Consensus conference definitions and recommendations on intra-abdominal hypertension (iah) and the abdominal compartment syndrome (acs) - the long road to the final publications, how did we get there?

Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine

ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20

CONSENSUS CONFERENCE DEFINITIONS AND RECOMMENDATIONS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND THE ABDOMINAL COMPARTMENT SYNDROME (ACS) - THE LONG ROAD TO THE FINAL PUBLICATIONS, HOW DID WE GET THERE? M.L.N.G. Malbrain, I. De laet & M. Cheatham To cite this article: M.L.N.G. Malbrain, I. De laet & M. Cheatham (2007) CONSENSUS CONFERENCE DEFINITIONS AND RECOMMENDATIONS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND THE ABDOMINAL COMPARTMENT SYNDROME (ACS) - THE LONG ROAD TO THE FINAL PUBLICATIONS, HOW DID WE GET THERE?, Acta Clinica Belgica, 62:sup1, 44-59, DOI: 10.1179/acb.2007.62.s1.007 To link to this article: http://dx.doi.org/10.1179/acb.2007.62.s1.007

Published online: 30 May 2014.

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CONSENSUS CONFERENCE DEFINITIONS AND RECOMMENDATIONS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND THE ABDOMINAL COMPARTMENT SYNDROME (ACS) - THE LONG ROAD TO THE FINAL PUBLICATIONS, HOW DID WE GET THERE?

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Original article – OA 6

CONSENSUS CONFERENCE DEFINITIONS AND RECOMMENDATIONS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND THE ABDOMINAL COMPARTMENT SYNDROME (ACS) THE LONG ROAD TO THE FINAL PUBLICATIONS, HOW DID WE GET THERE? M.L.N.G. Malbrain1, I. De laet1, M. Cheatham2

ABSTRACT Objective: There has been an exponentially increasing interest in intraabdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) over the last decade, and different definitions have been suggested. Nevertheless, there has been an impetus from experts in the field to modify these definitions to reflect our current understanding of the pathophysiology of these syndromes. An international multidisciplinary group of interested doctors met with the goal of agreeing on a set of definitions that could be applied to patients with ––––––––––––––– 1 Intensive Care Unit, ZiekenhuisNetwerk Antwerpen, campus Stuivenberg, Antwerpen, Belgium; 2 Department of Surgical Education, Orlando Regional Medical Center, Orlando, Florida, USA Address for correspondence: Dr. Manu Malbrain ICU Director Intensive Care Unit ZiekenhuisNetwerk Antwerpen Campus Stuivenberg Lange Beeldekensstraat 267 B-2060 Antwerpen 6 Belgium Tel: +32 3 217 7399 Fax: +32 3 217 7279 E-mail: [email protected]

Acta Clinica Belgica, 2007; 62-Supplement 1

IAH and ACS. The goal of this consensus group was to provide a conceptual and practical framework to further define ACS, a progressive injurious process that falls under the generalized term ‘IAH’ and that includes IAH-associated organ dysfunction. Design: In total, 21 North American, Australasian and European surgical, trauma and critical care specialists agreed to standardize the current definitions for IAH, ACS and related conditions in preparation for the second World Congress on Abdominal Compartment Syndrome (WCACS). The WCACS-meeting was endorsed by the European Society of Intensive Care Medicine (ESICM) and the World Society on Abdominal Compartment Syndrome (WSACS). Methods: The consensus conference (Noosa, Australia; December 7, 2004) was attended by 21 specialists from Europe, Australasia and North America and approximately 70 other congress participants. In advance of the conference, a blueprint for the various definitions was suggested. After the conference the participants corresponded electronically with feedback. A writing committee was formed at the conference and developed the final manuscript based on executive summary documents generated by each participant. The final report of the 2004 International ACS Consensus Definitions Conference has recently been published. This article will describe the long road towards this final publication with the evolution of the different definitions and recommendations from the initial



suggestions in 2004 to the further refinement and final publications in 2006 and 2007. It will try to explain how we got there and will also give the percentage of agreement with each proposed definition by the participants. Results: New definitions were offered for some terms, while others were discarded and not kept in the final manuscript. Different cut-offs for defining IAH and ACS were given, as well as broad definitions of primary, secondary and recurrent IAH/ACS. A classification system was introduced taking into account the duration, origin, and etiology of IAH. The use of an organ severity scoring method, by means of the Sequential Organ Failure Assessment (SOFA) score when dealing with ACS patients was not recommended as an adjunctive tool to assess morbidity in the final publication. Conclusion: This document reflects a process whereby a group of experts and opinion leaders suggested definitions for IAH and ACS. This document should be used as a reference for the next consensus definitions conference in March 2007.

INTRODUCTION There has been an exponentially increasing interest in intraabdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) over the last decade, and different definitions have been suggested. Nevertheless, there has been an impetus from experts in the field to modify these definitions to reflect our current understanding of the pathophysiology of these syndromes. Definitions of IAH and ACS and their threshold values stand or fall with the accuracy and reproducibility of the method to measure intraabdominal pressure (IAP) (1). Not only the absolute numbers but also the use of mean, median or maximal IAP values influence the prevalence and incidence of IAH and ACS (2, 3). Throughout the years different threshold values have been suggested for IAH and ACS and some have interchanged the terms IAH and ACS. Others have suggested terms such as primary or secondary ACS, but with ever-changing definitions. To date it is therefore very difficult to interpret the literature. At the cradle of a new era and in response to a loud cry for consensus definitions this article will summarize the long road towards the recently published consensus definitions and recommendations in order to give more insights

into the process and to provide a basis for the next consensus definitions conference in March 2007 (4, 5).

METHODS OF THE CONFERENCE A process to gain consensus was commenced in early 2004 with the intention of agreeing on a set of definitions that could be applied to patients with IAH and ACS. An international teleconference was held on May 28th 2004. The goals were to provide a conceptual and practical framework to define the ACS; a progressive injurious process that falls under the generalized term ‘IAH’ and that includes IAH-associated organ dysfunction. Several North American, Australasian and European surgical, trauma and critical care physicians preparing the second World Congress on Abdominal Compartment Syndrome (WCACS), to be held in Noosa, Australia, on December 6-8, 2004 agreed to standardise the current definitions for IAH, ACS and related conditions. The WCACS-meeting was endorsed by the European Society of Intensive Care Medicine (ESICM). The preceding “blueprinting” teleconference was attended by 18 specialists. The consensus conference at the WCACS was attended by 21 specialist leaders in the field from Europe, Australasia and North America and by approximately 70 congress participants. In advance of the conference, the authors suggested a blueprint for the different definitions. In total, about 50 participants gave their written feedback on the definitions that were suggested. After the conference the participants corresponded electronically and gave further feedback. A writing committee was formed at the conference and developed the recently published articles based on executive summary documents generated by each participant (4, 5). The present article will try to summarise the long road from 2004 until 2007 that led to publication of the final consensus reports.

THE EVOLVING DEFINITIONS: FROM THE SECOND WCACS IN 2004 UNTIL THE THIRD WCACS IN 2007 Table 1 and 2 summarise the changes and evolution in the consensus definitions and recommendations from 2004 until 2007.


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Table 1. Evolution in the consensus definitions, from initial suggestions to final publication Term IAP

FG

First Description (2004) The intraabdominal pressure is the pressure concealed within the abdominal cavity The intraabdominal pressure varies with respiration The abdominal perfusion pressure is calculated as the mean arterial pressure minus the intraabdominal pressure (APP = MAP – IAP) FG = GFP – PTP

FG

FG = MAP – 2 * IAP

IAP


APP

IAP

Modified Description (2005) The intraabdominal pressure is the pressure concealed within the abdominal cavity The intraabdominal pressure varies with respiration The abdominal perfusion pressure is calculated as the mean arterial pressure minus the intraabdominal pressure (APP = MAP – IAP) The FG is the mechanical force across the glomerulus and equals the difference between the glomerular filtration pressure (GFP) and the proximal tubular pressure (PTP). FG = GFP – PTP In the presence of IAH, PTP may be assumed to equal IAP, and thus GFP can be estimated as MAP - IAP. The FG can then be calculated by the formula: FG = MAP - 2*IAP The IAP should be expressed in mmHg and measured at end-expiration in the complete supine position, ensuring that abdominal muscle contractions are absent and the transducer zeroed at the level of mid-axillary line

Final Description (2006) IAP is the steady-state pressure concealed within the abdominal cavity. APP = MAP – IAP

FG = GFP – PTP = MAP – 2 * IAP

The IAP should be expressed in mmHg and IAP should be expressed in mmHg and measured at end-expiration in the complete measured at end-expiration in the comsupine position, ensuring that abdominal plete supine position after ensuring that muscle contractions are absent and the abdominal muscle contractions are abtransducer zeroed at the level of mid-axillary sent and with the transducer zeroed at line (the conversion factor from mmHg to the level of the mid-axillary line. cmH2O is 1.36 and conversely from cmH2O to mmHg is 0.74) IAP measurement The direct gold IAP measurement method is the pressure measured via direct needle puncture into the abdominal cavity (eg during peritoneal dialysis or laparoscopy) IAP measurement The indirect gold standard for intermittent The gold standard for (intermittent) IAP The reference standard for intermittent IAP measurement is via the bladder measurement is via the bladder IAP measurement is via the bladder with a maximal instillation volume of 25 mL of sterile saline. IAP measurement The maximal volume to be instilled into the bladder prior to IAP measurement is 50 ml of sterile saline IAP value The normal IAP is around 5 mmHg but can be The normal IAP is around 5-7 mmHg in Normal IAP is approximately 5-7 mmHg non-pathologically increased in the obese adults in critically ill adults IAP value The normal IAP is around 10-15 mmHg in obese patients IAH IAH is defined by an IAP value > 12 mmHg IAH is defined by a repeated or sustained IAH is defined by a sustained or repeated which is recorded by a minimum of three increase in IAP above 12 mmHg pathologic elevation of IAP > 12 mmHg. standardized pressure measurements that are conducted 4-6 hours apart IAH IAH is defined by an APP value < 60 mmHg which is recorded by a minimum of two standardized pressure measurements that are conducted 1-6 hours apart IAH Grading – Defined by IAP > 12 mmHg IAH can be – Grade I: IAP between 12 and 15 mmHg IAH is graded as follows: graded as: – Grade II: IAP between 16 and 20 mmHg • Grade I: IAP 12-15 mmHg Grade I: IAP between 12 and 15 mmHg – Grade III: IAP between 21 and 25 mmHg • Grade II: IAP 16-20 mmHg – Grade II: IAP between 16 and 20 mmHg – Grade IV: IAP greater than 25 mmHg • Grade III: IAP 21-25 mmHg – Grade III: IAP between 21 and 25 mmHg • Grade IV: IAP > 25 mmHg – Grade IV: IAP greater than 25 mmHg ACS ACS is defined as a peak IAP value of > 20 ACS is defined as the presence of both: ACS is defined as a sustained IAP ≥ 20 mmHg and/or APP < 50 mmHg recorded A sustained increase in IAP above 20 mmHg mmHg (with or without an APP < 60 during a minimum of two standardized (IAH grade III or IV) with or without an ab- mmHg) that is associated with new ormeasurements that are performed 1-6 hours dominal perfusion pressure (APP) below 60 gan dysfunction / failure. apart and that is associated with single or mmHg, together with: multiple organ system failure which was not single or multiple organ system failure which previously present (as assessed by the daily was not previously present SOFA or equivalent scoring system; organ failure is defined as a SOFA organ system score of >3). In contrast to IAH, the ACS should not be graded, ACS is an all or nothing phenomenon




IAH classification

For further fine-tuning and classification of IAH/ACS four questions need to be answered. 1. What is the duration of IAH/ACS? 2. Is an intra-abdominal problem responsible for the IAH/ACS? 3. What is the etiology of the IAH/ACS? 4. Is the IAH/ACS localised or generalised IAH Classification According to the duration of symptoms, we can classify IAH into 4 groups: 1. chronic IAH 2. acute IAH 3. subacute IAH 4. hyperacute IAH Chronic IAH acute IAH subacute IAH hyperacute IAH primary ACS

secondary ACS

recurrent ACS

IAH categories

IAH classification

Primary ACS is defined as a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional radiological intervention, or that develops following abdominal surgery (such as abdominal organ injuries that require surgical repair or damage control surgery, secondary peritonitis, bleeding pelvic fractures or other causes of massive retroperitoneal hematomas, liver transplantation). Patients that undergo an initial trial of nonoperative management for solid organ injuries who subsequently develop ACS are included in the Primary category. Secondary ACS refers to conditions that do not require early surgical or interventional radiological intervention (such as sepsis and capillary leak, severe acute pancreatitis, major burns and other conditions requiring massive fluid resuscitation). Tertiary ACS refers solely to the condition where ACS develops following prophylactic or therapeutic surgical or medical treatment of primary or secondary ACS (e.g. persistence of ACS after decompressive laparotomy – formerly termed the “open abdomen compartment syndrome – or the development of a new ACS episode following the definitive closure of the abdominal wall after the previous utilization of temporary abdominal wall closure). The presence of IAH/ACS whether primary, secondary or tertiary should always be viewed in the context of the underlying etiologies. We identify 4 major patient categories: 1. Surgical 2. Medical 3. Trauma 4. Burn To differentiate between localised and systemic IAH/ACS the bladder-to-gastric pressure difference should be measured. A localised problem is present when this difference exceeds 10 mmHg

For further fine-tuning and classification of IAH/ACS three questions need to be answered. 1. What is the duration of IAH/ACS? 2. Is an intra-abdominal problem responsible for the IAH/ACS? 3. What is the etiology of the IAH/ACS?

chronic IAH is defined as IAH that lasts for months or years acute IAH is defined as IAH that develops within hours subacute IAH is defined as IAH that develops within days hyperacute IAH is defined as IAH that only lasts for second or minutes Primary ACS is caused by a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or angioradiological intervention, or a condition that develops following abdominal surgery

Primary ACS is a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional radiological intervention.

Secondary ACS is caused by conditions that Secondary ACS refers to conditions that do not originate from the abdomo-pelvic re- do not originate from the abdominogion pelvic region.

Recurrent ACS is caused by condition in which ACS develops following prophylactic or therapeutic surgical or medical treatment of Primary or Secondary ACS

Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS.

The four IAH categories are: medical, surgical, trauma or burn


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Table 2. Evolution in consensus recommendations, from initial suggestions to final publication Term Risk factors for IAH

First Description (2004) Patients admitted to the ICU should at least once (preferably on admission) be screened for possible risk factors for the development of IAH or ACS.

Modified Description (2005) Patients admitted to the ICU should, preferably on admission, be screened for possible risk factors for the development of IAH or ACS. Indication for IAP If one or more risk factor is present a base- If one or more risk factors are monitoring line IAP measurement should be obtained for present, a baseline IAP measfuture reference. urement should be obtained.


IAP measurement

Epidemiology

Studies examining the prevalence and incidence of IAH/ACS should be based on the consensus definitions and classifications.

Epidemiology

Epidemiologic data should be given for mean, median and maximal IAP values on admission and during the study stay.

Treatment

Treatment for IAH/ACS is based on 3 principles: specific medical procedures to reduce IAP and the consequences of ACS general (intensive care) support of the critically ill patient optimisation after (surgical) decompression to perhaps counteract some of the specific adverse effects associated with decompression The medical treatment options should be targeted to specific goals and can be divided into 5 groups: 1. Improvement of abdominal wall compliance 2. Evacuation of intraluminal contents 3. Evacuation of peri-intestinal and abdominal fluids 4. Correction of capillary leak and positive fluid balance 5. Specific treatment (optimising APP, negative abdominal pressure,…)

Medical treatment


Final Description (2007) patients should be screened for IAH / ACS risk factors upon ICU admission and in the presence of new or progressive organ failure (GRADE 1B).

1) if two or more risk factors for IAH / ACS are present, a baseline IAP measurement should be obtained (GRADE 1B) and 2) if IAH is present, serial IAP measurements should be performed throughout the patient’s critical illness (GRADE 1C). studies should adopt the standardized IAP measurement method recommended by the consensus definitions OR provide sufficient detail of the technique utilized to allow accurate interpretation of the IAP data presented. (GRADE 2C) Prevalence and/or incidence incidence and prevalence estimates of IAH / ACS should estimates of IAH/ACS should be based upon the consensus definitions (GRADE 1C). be based upon the consensus definitions. In any study, mean, median, mean, median, and maximal IAP values should be proand maximal IAP values should vided both on admission and during the study period be provided both on admission (GRADE 2C). and during the study period. Appropriate treatment and management of IAH and/or ACS is based upon four general principles: 1. Serial monitoring of IAP. 2. Optimization of systemic perfusion and organ function in the patient with elevated IAP. 3. Institution of specific medical procedures to reduce IAP and the end-organ consequences of IAH / ACS. 4. Prompt surgical decompression for refractory IAH. Given the significant benefit and limited risk, we recommend that APP should be maintained above 50-60 mmHg in patients with IAH / ACS (GRADE 1C). As no prospective trials have yet been performed evaluating the benefits and risks of sedation and analgesia in IAH / ACS, no recommendations can be made at this time. a brief trial of neuromuscular blockade may be considered in selected patients with mild to moderate IAH while other interventions are performed to reduce IAP (GRADE 2C). the potential contribution of body position in elevating IAP should be considered in patients with moderate to severe IAH or ACS (GRADE 2C). To-date, however, no prospective trials have been performed to confirm the benefit of Nasogastric / Colonic Decompression, Prokinetic Motility Agents and no recommendations can be made at this time. fluid resuscitation volume should be carefully monitored to avoid over-resuscitation in patients at risk for IAH / ACS (GRADE 1B) and 2) hypertonic crystalloid and colloid-based resuscitation should be considered in patients with IAH to decrease the progression to secondary ACS (GRADE 1C). Diuretics and continuous venovenous hemofiltration / ultrafiltration have not been subjected to clinical study in IAH / ACS patients, however, and no recommendations can be made regarding their use. percutaneous catheter decompression should be considered in patients with intraperitoneal fluid, abscess, or blood who demonstrate symptomatic IAH or ACS (GRADE 2C).


Temporary abdominal closure (TAC)

It is not obligatory to use a vacuum assisted fascial closure (VAFC) as first time TAC since it is quite expensive and about one third of the patients can have their fascia closed at the second laparotomy.

surgical decompression should be performed in patients with ACS that is refractory to other treatment options (GRADE 1B), and 2) presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH / ACS (GRADE 1C). recommendations for definitive abdominal closure cannot be made at this time.


IAP measurement Future studies need to examine the ideal frequency for IAP measurement as well as the diurnal and nocturnal variations during continuous IAP monitoring. IAP and APP tresholds

ROC curves

IAP validation

IAP validation

Bias

Limits of agreement

Future studies need to examine the ideal frequency for IAP measurement as well as the impact of diurnal and nocturnal variations. Studies looking at IAP thresholds should be Evaluation of IAP and APP based on the analysis of receiver operating thresholds should be based characteristics (ROC) and the area under the on the analysis of receiver opROC-curve. erating characteristics (ROC) and the area under the ROCcurve. A good area under the ROC curve should be at least 0.75, and the best threshold needs to be identified with a sensitivity and/or specificity of at least, or close to 75%. Studies examining new devices to measure New IAP measurement techIAP should always compare the new IAP niques should be compared measurement method with some form of against a gold standard and gold standard. include a Bland and Altman analysis. The validation of the new technique should not be limited to the analysis of (significant) correlation coefficients with R2 but should also include an analysis according to Bland and Altman. The bias or the difference between 2 IAP The bias or difference between methods should be close to 0 mmHg (range the two methods should be -1 tot +1 mmHg). (Recommendation 13) close to 0 mmHg (range -1 to +1 mmHg) with maximum allowable limits of agreement (LA) within a range of 4 mmHg (LA = bias ± 4 mmHg). The maximal allowed limits of agreement (LA) when comparing 2 IAP methods should be within a range of 4 mmHg (LA = bias ± 4 mmHg).


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Intraabdominal Pressure (IAP) The IAP is the steady state pressure concealed within the abdominal cavity. The IAP shifts with respiration as evidenced by an inspiratory increase (diaphragmatic contraction) and an expiratory decrease (relaxation). The abdomen can be considered as a closed box which is partially rigid (spine and pelvis) and partially flexible (abdominal wall and diaphragm) with an anchorage above (costal arch) so that pressure values follow the hydrostatic laws. The degree of flexibility of the walls and the specific gravity of the abdominal contents would determine pressure at a given point at a given position (prone, supine…). However, n real life things are complicated by the movable diaphragm, the shifting costal arch, the contractions of the abdominal wall, and the intestines that may be empty or filled with air, fluid or fecal mass. The intraabdominal pressure is the pressure concealed within the abdominal cavity (Definition 1) Acceptance: by 95.5% of the consensus conference participants Remarks: the suggestion was made to add the recommendation that the pressure should be obtained in a steady-state situation. Some thought it would be advisable to highlight the consensus statements as such and suggested that these could somehow either form part of the abstract or be included in a single list as an ‘executive summary’ or similar at the beginning of the document. Result: modified definition kept in the final publication: “IAP is the steady-state pressure concealed within the abdominal cavity” (Final Definition 1)

APP = MAP – IAP (Definition 3) Acceptance: by 100% of the consensus conference participants Remarks: Abdominal perfusion pressure (APP) assesses not only the severity of IAP, but also the adequacy of the patient’s systemic perfusion. Result: definition kept in the final publication: “APP = MAP – IAP” (Final Definition 2) Filtration Gradient Renal perfusion pressure (RPP) and renal filtration gradient (FG) have been proposed as key factors in the development of IAP-induced renal failure. The FG is the mechanical force across the glomerulus and equals the difference between the glomerular filtration pressure (GFP) and the proximal tubular pressure (PTP). FG = GFP – PTP (Definition 4) Acceptance: by 95.5% of the consensus conference participants Remarks: none Result: definition kept in the final publication, but in combination with the following definition: “FG = GFP – PTP = MAP – 2 x IAP” (Final Definition 3) In the presence of IAH, PTP may be assumed to equal IAP, and thus GFP can be estimated as MAP - IAP. The FG can then be calculated by the formula: FG = MAP - 2*IAP (Definition 5)

Acceptance: by 97.7% of the consensus conference participants Remarks: none Result: definition not kept in the final publication

Acceptance: by 95.5% of the consensus conference participants Remarks: none Result: definition kept in the final publication (see above) Thus, changes in IAP will have a greater impact on renal function and urine production than changes in MAP. It should not be surprising, therefore, that decreased renal function, as evidenced by development of oliguria, is one of the first visible signs of IAH.

Abdominal Perfusion pressure Analogous to the widely accepted and utilized concept of cerebral perfusion pressure, calculated as mean arterial pressure (MAP) minus intracranial pressure (ICP), the abdominal perfusion pressure (APP), calculated as MAP minus IAP, has been proposed as a more accurate marker of critical illness and endpoint for resuscitation.

IAP measurement Since the abdomen and its contents can be considered as relatively non-compressive and primarily fluid in character, behaving in accordance to Pascal’s law, the IAP can be measured in nearly every part of it. Different direct and indirect measurement methods have been suggested (1).

The intraabdominal pressure varies with respiration (Definition 2)




The IAP should be expressed in mmHg and measured at end-expiration in the complete supine position, ensuring that abdominal muscle contractions are absent and the transducer zeroed at the level of midaxillary line (Definition 6) The conversion factor from mmHg to cmH2O is 1.36 and conversely, from cmH2O to mmHg it is 0.74 Acceptance: by 95.5% of the consensus conference participants Remarks: It was suggested to omit the conversion factor from the definition. Some also suggested to use the patient position at 30° head of bed (HOB) elevation as compared to the flat supine position, because most patients in the ICU are placed in the HOB 30° or 45° position to prevent ventilator associated pneumonia. Result: slightly modified definition kept in the final publication, supine position maintained because of lack of data and conversion from mmHg to cmH2O omitted: “The IAP should be expressed in mmHg and measured at end-expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line” (Final Definition 4) The direct gold standard IAP measurement method is the pressure measured via direct needle puncture into the abdominal cavity (eg. During peritoneal dialysis or laparoscopy) (Definition 7) Acceptance: by 77.3% of the consensus conference participants Remarks: Remarks were made that laparoscopy is not an ideal environment (the Verres needle can be blocked), and an invasive measurement can not be suggested as a gold standard. It is obvious that we can use different methods, but maybe only one gold standard should be withheld? Direct IAP measurement is not widely used in clinical practice. It was suggested to leave this out or to give it less visibility in the manuscript since it clouds the issue of ‘what should be used as the Gold Standard’ Result: definition not kept in the final publication The indirect gold standard for intermittent IAP measurement is via the bladder (Definition 8) Acceptance: by 90.9% of the consensus conference participants Remarks: Some argued that a description of the recommended technique for IAP measurement should

be given as follows: 1) connect the culture aspiration port of the urinary tubing to a transducer; 2) clamp the tubing distal to the aspiration port; 3) instil a maximal volume of 50 ml of sterile room temperature saline into the bladder with the patient in the complete supine position; 4) zero the transducer at the mid-axillary line; 5) after a stabilisation period of at least 30-60 seconds, mean IAP is read either on the bedside monitor or as the height of the urine column in the drainage tubing. It was also suggested that the maximal bladder instillation volume should be mentioned, and some suggested that 10 to 20ml is enough. Initially 50ml was agreed upon, but prior to the publication new data was published confirming that 20ml is more appropriate (6-8). Some participants suggested that also the type of instillation fluid should be specified: saline versus glucose versus urine as with the manometer techniques (9-11). Some suggested to use the patient’s own urine except in anuric patients. The reference level for intermittent measurement is important with regard to symphysis pubis or mid-axillary line as is the level of sedation, spontaneous versus controlled mechanical ventilation and the HOB position. Result: modified definition kept in the final publication, a maximal instillation volume of 25ml sterile saline was added: “The reference standard for intermittent IAP measurement is via the bladder with a maximal instillation volume of 25 mL of sterile saline” (Final Definition 5) The indirect gold standard for continuous IAP measurement is via a balloon-tipped catheter in the stomach (Definition 9) Acceptance: by 79.5% of the consensus conference participants Remarks: Continuous IAP monitoring lacks data and the IAP measurement definition still requires a “snapshot” approach due to the need for control of clinical variables. Intermittent bladder pressure checks are and should remain the gold standard for now. Gastric pressure measurement should not be part of any consensus statement at this point. At that time only one commercially method was available for continuous IAP monitoring namely via a balloon-tipped catheter in the stomach connected to the IAP monitor (Spiegelberg, Hamburg, Germany) (11, 12). During the congress a new study was presented validating continuous IAP monitoring via the bladder (13). Therefore some considered that a bias was introduced because of the affiliation of some congress participants to the industry: “the total clinical


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data on continuous monitoring is very limited and conducted only by single researchers, this needs to be confirmed in other institutions before we can call it a gold standard”. Nowadays continuous IAP monitoring is possible via the stomach (Spiegelberg or CiMON techniques), bladder (13) or directly intraperitoneally (14, 15), either via a fluid filled pressure transducer, an air or water capsule membrane or a solid state transducer (1, 16). Result: definition not kept in the final publication Normal and Pathologic IAP values In the strictest sense, only IAP values ranging from sub-atmospheric to zero mmHg can be considered normal. However, certain physiological characteristics, such as morbid obesity, can be associated with chronic increased IAP to which the patient has adapted, and the clinical significance of mild to moderate elevated values needs to be assessed in view of the initial ”steady state” of the individual patient. For example, it has been demonstrated that increased sagittal abdominal diameter in morbidly obese patients is associated with elevated IAP in the absence of other significant pathophysiology (17). The normal IAP is around 5mHg (Definition 10) Acceptance: by 83% of the consensus conference participants Remarks: It was suggested that baseline IAP may vary depending on body mass index, obesity or sagittal diameter. Absolute numbers pose problems especially in paediatric patients who have a lower mean arterial pressure such that lower IAP may result in poor abdominal perfusion pressures. Therefore ACS may occur in a neonate at an IAP of 8 to 12 mmHg, suggesting that APP will be a more appropriate way for determining definitions. Therefore it should be mentioned that all the definitions and thresholds given are only valid in adult patients since there are not enough data in children. The following definition was suggested: “The normal adult IAP is around 5 mmHg, but can be nonpathologically increased in the obese. Elevated IAP is a common finding among critically ill medical and surgical patients” Result: definition modified with regard to critically ill adults and kept in the final publication: “The normal IAP is approximately 5-7 mmHg in critically ill adults” (Final Definition 6)


Intra-Abdominal Hypertension (IAH) One point has to be made clear: simply putting the hand on the abdomen does not permit discrimination between IAP of 10 or 20mmHg (18, 19). The exact level of IAP that defines IAH still remains the subject of debate. In the early surgical literature the level of 15-18 mmHg (20 to 25 cmH2O) was put forward. Burch and co-authors defined a grading system of IAH/ACS to guide therapy (20): Converting from the units of cmH20 used in the original scale to values in mmHg, Grade I corresponds to a bladder pressure of 7.5-11 mmHg (10-15 cmH20), Grade II to 11-18 mmHg (15-25 cmH20), Grade III to 18-25 mmHg (25-35 cmH20), and Grade IV >25 mmHg (>35 cmH20). It was suggested that most of the patients with grade III and all of the patients with grade IV should undergo surgical abdominal decompression. In all grades adequate intravascular volume should be maintained whilst avoiding overfilling. Obviously, pathological IAP is a continuum ranging from mild increases in the IAP without clinically significant adverse effects to a substantial elevation of the IAP with grave consequences to almost all organ systems in the body. Although the use of a single IAP parameter to define IAH could be questioned, it is important that a consensus on this point be reached in the future. An accepted benchmark for the identification of IAH will facilitate the accurate interpretation of data derived from different institutions and individual studies. A recent multicenter study aimed at establishing the prevalence, etiology and predisposing factors associated with IAH in a mixed population of intensive care patients defined IAH as a maximal IAP value of 12 mmHg or more in at least one measurement (2). There are inherent variations and fluctuations in the IAP. When comparing values from continuous measurements to measurements taken during short intervals, the question of the relevance of using one maximal value of IAP to guide our therapeutic strategies, instead of using the mean or median of a set of measurements arises. With the lack of a consensus, and because the majority of institutions use maximal IAP values from individual bladder pressure measurements, all pressure values subsequently referred to herein correspond to the maximal IAP values from ”standardized” non-continuous bladder measurements, unless stated otherwise. Until a universally accepted consensus on the definition of IAH is established, and in order to exclude brief, temporary elevations of IAP that are not clinically significant, we suggest that IAH be defined as follows:



IAH is defined by a peak IAP value of > 12 mmHg which is recorded by minimum of two standardized pressure measurements that are conducted 4-6 hours apart. (Definition 11) Acceptance: by 75% of the consensus conference participants Remarks: Remarks made were that “peak” IAP should be omitted, that the rate of rise in IAP or the evolution over time as an indicator of a developing (surgical) catastrophe received little attention. Some disagreed with the 4-6 hours separation stipulated and suggested that 1-2 hours should be sufficient in a critically ill patient. This definition requires 12-18 hours prior to definition being met, which is probably too long, perhaps it would be better over a 6 hour period 1-2 hours apart. Baseline conditions are important since an IAP of 12 mmHg is not the same in an awake or sedated patient! Do we need to have different thresholds in medical versus surgical patients? What about patients with chronic IAH, when do we need to get worried there? Absolute numbers pose a problem especially in pediatric patients who have lower mean arterial pressure (see above). Continuous measurements and evolution over time are probably more important than individual measurements. Result: definition modified in the final publication: “IAH is defined by a sustained or repeated pathologic elevation of IAP > 12 mmHg” (Final definition 7) IAH is defined by a APP value of < 60 mmHg which is recorded by minimum of two standardized pressure measurements that are conducted 1-6 hours apart. (Definition 12) Acceptance: by 77.3% of the consensus conference participants Remarks: The following definition was suggested: “Intra-abdominal hypertension (IAH) is the pathologic elevation of IAP. IAH is defined by a sustained or repeated IAP > 12 mmHg or an APP < 60 mmHg”. This definition would define a patient with a MAP of 60 and an IAP of 5 mmHg as having IAH which obviously does not make any sense. An APP threshold value of 50mmHg would be better to harmonise with the ACS definition. Result: definition not kept in the final publication After establishing a minimum threshold for defining IAH, stratification of the pathological IAP values is needed to calibrate and quantify the ”threat” of the insult to produce clinically significant manifestations.

Ultimately such a stratification system could be used as an indication for various therapeutic interventions. With reference to the vascular system, although the classification ranges from mild to malignant, hypertension of any degree mandates intervention to prevent progressive organ dysfunction. The more severe the hypertension, the more urgent is the need for treatment. If this principle is applied to the abdomen, the pressure at which organ dysfunction becomes apparent may be used to define IAH. Therein lies the problem. Depending on the tools used, objective evidence of organ dysfunction and perfusion abnormalities may not be discovered before they are clinically apparent. To simplify things and as stated above, Burch et al. presented a four-level grading system upon which treatment could be based. In an analogous format, we suggest to use the following grading system for IAH in order to stratify patients. Defined by IAP>12 mmHg. IAH can be graded as: Grade I. IAH: IAP between 12-15 mmHg Grade II. IAH: IAP between 16-20 mmHg Grade III. IAH: IAP between 21-25 mmHg Grade IV. IAH: IAP greater than 25 mmHg (Definition 13) Acceptance: by 90.9% of the consensus conference participants Remarks: Some suggested the following threshold: “grade I from 15-20 mmHg, grade II from 20 to 25 mmHg, grade III from 25 to 30 mmHg and grade IV above 30 mmHg”. For research purposes, definitions with absolute or range of values will be necessary, however for clinical purposes the assessment of organ function will need to be part of the definition. Some commented “Considering the normal variation that does exist this grading does not seem relevant”, while others stated “Definitions for IAH and ACS should not cross grades”. Result: definition kept in the final publication (Final definition 8) Abdominal compartment syndrome (ACS) The ACS and IAH represent different stages of the same pathologic process, but they are not identical. IAH is a continuum with a critical level defining it that may vary from patient to patient and from moment to moment according to underlying etiologic factors, filling status, pre-existing organ failure and comorbidities. This level may be somewhere between 10 and 15mmHg (or 13.6 to 20.4 cmH2O) but is generally greater than 12


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mmHg. At this level changes at the microcirculatory level can take place even without obvious clinical signs of ACS. Subsequently, the exact level that defines ACS also remains subject to debate. Some interchange the terms IAH and ACS, and others define IAH after the onset of ACS, in fact the Grade I ACS (defined as from 10 to 15cmH20 or 7.5 to 11mmHg) in the Burch definition is mere IAH. Within the last statement rests the theoretical distinction between IAH and ACS, namely that IAH in combination with overt organ dysfunction represents ACS. This theoretically clear distinction may be difficult to make in clinical situations however, due to the indistinct margins of IAH and the difficulty in detecting subtle forms of organ dysfunction. In analogy to outcome prediction in the critically ill, the problems are rarely located at the far ends of the spectrum. Patients with low IAP and without new or progressive organ dysfunction are unlikely to benefit from abdominal decompression and patients with high IAP and timerelated progressive organ dysfunction clearly present with overt ACS, but in between these extremes, the distinction between IAH and ACS may be very difficult to make. Fietsam first described a syndrome in 4 surgical patients who developed oliguria, hypoxia, hypercarbia, high peak inspiratory pressures and a tense abdomen (21). To separate IAH from the clinical Abdominal Compartment Syndrome (ACS), Ivatury et al. characterized ACS by the presence of a tensely distended abdomen, elevated intra-abdominal and peak airway pressures, inadequate ventilation with hypoxia and hypercarbia, impaired renal function, and a documented improvement of these features after abdominal decompression (22). ACS was seen as a late manifestation of uncontrolled IAH. Similar characteristics in different combinations and with additions of persistently low pHi, labile blood pressure, diminished cardiac output, tachycardia with or without hypotension, or oliguria have subsequently been used by other authors. This was adapted by Morris and lead to the later generally accepted definition which is called the triad of ACS: 1) a pathologic state caused by an acute increase in IAP above 20 to 25 mmHg (or 27.2 to 34 cmH2O) 2) that adversely affects end-organ function or that can cause serious wound complications and 3) in which abdominal decompression has beneficial effects (23). A more accurate definition of the ACS will enhance the comparison of clinical data from different centers and will be helpful in future clinical trials. Reaching this milestone requires a definition which combines a cut-off


value for IAP with the significant clinical consequences of the prolonged IAH, i.e. the development of disturbances in the different organ systems. Meldrum et al. defined ACS as IAP >20 mmHg complicated by one of the following: peak airway pressure >40 cmH20, oxygen delivery index 3 (25). The SOFA score includes the sum of six organ system scores (respiratory, cardiovascular, renal, coagulation, liver and neurologic) ranging from 0 (normal) to 4 (severe derangement) for each organ system. The SOFA score is calculated using the worst values of the day. In addition to the calibration bias, the SOFA score does not account for organ systems which are not included in the score, of which the most important is the gastrointestinal system. Until a consensus agreement on a definition of ACS is reached, we submit the following to be used in future clinical studies: ACS is defined as a peak IAP value of > 20 mmHg and/or APP < 50 mmHg recorded during a minimum of two standardized measurements that are performed 1-6 hours apart and that is associated with single or multiple organ system failure which was not previously present (as assessed by the daily SOFA or equivalent scoring system; organ failure is defined as a SOFA organ system subscore of >3) (Definition14) Acceptance: by 72.7% of the consensus conference participants Remarks: This definition would define a patient with a MAP of 55 and an IAP of 8 mmHg as having ACS which obviously does not make any sense. Some suggested the following definition: “Abdominal Compartment Syndrome (ACS) is present when organ dysfunction occurs as a result of IAH. ACS is defined by a sustained or repeated IAP > 20 mmHg and/or APP < 60 mmHg in association with new-onset single or multiple organ system failure. In contrast to IAH, ACS is not be graded, but rather considered as an “all or nothing” phenomenon”. Definitions for IAH and ACS should not cross



grades. Some questioned whether the threshold of 20 mmHg is the same in spontaneously breathing versus mechanically ventilated patients, or in patients with chronic IAH? Three measurements to diagnose IAH or ACS are not necessary, a value of 25 mmHg in a postoperative patient is sufficient to diagnose ACS after correction for a ruptured abdominal aortic aneurysm. Some found that 20mmHg was too low as cut-off for ACS. Some felt that neonatal surgical correction of abdominal wall effects (gastroschisis, umbilical hernias,…) should be included somewhere in the definitions. Result: modified definition kept in the final publication: “ACS is defined as a sustained IAP ≥ 20 mmHg (with or without an APP < 60 mmHg) that is associated with new organ dysfunction / failure” (Final Definition 9) In contrast to IAH, the ACS should not be graded, ACS is an all or nothing phenomenon. The organ dysfunctions defining ACS however usually occur with Grade III-IV IAH but the individual tolerance of IAH varies as discussed previously. There is no single IAP value, above which ACS is uniformly present. Classification of IAH/ACS With the increasing recognition of ACS as a significant contributor to the development of multiple organ failure in critically ill patients, and the multitude of conditions associated with ACS, it is useful to categorize ACS according to the underlying pathology. In trauma patients, primary ACS has been defined as a recognized complication of damage control laparotomy, and secondary ACS as a condition reported in patients without abdominal injury who require aggressive fluid resuscitation (26). In the intensive care environment, primary ACS has been considered as surgical (e.g. ruptured abdominal aortic aneurysm, abdominal trauma) and secondary ACS as medical (e.g. pneumonia with septic shock, toxin release, capillary leak and massive fluid overload). Occasionally a combination of the two may occur, for example when a patient develops sepsis and capillary leakage with fluid overload after initial surgical stabilization for trauma. This overlap of clinical conditions and potential etiologies has added to the confusion regarding the definitions. Additional difficulty arises when patients develop ACS after previous surgical treatment for IAH.

For further fine-tuning and classification of IAH/ACS four questions need to be answered. 1. What is the duration of IAH/ACS? 2. Is an intra-abdominal problem responsible for the IAH/ACS? 3. What is the etiology of the IAH/ACS? 4. Is the IAH/ACS localised or generalised? (Definition15) Acceptance: by 97.7% of the consensus conference participants Remarks: Some suggested to add a fifth group namely acute on chronic IAH Result: definition not kept in the final publication Answering these four questions all IAH/ACS cases can be classified accordingly. Recognizing the importance of the presence or absence of pre-existing intraabdominal pathology and the crucial role of the role of early abdominal surgery, and with the lack of a widely accepted definition of primary and secondary ACS, the authors submit the following definitions as a basis for further debate: 1) What is the duration of symptoms? Many authors allude to the biphasic graded cardiovascular response to elevated IAP. During moderate elevation blood is squeezed from the splanchnic pool to the thoracic compartment, suddenly increasing venous return and CO. With ongoing increased IAP, CO drops as the abdominal capacitance vessels are emptied. This initial “autotransfusion” effect of increased IAP is classically observed during the application of a pneumatic anti-shock garment or MAST. This might also be the rationale after the so-called combined alternating thoracic and abdominal compression during CPR, which came forward in the basic life support literature a couple of years ago. Most of the above mentioned studies relate to the hemodynamically stable patient or laboratory animal without prior insult. Extrapolation of these results to a critically ill patient and from there to a trauma patient that experienced prior shock and resuscitation or thus multiple ischemia-reperfusion injury may be incorrect. Co-morbidities play an important role in aggravating the effects of raised IAP such as preexisting chronic renal failure, massive hemorrhage, hypovolemia, PEEP or pre-existing cardiomyopathy and these may reduce the threshold of IAH that causes clinical manifestation of ACS. In most cases it is the acuity of increase in IAP that is important and not necessarily the absolute increase


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According to the duration of symptoms, we can classify IAH into 4 groups: 1. chronic IAH 2. acute IAH 3. subacute IAH 4. hyperacute IAH (Definition 16) Acceptance: by 72.7% of the consensus conference participants Remarks: What about patients with chronic IAH, when do we need to get worried there? Result: definition not kept in the final publication Examples: Chronic IAH as morbid obesity, intra-abdominal tumor (large ovarian cyst, fibroma…), chronic ascites (liver cirrhosis or CAPD), or pregnancy, in those cases the abdominal wall adapt progressively during months or years to the increase in IAP and allows time for the body to adapt; Acute IAH which is mainly due to trauma or intraabdominal hemorrhage of any cause, and leads to ACS within hours; Subacute IAH as with most medical causes in the ICU that lead to IAH within days and results from a combination of etiologic factors and predisposing conditions; Hyperacute IAH that lasts only seconds or minutes as with laughing, straining, coughing, sneezing, defecation or physical activity. Only the second and third groups are of major importance in the critically ill population after ICU admission. 2) Is an intra-abdominal problem responsible for the IAH/ACS? Primary ACS is defined as a condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or radiological intervention, or that develops following abdominal surgery (such as abdominal organ injuries that require surgical repair or damage control surgery, secondary peritonitis, bleeding pelvic fractures or other causes of massive retroperitoneal hematomas, liver transplantation). Patients that undergo an initial trial of nonoperative management for solid organ injuries who subsequently develop ACS are included in the Primary category. (Definition 17)


Acceptance: by 95.5% of the consensus conference participants Remarks: None Result: modified and simplified definition kept in the final publication: “Primary ACS is a condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or interventional radiological intervention”. (Final Definition 10) Secondary ACS refers to conditions that do not require early surgical radiological intervention (such as sepsis and capillary leak, severe acute pancreatitis, major burns and other conditions requiring massive fluid resuscitation). (Definition 18) Acceptance: by 97.7% of the consensus conference participants Remarks: None Result: modified and simplified definition kept in the final publication: “Secondary ACS refers to conditions that do not originate from the abdomino-pelvic region” (Final Definition 11) Tertiary ACS refers solely to the condition where ACS develops following prophylactic or therapeutic surgical or medical treatment of primary or secondary ACS (e.g. persistence of ACS after decompressive laparotomy – formerly termed the “open abdomen compartment syndrome – or the development of a new ACS episode following the definitive closure of the abdominal wall after the previous utilization of temporary abdominal wall closure). (Definition 19) Acceptance: by 90.9% of the consensus conference participants Remarks: Some suggested that recurrent is a more appropriate term than tertiary, which makes it possible to categorize recurrent primary ACS or recurrent secondary ACS. Result: modified and simplified definition kept in the final publication: “Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS” (Final Definition 12)


3) What is the etiology?


The presence of IAH/ACS whether primary, secondary or tertiary should always be viewed in the context of the underlying etiologies. We identify 4 major patient categories: 1. Surgical 2. Medical 3. Trauma 4. Burn (Definition 21) Acceptance: by 93.2% of the consensus conference participants Remarks: None Result: definition not kept in the final publication Examples: Surgical or postoperative: postoperative hemorrhage (e.g. aorta suture leakage), any abdominal surgery (e.g. reduction of a massive parietal or diaphragmatic hernia), abdominal closure under excessive tension, postoperative application of abdominal belt, postoperative peritonitis or intra-abdominal abscess, postoperative edema (e.g. following extensive dissections in cancer patients), laparoscopic surgery with inflation of intra-abdominal air, postoperative ileus or acute gastric dilatation. Post-traumatic and Burns: external compression from a body cast (e.g. Military Anti-Shock Trousers or MAST), burn and multiple trauma patients, intra- or retroperitoneal bleeding (e.g. traumatic aortic rupture, liver or spleen rupture…), or visceral edema post fluid resuscitation. Medical causes of raised IAP: (chronic ambulatory) peritoneal dialysis, abdominal infection (e.g. fecal or bile peritonitis, intra-abdominal abscess, acute pancreatitis, spontaneous bacterial peritonitis…), edema or ascites secondary to massive fluid resuscitation (e.g. septic shock with capillary leakage), ascitic cirrhosis with decompensation, hemoperitoneum or hemoretroperitoneum (e.g. ruptured abdominal aortic aneurysm or LMWH associated psoas or rectus sheath hematoma), tension pneumoperitoneum, ileus of any origin (e.g. intestinal obstruction, paralytic, volvulus, pseudo-obstruction or Ogilvie syndrome, metabolic…). A frequently asked question is: “what is the effect of PEEP on IAP?”. Sussman studied the effects of increasing PEEP (from 0 to 15cmH2O) on IAP and concluded that PEEP of 15cmH2O or less had no effect on IAP (27).

4) Is the problem localised or generalised? The effects of IAH or ACS can be either localised or systemic. The IAP is usually measured via the bladder (IBP) but can be erroneously increased compared to gastric pressure (IGP). Recent data support the hypothesis that a high bladder-to-gastric pressure difference (IBP-IGP) is more a marker of localised ACS, that can be treated conservatively whereas a low bladder-to-gastric pressure difference is a marker of systemic ACS (28). To differentiate between localised and systemic IAH/ACS the bladder-to-gastric pressure difference should be measured. A localised problem is present when this difference exceeds 10 mmHg (Definition 21) Acceptance: by 68.2% of the consensus conference participants Remarks: Some believe that a localised ACS is not ACS. The concept of a localised ACS also is in contradiction with previous definitions. Localised ACS is due to inaccurate measurement of the ‘real’ IAP’, and therefore it was suggested to leave this out. Furthermore, these localized ACS patients do not develop organ dysfunction. Result: definition not kept in the final publication Underlying predisposing conditions for IAH The following conditions are reported in association with IAH/ACS: 1) acidosis defined as an arterial pH below 7.2; 2) hypothermia defined as a core temperature below 33°C; 3) polytransfusion defined as a rate of packed cell transfusion of more than 10 Units/24 hours; 4) coagulopathy defined as a platelet count below 55000/mm3 or an activated partial thromboplastin time (APTT) more than 2 times normal or a prothrombin time (PTT) below 50% or an international standardized ratio (INR) more than 1.5; 5) sepsis or septic shock defined according to the American - European consensus conference definitions with capillary leak (evidenced by a high CRP to albumin ratio); and 6) liver dysfunction (defined as decompensated or compensated cirrhosis or other liver failure with ascites (paraneoplastic, cardiac failure, portal vein thrombosis, ischemic hepatitis) The combination of acidosis, hypothermia and coagulopathy has been forwarded in the literature as the deadly triad.


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How common is intraabdominal hypertension? The problem in answering this question, as indicated earlier, is that studies have used different criteria to define IAH. Sugrue et al in a study of 100 patients admitted to a single intensive care unit following laparotomy used a level of 20mmHg to define IAH (29). Of the 88 patients eligible for final analysis 29 (33%) had elevated pressures. If a lower level of 15mmHg had been used, 38 (43%) patients would have been defined as having excessive IAP. Of the 57 patients undergoing emergency surgery 23 (40%) had pressures greater than 20mmHg, whereas of the 31 patients who underwent elective surgery only 6 (19%) fulfilled the criterion. Although not achieving statistical significance this must be viewed as a clinically significant finding. In a series of 70 patients suffering life-threatening abdominal injury, 23 (33%) were regarded as having IAH using a level of 25mmHg as the definition (30). This study may be criticized, however, for containing a specific group of patients at high risk of this complication and does not necessarily portray the true incidence. As suggested by the authors, however, the critical level of IAH that needs treatment has not been established. In a prospective study of 405 patients admitted to intensive care the overall incidence of IAH was 17.5% using a cut-off point of 12mmHg (31). Of patients admitted following emergency surgery 39% fulfilled the criterion compared to only 6% of those undergoing elective surgery. The incidence in medical patients was 20%. Surprisingly, despite the use of three different levels of IAP to define IAH, the incidence is very similar especially in patients who have undergone emergency surgery. Studies examining the prevalence and incidence of IAH/ACS should be based on the above cited definitions and classifications. The results should be given for mean, median and maximal IAP values on admission and during the study stay. (Definition 22) Acceptance: by 95.5% of the consensus conference participants Remarks: This definition is a question of “blue printing” existing trials and publications. Result: definition not kept in the final publication Studies looking at IAP and APP thresholds should be based on the analysis of receiver operating characteristics (ROC) and the area under the ROC-curve. (Definition 23)


Acceptance: by 88.6% of the consensus conference participants Remarks: This definition is a question of “blue printing” existing trials and publications. Result: definition not kept in the final publication Studies examining new devices to measure IAP should always compare the new IAP measurement method with some form of gold standard. (Definition 24) Acceptance: by 97.7% of the consensus conference participants Remarks: This definition is a question of “blue printing” existing trials and publications. Result: definition not kept in the final publication The validation of the new technique should not be limited to the analysis of correlation, but it should also include a Bland and Altman analysis. (Definition 25) Acceptance: by 88.6% of the consensus conference participants Remarks: This definition is a question of “blue printing” existing trials and publications. It was suggested that the bias should be as close to 0 mmHg as possible and that the maximal allowed limits of agreement were plus or minus 4 mmHg with a percentage error of 25%. Result: definition not kept in the final publication

SUMMARY Every definition of a clinical situation or syndrome fails to include all possible conditions and variations of an inherently complex phenomenon. Nevertheless, in order to approach scientific accuracy in comparing different clinical reports, and to plan for future clinical trials, definitions are required which are comprehensive, detailed, simple, practical and acceptable to the majority of the scientific community working in the particular field. This chapter does not, and cannot, provide bullet-proof definitions for all issues associated with increased IAP, but puts forward arguments and suggestions that may serve as a springboard for further consensus building endeavors. These definitions also allow better comparisons of data between groups of researchers and may lead to refined and better definitions themselves.



REFERENCES 1. Malbrain ML. Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Intensive Care Med. 2004; 30: 357-71. 2. Malbrain ML, Chiumello D, Pelosi P, Wilmer A, Brienza N, Malcangi V, et al. Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre epidemiological study. Intensive Care Med. 2004; 30: 822-9. 3. Malbrain ML, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, 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. 4. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med. 2006; 32: 1722-32. 5. Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med. 2007; in press. 6. De Waele J, Pletinckx P, Blot S, Hoste E. Saline volume in transvesical intra-abdominal pressure measurement: enough is enough. Intensive Care Med. 2006; 32: 455-9. 7. Malbrain ML, Deeren DH. Effect of bladder volume on measured intravesical pressure: a prospective cohort study. Crit Care. 2006; 10: R98. 8. Ball CG, Kirkpatrick AW. ‘Progression towards the minimum’: the importance of standardizing the priming volume during the indirect measurement of intra-abdominal pressures. Crit Care. 2006; 10: 153. 9. Harrahill M. Intra-abdominal pressure monitoring. J Emerg Nurs. 1998; 24: 465-6. 10. Lee SL, Anderson JT, Kraut EJ, Wisner DH, Wolfe BM. A simplified approach to the diagnosis of elevated intra-abdominal pressure. JTrauma. 2002; 52: 1169-72. 11. De Potter TJ, Dits H, Malbrain ML. Intra- and interobserver variability during in vitro validation of two novel methods for intraabdominal pressure monitoring. Intensive Care Med. 2005; 31: 747-51. 12. Schachtrupp A, Tons C, Fackeldey V, Hoer J, Reinges M, Schumpelick V. Evaluation of two novel methods for the direct and continuous measurement of the intra-abdominal pressure in a porcine model. Intensive Care Med. 2003; 29: 1605-8. 13. Balogh Z, Jones F, D’Amours S, Parr M, Sugrue M. Continuous intra-abdominal pressure measurement technique. Am J Surg. 2004; 188: 679-84. 14. Risin E, Kessel B, Ashkenazi I, Lieberman N, Alfici R. A new technique of direct intra-abdominal pressure measurement: a preliminary study. Am J Surg. 2006; 191: 235-7. 15. Risin E, Kessel B, Lieberman N, Schmilovich M, Ashkenazi I, Alfici R. New technique of direct intra-abdominal pressure measurement. Asian J Surg. 2006; 29: 247-50. 16. Schachtrupp A, Henzler D, Orfao S, Schaefer W, Schwab R, Becker P, et al. Evaluation of a modified piezoresistive technique and a water-capsule technique for direct and continuous measurement of intra-abdominal pressure in a porcine model. Crit Care Med. 2006; 34: 745-50.

17. Sugerman H, Windsor A, Bessos M, Wolfe L. Intra-abdominal pressure, sagittal abdominal diameter and obesity comorbidity. J Intern Med. 1997; 241: 71-9. 18. Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg. 2000; 43: 207-11. 19. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, et al. Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg. 2002; 26: 1428-31. 20. Burch JM, Moore EE, Moore FA, Franciose R. The abdominal compartment syndrome. Surg Clin North Am. 1996; 76: 83342. 21. Fietsam R, Jr., Villalba M, Glover JL, Clark K. Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg. 1989; 55: 396-402. 22. Ivatury RR, Diebel L, Porter JM, Simon RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am. 1997; 77: 783-800. 23. Morris JA, Jr., Eddy VA, Blinman TA, Rutherford EJ, Sharp KW. The staged celiotomy for trauma. Issues in unpacking and reconstruction. Ann Surg. 1993; 217: 576-84. 24. Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia A, Burch JM. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997; 174: 667-72. 25. Vincent JL, Moreno R, Takala J, Willatts S, De Mendonca A, Bruining H, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996; 22: 707-10. 26. Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Valdivia A, Sailors RM, et al. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg. 2003; 138: 637-42; discussion 42-3. 27. Sussman AM, Boyd CR, Williams JS, DiBenedetto RJ. Effect of positive end-expiratory pressure on intra-abdominal pressure. South Med J. 1991; 84: 697-700. 28. Malbrain MLNG, Deeren DH, De Potter T, Libeer C, Dits H. Abdominal compartment syndrome following rectus sheath hematoma: bladder-to-gastric pressure difference as a guide to treatment. ANZ Journal of Surgery. 2005; 75: A8. 29. Sugrue M, Buist MD, Hourihan F, Deane S, Bauman A, Hillman K. Prospective study of intra-abdominal hypertension and renal function after laparotomy. Br J Surg. 1995; 82: 235-8. 30. Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intraabdominal 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; discussion 21-3. 31. Malbrain ML. Abdominal pressure in the critically ill: measurement and clinical relevance. Intensive Care Med. 1999; 25: 14538.


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Mesenteric ischemia, intra-abdominal hypertension, and the abdominal compartment syndrome.

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Clinical studies on intra-abdominal hypertension and abdominal compartment syndrome.

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Abdominal compartment syndrome and intraabdominal sepsis: two of the same kind?

Abdominal compartment syndrome (ACS) in a severely burned patient.

Pediatric acute respiratory distress syndrome: consensus recommendations from the Pediatric Acute Lung Injury Consensus Conference.

The secondary and recurrent abdominal compartment syndrome.

Management of intra-abdominal infections: recommendations by the WSES 2016 consensus conference.

Microfluidics for the analysis of membrane proteins: how do we get there?

Beta-blockers in hypertension: how to get the best results.

How Did It Get Late So Soon?

Tissue engineering of the bladder--when will we get there?

How did that get there? A population-based analysis of nasal foreign bodies.

Fourth Canadian Consensus Conference on the Diagnosis and Treatment of Dementia: recommendations for family physicians.

The current status of anatomy knowledge: where are we now? Where do we need to go and how do we get there?

Recognition and management of intra-abdominal hypertension and abdominal compartment syndrome; a survey among Dutch surgeons.

Pattern selection: the importance of "how you get there".