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Overview of Abdominal Compartment Syndromes PowerPoint Presentation

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  • Slide 1 - Intra-Abdominal Hypertension (IAH) Abdominal CompartmentSyndrome (ACS) & By: Tim Wolfe, MD Email: twolfe@wolfetory.com
  • Slide 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?
  • Slide 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
  • Slide 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 Care withdrawn at later time and allowed to expire.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
  • Slide 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
  • Slide 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.
  • Slide 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
  • Slide 8 - 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
  • Slide 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
  • Slide 10 - Physiologic Insult/Critical Illness Ischemia Inflammatory response Capillary leak Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension Fluid resuscitation
  • Slide 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?
  • Slide 12 - Intra-abdominal Hypertension &Abdominal Compartment Syndrome Physiologic Sequelae
  • Slide 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
  • Slide 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)
  • Slide 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
  • Slide 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!
  • Slide 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
  • Slide 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
  • Slide 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.
  • Slide 20 - Management of IAH and ACS
  • Slide 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
  • Slide 22 - IAH/ACS Management: Decompressive Laparotomy
  • Slide 23 - Decompressive Laparotomy Delay in abdominal decompression may lead to intestinal ischemia Decompress early!
  • Slide 24 - Intra-Abdominal Pressure Monitoring
  • Slide 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)
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 31 - WSACS GuidelinesCheatham, ICM 2006
  • Slide 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
  • Slide 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
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