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Published on January 10, 2008

Author: Monica

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Intra-Abdominal Hypertension (IAH):  Intra-Abdominal Hypertension (IAH) Abdominal Compartment Syndrome (ACS) & By: Tim Wolfe, MD Email: twolfe@wolfetory.com What was their intra-abdominal pressure?:  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? 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: Dyspnea in ER:  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 Care withdrawn at later time and allowed to expire.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:  Case: Aspiration patient 77 y.o. male aspirated on ward. Transferred to ICU where he required intubation, developed hypotension 10 liters IVF overnight, Norepi 1.0 mcg/kg/min. Anuric (35 ml urine in 8 hours). Lactate = 4.6 IAP = 31 mm Hg. KUB – massively distend small and large bowel. US shows no free ascitic fluid. Surgeon consulted for possible decompressive surgery Rx: NGT, Rectal Tube, oral cathartics, neuromuscular blockade 1 hour later: IAP 12 mm Hg, UOP 210 ml, norepinephrine discontinued. Cheatham, WSACS 2006 Case Points:  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. Outline / Objectives:  Outline / Objectives Definition – what is it? Causes Physiologic Manifestations Prevalence Outcome Treatment Detection: Bladder pressure monitoring University of Utah/WSACS treatment algorithm Definitions WCACS, Antwerp Belgium 2007:  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:  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 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 (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 Physiologic Insult/Critical Illness:  Physiologic Insult/Critical Illness Ischemia Inflammatory response Capillary leak Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension Fluid resuscitation Causes of Intra-abdominal Pressure (IAP) Elevation:  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? Slide13:  Right Here!! Intra-abdominal Hypertension & Abdominal Compartment Syndrome:  Intra-abdominal Hypertension & Abdominal Compartment Syndrome Physiologic Sequelae 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, decreased ScvO2 Misleading elevations of CVP and PAWP Cardiac insufficiency Cardiac arrest Slide16:  PEEP PIP Intra-abdominal pressure Thoracic cage Compliance pressure Pleural Pressure Lung compliance pressure Airway resistance pressure Intra-cardiac pressure Catheter PA Changing Ventricular compliance, Valvular disease Pressure  Volume CVP, PAOP & CI in the presence of Intra-abdominal Hypertension:  CVP, PAOP & CI in the presence of Intra-abdominal Hypertension r = -0.33 r = -0.33 Poor, inverse correlation between CVP, PAOP and Cardiac Index Cheatham, Malbrain 2005 Slide18:  Ridings, et al 1995 Slide19:  Cheatham, Malbrain 2005 Physiologic Sequelae:  Physiologic Sequelae Pulmonary: Increased intra-abdominal pressures causes: Elevation of the diaphragms with reduction in lung volumes, stiffening of thoracic cage, reduced alveolar inflation, increased intersitial fluid 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 - VILI, 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 IAP vs Organ perfusion:  IAP vs Organ perfusion Δ – hepatic a. flow; O – cardiac output; ◊ - SMA flow; □ - intest. flow Diebel, J Trauma 1992 Physiologic Sequelae:  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) FG = GFP-PTP so FG = (MAP-IAP)-IAP so FG = MAP-(2 x IAP) Renal failure, oliguria/anuria Top 4 causes of renal impairment in SICU: hypotension, sepsis, age > 60 and elevated IAP Mortality of renal failure in ICU is over 50% - DO NOT WAIT for this to occur! Normal Abdominal CT:  Normal Abdominal CT Inferior Vena Cava Note that abdomen is oval, not round Normal kidney Abdominal CT in ACS – Renal compression:  Retroperitoneal hemorrhage Note that abdomen is round, not oval Kidneys are compressed, patient is anuric Pickhardt, AJR 1999 Abdominal CT in ACS – Renal compression Flattened Inferior Vena Cava 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 Maryland Shock Trauma unit now decompresses abdomens in patients with intractable intra-cranial hypertension 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) Slide28:  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 common – Septic* Patients :  How common – Septic* Patients Efstathiou et al, Intensive Care Med 2005;31 supp1 1: S183 Abs 703 *Hernandez showed 51% incidence of IAP > 20 mm Hg in septic shock patients at the same conference. Slide32:  Beware of IAH/ACS!! Early Goal Directed Therapy Algorithm Fluids Vasoconstriction Ischemia How good is clinical judgment for detecting elevated IAP? :  How good is clinical judgment for detecting elevated IAP? Prospective, blinded trial - Staff physician judgment Results: < 50% of the time was the clinician able to determine when IAP was elevated. “…findings suggest that more routine measurements of bladder pressure…” Kirkpatrick, Can J Surg 2000 Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? IAH predicted mortality IAH > 12 mortality 38.8% No IAH - mortality: 22.2% Malbrain, Crit Care Med, 2005 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 < 18 mm Hg (25 cm H2O) : 19% SIRS & MODS 0 % mortality Mean ICU LOS 9 days 11 cases with IAP > 18 mm Hg (25 cm H2O) : 64% SIRS & MODS 36 % mortality Mean ICU LOS 21 days Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? Ivatury, J Trauma, 1998: Intra-abdominal hypertension after damage control surgery. 70 patients monitored for IAP > 18 mm Hg (25 cm H2O) 25 had facial closure at time of surgery: 52% developed IAP > 18 mm Hg 39% Died 45 cases had abdomen left “open”: 22% developed IAP > 18 mm Hg 10.6% Died Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? Cheatman, Is the evolving management of IAH/ ACS improving survival? Acta Clinica Belgica 2007;62 supp1 1:268 Abs O61 Prospectively collected data base in hospital with >10 yrs of ACS experience Year 2002: 53 cases of abdominal decompression for IAH/ACS 34% successful same admission closure 49% mortality Median hospital LOS 28 days Year 2005: Implementation of IAH treatment protocol Year 2006: 75 cases of abdominal decompression for IAH before or early after the onset of ACS 61% successful same admission closure 29% mortality Median hospital LOS 18 days Author points: Despite same age and severity of illness they achieved a much better outcome with similar or less resource utilization by implementing aggressive treatment protocol. Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient 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:  Management of IAH and ACS IAH/ACS Management:  IAH/ACS Management Position 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 (> 60 mm Hg) optimize fluids, then add vasopressors Sedation, Paralytics NGT / Cathartics / enema to clear bowel? Colloids / diuretics? Hemofiltration Paracentesis Surgical decompression IAH/ACS Management : Positioning:  IAH/ACS Management : Positioning Malbrain, CCM 2003 IAH/ACS Management: Optimize fluids, consider colloids:  IAH/ACS Management: Optimize fluids, consider colloids Issues: Judicious fluid management may prevent IAH Too much fluid leads to increased capillary leak but elevated IAP elevates CVP potentially causing inadequate fluid resuscitation. Suggestions for resuscitation: Serial IAP measurements – once IAP rises over 10, do not rely on CVP, PAWP measurements Assess volumes status using volume index catheter, echo, pulse contour analysis to assist in determining ventricular filling Resuscitate with crystalloids - consider HS, colloids Assess afterload, RVEF (or GEF) to determine next step in patients who have not met perfusion parameters Low afterload – vasopressor, Normal EF – fluids, Low EF - inotropes 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 (esp. pediatrics). 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 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 (maintained adequate serum oncotic pressure with albumin) 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 Multiple case series reporting successful treatment of IAH and ACS: Latenser 2002: Burn patient management Reckard 2005: Peripancreatic fluid filled mass Sharp 2002: Pediatric blunt trauma Etzion 2004: Malignant ascites therapy IAH/ACS Management: Paracentesis:  IAH/ACS Management: Paracentesis Sun, 2006: Indwelling peritoneal catheter vs conservative measures in fulminant acute pancreatitis. 110 cases of severe fulminant pancreatitis - RCT Control group: Routine ICU supportive care Study group: Routine ICU supportive care PLUS IAP monitoring (mean pressure 21 mm Hg on day 1) Indwelling peritoneal drain catheter (drain 1800 cc on day 1) Outcome: Control - 20.7% mortality Study group - 10.0% mortality (p<0.01) IAH/ACS Management:  IAH/ACS Management Decompressive Laparotomy: Err on the side of early vs late intervention Less bowel edema or cell damage, better chance of early closure and early recovery. Be aware that delaying care until this complication occurs is VERY expensive – more expensive the longer you wait: Vanderbilt costs for open abdomen: Same admission closure - $150,000 Failure to close on initial admission $250,000 (estimate at least as much over next year by time ventral hernia finally repaired). IAH/ACS Management: Decompressive Laparotomy:  IAH/ACS Management: Decompressive Laparotomy Rigid Abdomen in ACS Post decompressive laparotomy 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 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 Craniotomy, etc.. Chest tube Pericardiocentesis Fasciotomy Management of Compartment Syndromes:  Management of Compartment Syndromes Abdominal compartment syndrome = Emergent Surgical Disease. Intra-abdominal hypertension = Urgent Medical Disease. 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 (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” 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 – therefor 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:  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 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 Standardized measurement No reproducibility errors AbViser: Reproducibility Study :  AbViser: Reproducibility Study Inter-observer Scatterplot (r = 0.922, p < 0.001) Kimball, Int Care Med 2007 Intra-Abdominal Pressure Monitoring:  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 Pediatric data shows 1 ml/kg best (Davis, 2005) 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 IAP transduction to monitor:  IAP transduction to monitor Proper transduction clues: Respiratory variation noted Oscillation test positive Reproducible over several measurements WSACS Guidelines Cheatham, ICM 2006:  WSACS Guidelines Cheatham, ICM 2006 University of Utah IAP monitoring & treatment algorithm:  University of Utah IAP monitoring & treatment algorithm Entry criteria defined in prior table Nurse is empowered to enter any patient fulfilling those criteria IAH/ACS Medical Management:  IAH/ACS Medical Management IAH Perform measurement Q2-4h until < 12 mmHg Medical therapy for IAH ACS Primary…decompression Secondary…medical tx with surgical backup IAP Monitoring Protocol:  IAP Monitoring Protocol IAP monitoring Q 2 hours for first 24-48 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 >20-25 mm Hg or evidence of organ dysfunction/ ischemia (ACS) Optimize Abdominal perfusion pressure Careful fluid management 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 Medical Management Sedation/pain control Empty GI tract Gastric suction, cathartics Rectal tube/enemas Neuromuscular blockade Colloids/diuretics Paracentesis CVVH plus Colloids Consider 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: www.abdominal-compartment-syndrome.org WSACS.org My email: twolfe@wolfetory.com References:  References Ridings PC, et al. Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma 1995;39:1071-5. Citerio G, et al. Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med 2001;29:1466-71. Malbrain ML, et al. Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre study. Intensive Care Med 2004;30:822-9. Kirkpatrick AW, et al. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critical patients? Can J Surg 2000;43:207-11. Ivatury RR, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma 1998;44:1016-21. De Waele JJ, et al. A role for muscle relaxation in patients with abdominal compartment syndrome? Intensive Care Med 2003;29:332. References:  References Malbrain ML, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med 2005;33:315-22. O'Mara MS, et al. A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma 2005;58:1011-8. Oda S, et al. Management of Intra-abdominal Hypertension in Patients With Severe Acute Pancreatitis With Continuous Hemodiafiltration Using a Polymethyl Methacrylate Membrane Hemofilter. Ther Apher Dial 2005;9:355-61. Syndrome WSoAC. Consensus Definitions and Recommendations [WSACS web site]. Available at: http://www.wsacs.org/. 2005. Reckard JM, et al. Management of intraabdominal hypertension by percutaneous catheter drainage. J Vasc Interv Radiol 2005;16:1019-21. Summary Are your patients at risk for ACS?:  Summary Are your patients at risk for ACS? 30-50+% of all ICU patients have some IAH and are at risk for ACS 1 In 11 suffer full blown abdominal compartment syndrome Summary Should you monitor bladder pressures ?:  Summary Should you monitor bladder pressures ? IAP is directly related to organ failure and mortality Directly impacts other important monitoring capabilities Clinical exam is very inaccurate Summary Can you make a difference?:  Summary Can you make a difference? Early intervention and management can impact patient survival Does IAH / ACS affect patient outcome?:  Does IAH / ACS affect patient outcome? Joseph 2004: Decompressive laparotomy to treat intractable intracranial hypertension 17 patients with intractable ICP despite maximal therapy (including decompressive craniectomy in 14) Mean ICP 30 mm Hg, Mean IAP 27 mm Hg All 17 underwent decompressive laparotomy 100% had drop in the ICP immediately or in few hours To mean of 17 mm Hg 11 had persistent reduction in ICP These 11 all survived and with “good neurologic outcome” “Decompression should almost certainly be performed before obvious symptoms of abdominal compartment syndrome are manifest.”

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