Abdominal compartment syndrome[1]

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Abdominal compartment syndrome[1]

  1. 1. Abdominal Compartment Syndrome :An Unrecognised Cause of AKI SAID KHAMIS (MD, KUL Belgium) Professor Of Medicine Nephrology Consultant Menofia University Hospitals
  2. 2. Agenda - IAH and ACS Definition – what is it? Causes Recent increase in recognition Physiologic Manifestations Prevalence Outcome Treatment Detection:  Bladder pressure monitoring
  3. 3. Abdominal Compartment SyndromeDefinition“…….. multiple organ dysfunction caused by elevated intra-abdominal pressure.” Tim Wolfe, MD
  4. 4. What intra-abdominal pressures are concerning?Pressure (mm Hg) Interpretation 0-5 Normal 5-10 Common in most ICU patients > 12 Intra-abdominal hypertension15-20 Dangerous IAH - consider non- invasive interventions>20-25 Impending abdominal compartment syndrome - strongly consider decompressive laparotomy
  5. 5. Causes of Intra-abdominal Pressure(IAP) Elevation Retroperitoneal: pancreatitis, retroperitoneal or pelvic bleeding, contained AAA rupture, aortic surgery, abscess, visceral edema Intraperitoneal: intraperitoneal bleeding, AAA rupture, acute gastric dilatation, bowel obstruction, ileus, mesenteric venous obstruction, pneumoperitoneum, abdominal packing, abscess, visceral edema secondary to resuscitation (SIRS)
  6. 6. Causes of Intra-abdominal Pressure(IAP) Elevation Abdominal Wall: burn eschar, repair of gastroschisis or omphalocele, reduction of large hernias, pneumatic anti-shock garments, lap closure under tension, abdominal binders Chronic: central obesity, ascites, large abdominal tumors, PD, pregnancy
  7. 7. Are we seeing more ACS? Increased Incidence?  Syndromes created by medical “progress”  ICU’s full of sicker patients  Fluid resuscitation due to early goal directed therapy for sepsis? Increased Recognition?
  8. 8. ACS Literature: Publicationexplosion 140 120 100 80 60 Research Publications 40 20 0 83- 87- 91- 95- 99- 00 84 88 92 96 00 3- 04
  9. 9. Physiologic Insult Ischemia Inflammatory response Capillary leakFluid resuscitation Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension
  10. 10. Physiologic SequelaeCardiac: Increased intra-abdominal pressures causes:  Compression of the vena cava with reduction in venous return to the heart  Elevated ITP with multiple negative cardiac effects The result:  Decreased cardiac output increased SVR  Increased cardiac workload  Decreased tissue perfusion, SVO2  Misleading elevations of PAWP and CVP  Cardiac insufficiency Cardiac arrest
  11. 11. Physiologic SequelaePulmonary: Increased intra-abdominal pressures causes:  Elevation of the diaphragms with reduction in lung volumes  Cytokines release, immune hyper-responsiveness The 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)
  12. 12. Physiologic SequelaeGastrointestinal: 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, cytokine release, neutrophil priming  Bacterial translocation  Development and perpetuation of SIRS  Further increases in intra-abdominal pressure
  13. 13. Physiologic SequelaeRenal: Elevated intra-abdominal pressure causes:  Compression of renal veins and arteries  Reduced cardiac output to kidneys The Result:  Decreased renal artery and vein flow  Renal congestion and edema  Decreased glomerular filtration rate (GFR)  Acute tubular necrosis (ATN)  Renal failure, oliguria/anuria
  14. 14. Physiologic SequelaeNeuro: 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 CVP and IJ pressure  Increased intracranial pressure  Decreased cerebral perfusion pressure  Cerebral edema, brain anoxia, brain injury
  15. 15. Physiologic Sequelae Direct impact of IAP on common pressure measurements:  IAP elevation causes immediate increases in ICP, IJP and CVP (also in PAOP)15 liter bag placed on abdomen(Citerio 2001)
  16. 16. Physiologic SequelaeMiscellaneous Elevated intra-abdominal pressure causes:  Reduces perfusion of surgical and traumatic wounds  Reduced blood flow to liver, bone marrow, etc.  Blood pooling in pelvis and legs  “Second hit” in the two event model of MOF? The Result:  Poor wound healing and dehiscence  Coagulopathy  Immunosuppression  DVT and PE risks
  17. 17. Circling the Drain Intra-abdominal Pressure Capillary leak Mucosal Decreased O2 delivery Breakdown Free radical formation Anaerobic metabolism (Multi-System Organ Failure) Bacterial translocation Acidosis
  18. 18. How common is this syndrome?Malbrain, Intensive Care Medicine (2004):Abdominal Total MICU SICUpressure: Prevalence prevalence prevalence IAP > 12 58.8% 54.4% 65%IAP > 15 28.9% 29.8% 27.5%IAP > 20 8.2% 10.5% 5.0% plus organ failure
  19. 19. Does IAH / ACS affect patient outcome?Ivatury, J Trauma, 1998: Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. 70 patients with monitored for IAP > 25 mm Hg  25 had facial closure at time of surgery:  52% developed IAP > 25  39% Died  45 cases had abdomen left “open”:  22% developed IAP > 25  10.6% Died
  20. 20. Does IAH / ACS affect patient outcome?Points: Clinical signs of IAH are unreliable and only show up late in clinical course (once ACS occurs). IAH and ACS increase morbidity, mortality and ICU length of stay. Preventive therapy plus early detection and intervention can reduce these complications in many patients. Monitoring early (not waiting for clinical signs) in all high risk patients allows early detection and early intervention.
  21. 21. IAH/ACS Management Fluids – two edged sword  Fluids will absolutely improve cardiac indices if the patient has inadequate RV filling- so early in the course they are necessary  However, over resuscitation will lead to worsened edema Abdominal perfusion pressure - optimize fluids first then add vasopressors. Shoot for a perfusion pressure > 60 mm Hg Sedation, Paralytics Cathartics / enema to clear bowel? Colloids Hemofiltration Paracentesis  Need significant free fluid on US Decompressive laparotomy
  22. 22. IAH/ACS Management : Abdominal Perfusion Pressure 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 Cheatham 2000  Optimizing APP reduced incidence of  ACS - 64% versus 48%  Death - 44% versus 28%
  23. 23. IAH/ACS Management: Decompressive LaparotomyRigid Abdomen in ACS Post decompressive laparotomy
  24. 24. Surgical Management of Compartment Syndromes PathophysiologyCompartment Surgical Management ICP elevationCranium Mannitol, Craniectomy, etc.. TensionChest pneumothorax Chest tubePericardium Cardiac tamponade Pericardiocentesis ExtremityLimb compartment Fasciotomy syndrome
  25. 25. Decompressive Laparotomy  Delay in abdominal decompression may lead to intestinal ischemia  Decompress Early!
  26. 26. Decompressive LaparotomyPost-operative dressing Several days post-op
  27. 27. Intra-Abdominal PressureMonitoringBladder 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 (Bailey, Crit Care 2000)  More reliable and reproducible than clinical judgment (Kirkpatrick, CJS 2000; Sugrue World J Surg 2002)
  28. 28. “Home Made” Pressure Transducer TechniqueHome-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
  29. 29. University of Utah: IAP monitoring algorithm Entry criteria defined in table Nurse is empowered to enter any patient fulfilling these criteria
  30. 30. Final ThoughtDo NOT wait for signs of ACS to be present before you decide to check IAP  By then the patient has one foot in the grave!  You have lost your opportunity for medical therapyMonitor ALL high risk patients early and often:  TREND IAP like a vital sign  Intervene early, before critical pressure develops
  31. 31. QUESTIONS? IAH and ACS Educational Web sites: www.Abdominalcompartmentsyndrome. org

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