IntraAbdominal Hypertension IAH Abdominal Compartment Syndrome ACS By

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

• 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. De. Cou, 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 • Care withdrawn at later time and allowed to expire.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 abdominopelvic 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 noninvasive 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 Capillary leak Mucosal Breakdown Decreased O 2 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) – Ci. Mon (Gastric) – Spiegelberg (Gastric) – Ab. Viser – (Bladder transduction) Advantages – Simple, standardized, reproducible, time-efficient, sterile

Ab. Viser 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