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Information about slideshow081505 abridged

Published on January 11, 2008

Author: Rachele


Intra-Abdominal Hypertension (IAH) & :  Intra-Abdominal Hypertension (IAH) & By: Tim Wolfe, MD Associate Professor, University of Utah Medical Director, Wolfe Tory Medical Abdominal Compartment Syndrome (ACS) Case: Septic child:  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 Case: Complicated pulmonary embolism:  Case: Complicated pulmonary embolism 46 yo male with PE on SQ enoxaparin Acutely decompensated, requiring IVF, vasopressors and blood for retroperitoneal hematoma Became anuric, BP dropped again, difficult to ventilate IAP measured at 68 cm H2O (50 mm Hg) Decompression resulted in immediate resolution of anuria, hypotension and ventilator pressure issues Eventually discharged alive and well Dabney, Intensive Care Med 2001 Case: Dyspnea in ER:  Case: Dyspnea in ER 67 y.o. female presenting to ER with pleurisy, dyspnea Initially vitals stable, H&P suggest liver dz Over 2 hours developed agitation, hypotension, hypoxemia, oliguria & hypercarbia. IAP = 45 mm Hg, abdominal ultrasound showed tense ascites paracentesis of 4500 cc fluid. Immediate resolution of renal, pulmonary and hemodynamic compromise. Pathology showed malignant effusion – pancreatic CA. Care withdrawn at later time and allowed to expire. Etzion, Am J EM 2004 Case Points:  Case Points Intra-abdominal hypertension and ACS occur in many ICU settings (PICU, MICU, SICU). Trauma is not required for ACS to develop. Bladder pressure measurements are valuable in assessing whether IAH is contributing to organ dysfunction. “Spot” IAP checks when clinical syndrome has developed result in delayed diagnosis IAP monitoring allows early detection and early intervention for IAH before ACS develops. Outline - IAH and ACS:  Outline - IAH and ACS Definition – what is it? Causes Recent increase in recognition Physiologic Manifestations Prevalence Outcome Treatment Detection: Bladder pressure monitoring University of Utah treatment algorithm Abdominal Compartment Syndrome (ACS): Definition:  Abdominal Compartment Syndrome (ACS): Definition “…….. multiple organ dysfunction caused by elevated intra-abdominal pressure.” Tim Wolfe, MD What intra-abdominal pressures are concerning?:  What intra-abdominal pressures are concerning? Pressure (mm Hg) Interpretation 0-5 Normal 5-10 Common in most ICU patients > 12 Intra-abdominal hypertension 15-20 Dangerous IAH - consider non- invasive interventions >20-25 Impending abdominal compartment syndrome - strongly consider decompressive laparotomy Intra-abdominal pressure vs organ dysfunction:  Intra-abdominal pressure vs organ dysfunction Slide10:  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) 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 Recent increases in ACS Recognition:  Recent increases in ACS Recognition Are we seeing more ACS?:  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? ACS Literature: Publication explosion:  ACS Literature: Publication explosion Intra-abdominal Hypertension & Abdominal Compartment Syndrome:  Intra-abdominal Hypertension & Abdominal Compartment Syndrome Physiologic Sequelae Physiologic Insult:  Physiologic Insult Ischemia Inflammatory response Capillary leak Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension Fluid resuscitation Physiologic Sequelae:  Physiologic Sequelae Cardiac: 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 Slide17:  Ridings, et al 1995 Physiologic Sequelae:  Physiologic Sequelae Pulmonary: 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) Physiologic Sequelae:  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, cytokine release, neutrophil priming Bacterial translocation Development and perpetuation of SIRS Further increases in intra-abdominal pressure Physiologic Sequelae:  Physiologic Sequelae Renal: 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 Physiologic Sequelae:  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 Physiologic Sequelae:  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) Physiologic Sequelae:  Physiologic Sequelae Miscellaneous 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 Slide24:  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 How common is this syndrome?:  How common is this syndrome? Malbrain, Intensive Care Medicine (2004): Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre epidemiological study. Prospective, multi-center trial 13 ICU’s, 6 countries Every patient in ICU with expected stay > 24 hours had IAP measured q6 hours. 97 patients entered How common is this syndrome?:  How common is this syndrome? Malbrain, Intensive Care Medicine (2004): How good is clinical judgment for detecting elevated IAP?:  How good is clinical judgment for detecting elevated IAP? Kirkpatrick, Can J Surg (2000). Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Prospective, blinded trial - Staff physician judgment Results: Less than 50% of the time was the clinician able to determine when IAP was elevated. “These findings suggest that more routine measurements of bladder pressure in patients at risk for intra-abdominal hypertension should be performed.” Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? Pupelis, 2002: Clinical significance of increased intra-abdominal pressure in severe acute pancreatitis. 37 cases of severe pancreatitis 26 cases with IAP < 25 mm Hg: 19% SIRS & MODS 0 % mortality Mean ICU LOS 9 days 11 cases with IAP > 25 mm Hg: 64% SIRS & MODS 36 % mortality Mean ICU LOS 21 days Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? Biancofiore 2004: Intra-abdominal pressure in liver transplant recipients: incidence and clinical significance. Prospective observational study in 108 liver transplants 32% developed IAP > 25 mm Hg: Renal failure in 32%; permanent dialysis 9%, higher mortality 68 with IAP < 25 mm Hg: Renal failure 8%; permanent dialysis 0% “The critical IAP values… with the best sensitivity specificity, were 23 mm Hg for postoperative ventilatory delayed weaning (P <.05), 24 mm Hg for renal dysfunction (P <.05), and 25 mm Hg for death (P <.01).” Does IAH / ACS affect patient outcome?:  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 Does IAH / ACS affect patient outcome?:  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. IAH/ACS Management:  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 IAH/ACS Management : Abdominal Perfusion Pressure:  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% IAH/ACS Management: Paralysis:  IAH/ACS Management: Paralysis De Waele, Crit Care Med 2003 UOP IAP IAH/ACS Management: Colloids:  IAH/ACS Management: Colloids O’Mara, 2005: Prospective randomized evaluation of IAP with crystalloid and colloid resuscitation in burns 31 cases with >25% burn plus inhalation or >40% burn without inhalation Randomized to saline vs plasma Results post resuscitation: Crystalloid IAP mean 26.5 mm Hg Plasma IAP mean 10.6 mm Hg IAH/ACS Management: Hemofiltration:  IAH/ACS Management: Hemofiltration Oda, 2005: Management of IAH in patients with severe acute pancreatitis using continuous hemofiltration. 17 cases of severe pancreatitis and IAH Treated with hemofiltration PRIOR to developing renal insufficiency Results: Interleukin (IL-6) cytokine levels cut in half Reduced vascular permeability and interstitial edema Mean IAP value dropped from 15 mm to less than 10 mm 16 of 17 patients discharged alive without complications IAH/ACS Management: Paracentesis:  IAH/ACS Management: Paracentesis Latenser, 2002: Percutaneous decompression for abdominal compartment syndrome in burn patients. 9 cases with IAP > 25-30 mm Hg Treated with percutaneous catheter (paracentesis) to drain ascitic fluid Results: 5 responded with drop in IAP - 60% survival 4 failed to respond and IAP increased - 0% survival IAH/ACS Management: Decompressive Laparotomy:  IAH/ACS Management: Decompressive Laparotomy Rigid Abdomen in ACS Post decompressive laparotomy Surgical Management of Compartment Syndromes:  Surgical Management of Compartment Syndromes Compartment Cranium Chest Pericardium Limb Pathophysiology ICP elevation Tension pneumothorax Cardiac tamponade Extremity compartment syndrome Surgical Management Mannitol, Craniectomy, etc.. Chest tube Pericardiocentesis Fasciotomy Decompressive Laparotomy:  Decompressive Laparotomy Delay in abdominal decompression may lead to intestinal ischemia Decompress Early! Decompressive Laparotomy:  Decompressive Laparotomy Post-operative dressing Several days post-op Intra-Abdominal Pressure Monitoring:  Intra-Abdominal Pressure Monitoring 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 (Bailey, Crit Care 2000) More reliable and reproducible than clinical judgment (Kirkpatrick, CJS 2000; Sugrue World J Surg 2002) How much fluid should be infused into bladder?:  How much fluid should be infused into bladder? Volume of infusion (ml) IAP Measured (mm Hg) Non-compliant bladder: Measured pressure increases as volumes exceed 50 ml of infusion Compliant bladder: Measured pressure changes very little with higher volumes of fluid infusion “Home Made” Pressure Transducer Technique:  “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:  “Home Made” Pressure Transducer Technique PROBLEMS: Home-made: No standardization Sterility issues Time consuming – Done infrequently Data reproducibility errors - what are the costs / morbidity of inaccurate information? Other: Needle stick, Recurrent penetration of sterile system, Leaks, re-zeroing problems/errors AbViser Intra-Abdominal Pressure Monitoring Kit:  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 AbViser Intra-Abdominal Pressure Monitoring Kit:  AbViser Intra-Abdominal Pressure Monitoring Kit Advantages: Kit contains everything you need Standardized measurement No reproducibility errors Ease & simplicity of use Time savings 30 seconds to get data. Closed system No needles No contamination risks AbViser: Reproducibility Study :  AbViser: Reproducibility Study Inter-observer Scatterplot (r = 0.922, p < 0.001) AbViser: Purchase Justification:  AbViser: Purchase Justification If you SPOT CHECK to confirm clinical suspicion of advanced disease (i.e. to confirm ACS): The AbViser is not for you. If your goal is to: Detect IAH early Establish a trend in IAP to assist in clinical management Utilize IAP to accurately interpret hemodynamics and other organ function Prevent abdominal compartment syndrome Decrease patient morbidity, mortality and LOS Then the AbViser is your tool University of Utah: IAP monitoring algorithm:  University of Utah: IAP monitoring algorithm Entry criteria defined in table Nurse is empowered to enter any patient fulfilling these criteria University of Utah: IAP Monitoring Protocol:  University of Utah: IAP Monitoring Protocol IAP monitoring Q1-2 hours for first 12 hours IAP consistently <12 mm Hg IAP 12 to 15 mm Hg IAP 15-20 mm Hg with no evidence of organ dysfunction/ ischemia (ACS) IAP >20 mm Hg OR APP< 50-60 mm Hg? Plus evidence of organ dysfunction/ ischemia (ACS) Optimize Abdominal perfusion pressure Careful fluid management Pressors Reduce IAP measurements to Q4-6 hours for 24 hours “Second Hit” pt. develops new indication for IAP monitoring IAP remains <12 mm Hg discontinue monitoring Consider Medical Management Sedation/Neuromuscular blockade Paracentesis of free fluid Other options Gastric suction, cathartics Rectal tube/enemas Continuous filtration Colloids Surgical Decompression Final Thought:  Final Thought Do 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 therapy Monitor ALL high risk patients early and often: TREND IAP like a vital sign Intervene early, before critical pressure develops QUESTIONS?:  QUESTIONS? IAH and ACS Educational Web sites: My email:

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