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Intra-abdominal hypertension and abdominal compartment syndrome--making progress?

In this issue, Kim et al provide us with prospective, observational data documenting the incidence, associated risk factors and outcome of intra-abdominal hypertension (IAH) in critically ill patients (1). As with many pathological conditions, once intra-abdominal pressure (IAP) is raised, there is a continuum of severity of IAH, from mild to severe. There are very different treatment and prognostic consequences, dependent on the severity of IAH, and therefore clearly defining where individuals fall within this continuum is important. The World Society of Abdominal Compartment Syndrome (WSACS) definitions provide for such a grading of severity (2). Like other consensus definitions (3), the WSACS definitions are not perfect for use in the clinical context, but have the advantage of allowing proper comparison of epidemiological studies, and should facilitate more consistent characterisation of participants in clinical trials when they are used. Kim et al's data are particularly informative because they utilise recent consensus definitions and meticulous measurement technique, in accordance with the definitions and standards agreed by the WSACS (2).

Because the incidence and severity of IAH are also strongly determined by case mix (4), it is likely admission patterns will influence epidemiological data and some results are likely to be a reflection of regional intensive care unit (ICU) admission patterns. Similarly, clinical management may vary regionally. There is increasing evidence that clinical management may influence the incidence and severity of IAH and abdominal compartment syndrome (ACS), for example much observational evidence suggests that an excessively positive fluid balance may be associated with an increased incidence and severity of IAH (5-7). Thus the data provided by Kim et al's study uniquely provides epidemiological data resulting from Australasian ICU admission patterns and management practices. In a representative Australasian ICU, Kim et al found that IAH was common, affecting about 40% of the general ICU patients, and that ACS occurred in 4% of patients studied. While the incidence of IAH and ACS was similar to that observed internationally, the condition was apparently more benign with fewer consequences in terms of organ failure and mortality (8). The apparently benign nature of the condition possibly reflects differences in practice in Australasian ICUs compared to those in other parts of the world. As the authors point out, differences in management, such the judicious use of fluid resuscitation, and maintenance of robust mean arterial pressure may have been responsible for the relatively mild nature and consequences of IAH reported in this study (1).

The current WSACS definitions, incorporating the grades of severity of IAH, are based on expert consensus and an understanding of the known pathophysiology of IAH (2). This understanding is largely derived from animal studies and uncontrolled human observations. The use of these definitions to guide diagnosis and management in the clinical setting has been proposed (9), but has not been rigorously tested. The current study raises some questions regarding these definitions and subsequent recommendations (2,9). In the patients meeting criteria for IAH, and those for whom interventions are recommended, significant excess morbidity and mortality was not evident (1). Although the presence or nature of possible therapeutic interventions was not recorded, it raises the question of whether treatment recommendations for this degree of IAH are justified. Previously reported data from Europe and North America do suggest that IAH is independently associated with increased morbidity and mortality (8,10), but in light of Kim et al's data, further data are required to resolve whether mild to moderate IAH requires therapeutic intervention.

Previous data have suggested that a low abdominal perfusion pressure (APP), less than 50 mmHg, may be a superior predictor of poor outcomes than IAH alone (10). In Kim et al's study it is notable that APP, defined as mean arterial pressure-IAP, although decreased in those with IAH, was still higher than 65 mmHg on average (1). Even in the four patients with ACS, APP was generally well maintained and morbidity and mortality were low. Although one patient with ACS demonstrated a low APP, it is unclear for how long this abnormality was present. Thus it would seem that despite the presence of IAH, the robust maintenance of APP, particularly with the use of vasopressors in the presence of conservative fluid resuscitation, may have been sufficient to prevent significant adverse consequences of IAH1. Although this hypothesis is attractive, there remains no high quality evidence supporting the concept of therapeutic maintenance of APP in the management of IAH. In fact, a search for high quality evidence supporting any management strategy for the management of IAH reveals disappointing results.

Given the lack of evidence-based interventions for the treatment of IAH, how do we progress from here? The investigators correctly point out that, on the basis of their observations, to power a clinical trial in similar Australian ICUs for a reasonable clinical endpoint such as a reduction of the incidence of ACS would require about 5000 patients (1). This would be a hugely expensive and difficult task. To target mortality improvement from ACS itself may be an alternative strategy, but the epidemiology of the condition is not well defined, and cases are infrequent in general ICUs. To choose ICUs that specialise in the management of patients at high-risk ACS, such as major trauma or burns units, would seem an alternative, however such units are not numerous. Given the likely practical difficulties and costs of achieving this goal by clinical trial methodology, what are the options available to help develop useful interventions?

It is perhaps worth taking a step back and critically assessing our knowledge of IAH and its effects. Although our knowledge of the pathophysiology and clinical consequences of IAH has advanced over the last two decades, it remains rudimentary. As discussed by Kim et al, associations between possible aetiology, risk factors for causation, and the consequences of IAH are not yet clearly delineated. For example, does a high central venous pressure indicate fluid overload causing IAH, or does IAH simply cause a mechanical, pressure-induced increase in central venous pressure? In many instances it is not even clear what conditions cause IAH, and what conditions are a consequence of IAH. In addition, the magnitude and the duration of IAH are likely to have important implications for the development of organ dysfunction (11), and therefore also for the timing of treatment strategies. There is little data from the current study, or others, informing us of the consequences of prolonged raised IAH in individual patients, or how the magnitude and duration of IAH may interact to cause pathological consequences. This information is needed to allow the development of treatment strategies, especially those that may be time sensitive.

We believe that many of these fundamental questions can be best answered in the first instance, by high quality animal studies. Animal studies could be designed to answer some of the questions of causation discussed above, should be able to identify relevant causative factors and readily clarify uncertainties of pathophysiology. Attention should be paid to developing experimental models relevant to the human condition of IAH. In particular, while most existing animal studies have explored the effects of IAP in healthy animal models, there are few that examine the effects of increased IAP under conditions where the experimental animal has systemic inflammatory response syndrome, sepsis or is shocked. It would be unusual for ICU patients to have IAH without some form of critical illness-induced systemic inflammatory response and our experimental models should replicate this as far as possible. Similarly, studies testing the effects of the duration of the varying grades of IAH on outcome may be more readily achieved in experimental models. Reliable knowledge gained from animal studies could then be used to design further experimental models testing possible interventions, such as the likely benefit of the maintenance or restoration of APP with the use of vasopressors.

While the study by Kim et al provides us with important human epidemiological data, it also serves to highlight our lack of understanding of many of the basic pathophysiological processes associated with IAH. Only when pathophysiology of IAH and ACS is more clearly understood, and possible interventions are robustly tested under experimental conditions, will we be able to begin to plan rational and rigorous clinical trials in human patients.

REFERENCES

(1.) Kim B, Prowle J, Baldwin I, Bellomo R. Incidence, risk factors and outcome associations of intra-abdominal hypertension in critically ill patients. Anaesth Intensive Care 2012; 40:79-89.

(2.) 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; 32:1722-1732.

(3.) Bone RC, Sibbald WJ, Sprung CL. The ACCP-SCCM consensus conference on sepsis and organ failure. Chest 1992; 101:1481-1483.

(4.) Joynt GM, Ramsay SJ, Buckley TA. Intra-abdominal hypertension --implications for the intensive care physician. Ann Acad Med Singapore 2001; 30:310-319.

(5.) 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; 138:637-642.

(6.) Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary abdominal compartment syndrome after severe extremity injury: are early, aggressive fluid resuscitation strategies to blame? J Trauma 2008; 64:280-285.

(7.) O'Mara MS, Slater H, Goldfarb IW, Caushaj PF. A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma 2005; 58:1011-1018.

(8.) 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; 33:315-322.

(9.) 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; 33:951-962.

(10.) Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma 2000; 49:621-626.

(11.) Cheatham ML, Safcsak K. Intra-abdominal hypertension and abdominal compartment syndrome: the journey forward. Am Surg 2011; 77 (Suppl 1):S1-S5.

G. M. Joynt

J. K. M. Wa

Department of Anaesthesia and Intensive Care, Chinese University of Hong Kong and Intensive Care Unit, Prince of Wales Hospital, Shatin, Hong Kong
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Title Annotation:Editorials
Author:Joynt, G.M.; Wai, J.K.M.
Publication:Anaesthesia and Intensive Care
Article Type:Editorial
Geographic Code:1USA
Date:Jan 1, 2012
Words:1714
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