACS, Antwerp Belgium 2007 • Primary – Injury/disease of abdomino-pelvic region, “surgical” • Secondary – Sepsis, capillary leak, burns, “medical” • Recurrent – ACS develops despite surgical intervention

9. 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

10. Physiologic Insult/Critical Illness Inflammatory response Ischemia Fluid resuscitation Capillary leak Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension

11. 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?

12. Intra-abdominal Hypertension &Abdominal Compartment Syndrome Physiologic Sequelae

13. 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

14. 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)

15. 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

16. 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!

17. 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

18. Circling the Drain Intra-abdominal Pressure Mucosal Breakdown (Multi-System Organ Failure) Bacterial translocation Acidosis Decreased O2 delivery Anaerobic metabolism Capillary leak Free radical formation MSOF

19. 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.

20. Management of IAH and ACS

21. 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

22. IAH/ACS Management: Decompressive Laparotomy

23. Decompressive Laparotomy • Delay in abdominal decompression may lead to intestinal ischemia • Decompress early!

24. Intra-Abdominal Pressure Monitoring

25. 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)

26. “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

27. “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

28. 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

29. 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

30. 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

31. WSACS GuidelinesCheatham, ICM 2006

32. 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

33. 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