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
THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME A.W. Kirkpatrick, J.J. De Waele, C.G. Ball, K. Ranson, S. Widder & K.B. Laupland To cite this article: A.W. Kirkpatrick, J.J. De Waele, C.G. Ball, K. Ranson, S. Widder & K.B. Laupland (2007) THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME, Acta Clinica Belgica, 62:sup1, 60-65 To link to this article: http://dx.doi.org/10.1179/acb.2007.62.s1.008
Published online: 30 May 2014.
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Original article – OA 7
THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME A.W. Kirkpatrick1,2,3, J.J. De Waele4, C.G. Ball3, K. Ranson1, S. Widder2,3, K.B. Laupland5
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Key words: intra-abdominal pressure, intra-abdominal hypertension, secondary abdominal compartment syndrome, recurrent abdominal compartment syndrome
ABSTRACT Introduction: The Secondary Abdominal Compartment Syndrome (SACS) refers to cases of the ACS that do not originate from the abdominopelvic region. With greater awareness of the physiologic consequences of raised intra-abdominal hypertension (IAH), cases of the SACS are being increasingly described. The prior treatment or the presence of a partially open abdomen does not preclude the ACS if the abdomen and viscera continue to swell or the clinician is not vigilant in monitoring intra-abdominal pressure (IAP). Such recurrent cases (RACS) have been defined as those
––––––––––––––– 1 Regional Trauma Services, and the Departments of 2 Critical Care Medicine, 3 Surgery, and 5 Faculty of Medicine, Foothills Hospital, University of Calgary Calgary, Alberta, Canada; 4 Intensive Care Unit, Ghent University Hospital Gent, Belgium Address for correspondence: A.W. Kirkpatrick, MD, FRCSC Department of Surgery Foothills Medical Centre 1403 – 29th Street N.W. Calgary, Alberta T2N 2T9 Tel: +1 403 944 4262 Fax: +1 403 944 1277 E-mail: [email protected]
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which redevelop following the previous medical or surgical treatment of primary or SACS. Although there has been a diverse range of etiologies implicated, these cases seem to be linked by the common occurrence of severe shock requiring aggressive fluid resuscitation. The aim of this paper is to thus to review the historical background, awareness, definitions, pathophysiological implications and treatment options for SACS and RACS. Methods: This review will focus on the available literature regarding SACS and RACS. A Medline and Pubmed search was performed using the keywords; secondary abdominal compartment syndrome AND secondary AND tertiary AND recurrent AND abdominal compartment syndrome AND intraabdominal pressure AND intra-abdominal hypertension. Bibliographies of recovered papers were hand-searched for other appropriate references. The resulting references were included in the current review on the basis of relevance and scientific merit Results: There has been remarkably little specific study of these entities outside of specific groups such as those injured by thermal or traumatic injury. The epidemiology, risk factors for, treatment of and most importantly, strategies for prevention all remain scientifically unknown and therefore based on opinion. Notable, although small, studies suggest that specific resuscitation practices may avert these conditions. Conclusions: ACS can occur in any patient who is critically ill and subject to visceral and somatic swelling, regardless of whether the inciting pathology is extra-abdominal. The ACS may also reoccur with recurrent shock and swelling even
THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME
if previous therapies had partially addressed IAH. Therefore IAP measurements should be considered a routine monitoring for the critically ill, especially those subjected to shock and requiring a subsequent resuscitation. Much further study is required to understand the differences in etiology, diagnosis, pathophysiology, and treatment for all cases of the ACS.
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INTRODUCTION The abdominal compartment syndrome (ACS) has generally been recognized as an adverse physiological state resulting from sustained increases in intra-abdominal pressure, that most obviously affects the cardiovascular, respiratory, and renal systems (1-4). The ACS has typically been recognized as a complication occurring in patients who have suffered either intraabdominal trauma or other intra-abdominal catastrophes such as ruptured aortic or other visceral aneurysm, mesenteric ischemia, and severe pancreatitis (1,2,5-8). The ACS independently predicts multi-system organ dysfunction and death (9). With greater attention and knowledge of the salient features of ACS, cases are being noted in those instances where there has been no direct abdominal injury. Cases of ACS without primary abdominal pathology or “secondary” ACS (SACS) have been reported to occur after vigorous resuscitation for burns, extra-abdominal injuries and systemic infections (10-12). A diverse range of inciting etiologies such as extraperitoneal trauma, severe burns, sepsis, and even unusual conditions such as hypothermia, lightning strikes, and pneumoperitoneum secondary to uncontrolled scuba diving ascents have been reported (3,5,13-16). These cases, termed secondary, appear to be related to resuscitation-induced bowel and abdominal wall edema and ascites (9,14,17-20). In this review, we will give an overview of the clinical conditions commonly associated with SACS and recurrent ACS (RACS), the presumed pathophysiological mechanisms involved, and potential strategies to prevent either condition.
CLINICAL CONDITIONS ASSOCIATED WITH SACS 1. Post-traumatic Secondary ACS The precise incidence of ACS in critically ill patients is unclear, but may occur in up to 1 to 14% of some high-risk populations (9,18,21). Clinicians are now preventing primary ACS after trauma or abdominal surgical diseases by prophylactically leaving the peritoneal cavity open after laparotomy (22,23). When the abdomen was closed after damage-control, high rates of primary ACS were reported. Offner reported on the outcomes of damage-control surgery, noting an 80% rate of ACS with primary fascial closure, 24% with skin closure only, and 18% with the Bogotá bag, despite an assumed bias for primary closure in more favorable patients (24). Now, in institutions that are familiar with, and which have a high degree of suspicion for, IAH, the incidence of secondary post-traumatic ACS may equal or exceed primary ACS. Balogh reported an incidence of secondary ACS of 8% compared to a 6% incidence of primary, in severely injured trauma patients presenting in shock with a mean ISS 28 in one cohort of patients (9), and 9% in another presenting in shock from severe injuries, which was 0.7% of all admissions to the shock trauma ICU (18). These patients all developed early SACS within the first 24 hours of hospital admission, and had severe shock from extra-abdominal bleeding from pelvic trauma, multiple long-bone fractures, or penetrating chest injuries (9). Balogh compared patients with primary and secondary ACS, and noted that the SACS patients tended to spend longer in the emergency department where they received significantly more crystalloid fluids (19). These patients often require aggressive fluid resuscitation and become grossly edematous. Rodas and colleagues also described a hyperacute subset of SACS that develops intra-operatively in settings requiring massive resuscitation for extra-abdominal injuries (25). 2. Secondary ACS and burns Thermal injury also induces the SACS, especially those with burns greater than 70% surface area or inhalational injury (26). Circumferential eschar is not required (26). Retrospective reviews have reported incidence of 1% of serious burns having required surgical decompression, when clinical monitoring was relied upon, potentially under-diagnosing this condition (27). SACS occurs either early during the acute burn resuscitation or during a later septic episode (26,27).
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3. Secondary ACS and Critical Illness Suggested markers of increased risk of the SACS essentially include anyone who is critically ill, and who requires fluid resuscitation in the setting of increased microvascular permeability (28). In a multi-institutional study of the point prevalence of IAH involving 6 countries, half of all patients were shown to have mild (> 12 mmHg) IAH, and 8% to have the ACS (IAH > 20mmHg and failure of 1 or more organs) (28). The volumes of fluid that have been noted to be associated with intra-abdominal hypertension are relatively modest considering current ICU practice. Malbrain considers the administration of as little as 3.5 liters of colloids or 10.5 liters of crystalloids in a 24 hour period as risk factor for IAH (29, M Malbrain, personal communication). Such volumes of fluid may be quite easily infused during aggressive resuscitation of the critically ill, especially in centres that rely primarily on crystalloid fluids. Malbrain and colleagues followed their single-day point prevalence study with a prospective study during which they followed 265 patients in six counties for a week or until death or discharge from the ICU with twice daily IAP measurements. They noted that 32% of all patents had IAH on admission, and 4.2% had ACS, although only one underwent a decompressive laparotomy (29). The mortality rate in those with IAH was significantly higher than in those without (29). They also found that the occurrence of IAH during the intensive care unit stay was an independent predictor of mortality, even using the modest threshold value of 12 mmHg (29). Although we suspect that IAH/ACS may frequently influence the outcome of the critically ill as either SACS or in a multi-factorial interaction, occurrences of the SACS after systemic sepsis, have only rarely been reported. When they have though, the outcomes have been markedly worse compared to post-surgical primary cases. This has been attributed to a lack of suspicion, leading to delayed recognition (5). We also speculate that this may relate to a lack of surveillance in non-surgical populations despite recommendations for screening available from other high risk patient groups. Such recommendations have noted thresholds of receiving 10L of crystalloid or 10 units of PRBC’s after trauma (14); or receiving 250 ml/kg of fluid after burns (15), or receiving 6L or more of crystalloids after being acutely resuscitated from shock (5). As essentially all critically ill patients are typically administered fluids and most suffer microvascular abnormalities, it is likely that almost all critically ill patients are at risk, although this has largely been overlooked by the medical community.
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This inattention is not limited though to any one institution or even nation. To date all commonly used organ dysfunction scoring systems to predict outcome in critically ill patients have disregarded the potential effects of IAH, including the APACHE II (30), SAPS II (31), SOFA (32), and MODS score (33).
PATHOPHYSIOLOGY OF THE SACS This ever increasing list of inciting conditions seems to have the unifying presence of a shock state requiring aggressive resuscitation with crystalloid fluids (34). The recognition that the shock state necessitated an obligatory loss of fluid to the intra-cellular space or “third space” has been recognized as a major advance in trauma care that has undoubtedly saved lives, and has all but eliminated renal failure as a complication of burn injury (35,36). It appears possible though, that “you can have too much of a good thing”, and that excess resuscitation with crystalloid fluids may be harming our patients and contributing to an increased occurrence of the ACS (9,20,37). Further, it appears that once IAH/ ACS is initiated that this may further potentiate systemic inflammation generating a vicious cycle culminating in multiple organ failure (34,38-40).
SACS: ARE WE CONTRIBUTING TO THE PROBLEM? The optimal fluid resuscitation strategy for the critically ill remains intensely controversial and unresolved (41,42). While some studies have identified a positive fluid balance as early as day 1 to 3 of an ICU admission as a marker of poor outcome (29,43,44), others have noted improved survival after the rapid and aggressive correction of the hemodynamic status with aggressive fluid resuscitation (45). Fluid resuscitation in these patients may influence IAP both by increasing intra-abdominal volume due to retroperitoneal and bowel wall edema, and the formation of ascites. Also ileus of the gastrointestinal tract may add to the observed increase in IAP. Often abdominal wall compliance is reduced which leads to a shift of the P/V curve of the abdomen upwards and to the left. Other current initiatives in critical care medicine may further increase the risk of the SACS. Severe sepsis (infection-induced organ dysfunction or hypoperfusion abnormalities) is a leading cause of death in critical care units through-out the world. The documented world-wide incidence is believed
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to be falsely low such that the estimated number of cases may be approaching 18 million, and is a leading cause of death worldwide (46,47). As it is acknowledged that the mortality rate of the most severe sepsis syndromes (severe sepsis or septic shock) remains unacceptably high, an international effort is underway dedicated to raising awareness of these syndromes and to promulgate guidelines intended to address severe sepsis (48,49). The first recognized priority in the subsequent “bundle” recommends fluid resuscitation to obtain a central venous pressure reading of between 8 – 12 mmHg, typically entailing aggressive fluid administration. If increased intra-thoracic or intra-abdominal pressure is recognized, even higher CVP’s will be targeted (48). These recommendations recognize that “large amounts of fluid may be administered over short periods of time” and with “venodilation and ongoing capillary leak, most patients require continuous aggressive fluid resuscitation during the first 24 hours of management” (48). Whether this increased emphasis on aggressive fluid resuscitation in the setting of sepsis induced microvascular “leakiness” will lead to an increased incidence of intra-abdominal hypertension, or even whether intra-abdominal hypertension influences outcomes in systemic sepsis, remains essentially unknown and must be studied.
THE RECURRENT ABDOMINAL COMPARTMENT SYNDROME Despite increasing use of abbreviated and decompressing abdominal closures, it has become apparent that protection from the adverse effects of IAH relies on documentation of the return to normal pressures. With marked progression in the swelling of the viscera and/or abdominal wall, cases of the abdominal compartment syndrome are being reported with increasing frequency. While the WSACS defines these cases as a condition in which the ACS redevelops following previous surgical or medical treatment of primary or SACS (3,50). Other synonyms have included the open abdomen compartment syndrome, or tertiary ACS (51,52). The important message is that an “open abdomen” in itself does not preclude the ACS, and that vigilant if not routine monitoring is required. Although the RACS has been described exclusively in a trauma population, it may also occur in the patient typically at risk for SACS. Especially in patients in the later stages after multiple surgical procedures for infectious problems or fistulas, also referred to as tertiary
peritonitis, the “frozen abdomen” that consists of a block of adherent, chronically inflamed bowel loops that cannot be mobilized, may lead to elevated IAP in patients with an open abdomen, and make abdominal decompression in these patients impossible. Often, extensive abdominal wall edema adds to the increased abdominal pressure.
PREVENTION OF SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME At this point in time it remains truly unknown as to whether the SACS can be prevented in the most critically ill patients. The importance of early control of the inciting cause of shock is crucial, such as providing hemorrhage control for bleeding, or source control for sepsis. Despite this, some measure of fluid resuscitation is necessary to provide for tissue perfusion or to manage obligatory third-space fluid losses. Which is the correct fluid to use remains an intense debate and is beyond the scope of this review. The majority of critically injured patients will be adequately resuscitated with crystalloid fluid or blood (19). It has been suggested though that smaller volumes of higher-tonicity fluids may limit edema generation and secondary IAH (53). Small prospective trials of both a plasma-based (randomized) or a hypertonic saline (non-randomized) resuscitation strategy versus crystalloid fluids in severe burns have shown decreased intra-abdominal and ventilatory pressures, although survival advantages have not yet been demonstrated (37,54).
CONCLUSIONS The relative importance of SACS will undoubtedly increase significantly in the near future. The increased awareness of SACS in conditions associated with massive fluid resuscitation will coincide with the decreased incidence of primary ACS, as more preventive measures such as temporary abdominal closure devices are used in patients undergoing abdominal surgery. Primary ACS should be something that is rarely observed in the ICU, and that is dealt with promptly when it does occur. The true role of SACS however, in other than trauma associated conditions, remains to be elucidated and should be the focus of collaborative research efforts in the next few years. The secondary and recurrent ACS represent
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the worst case scenarios of IAH. These conditions are most related to edema of the viscera, retroperitoneum, and abdominal wall as well as intra-peritoneal ascites. When the ACS develops these conditions are potentially lethal unless dealt with urgently. What is currently unknown is to what extent lesser degrees of secondary IAH contribute in a multi-factorial way to the mortality and morbidity of the critically ill, and whether novel or modified resuscitation strategies might influence the outcome. Urgent study is currently required to evaluate the true incidence, outcomes of secondary ACS/IAH, and to consider strategies to avoid their occurrence.
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ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME A.W. Kirkpatrick, J.J. De Waele, C.G. Ball, K. Ranson, S. Widder & K.B. Laupland To cite this article: A.W. Kirkpatrick, J.J. De Waele, C.G. Ball, K. Ranson, S. Widder & K.B. Laupland (2007) THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME, Acta Clinica Belgica, 62:sup1, 60-65 To link to this article: http://dx.doi.org/10.1179/acb.2007.62.s1.008
Published online: 30 May 2014.
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Original article – OA 7
THE SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME A.W. Kirkpatrick1,2,3, J.J. De Waele4, C.G. Ball3, K. Ranson1, S. Widder2,3, K.B. Laupland5
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Key words: intra-abdominal pressure, intra-abdominal hypertension, secondary abdominal compartment syndrome, recurrent abdominal compartment syndrome
ABSTRACT Introduction: The Secondary Abdominal Compartment Syndrome (SACS) refers to cases of the ACS that do not originate from the abdominopelvic region. With greater awareness of the physiologic consequences of raised intra-abdominal hypertension (IAH), cases of the SACS are being increasingly described. The prior treatment or the presence of a partially open abdomen does not preclude the ACS if the abdomen and viscera continue to swell or the clinician is not vigilant in monitoring intra-abdominal pressure (IAP). Such recurrent cases (RACS) have been defined as those
––––––––––––––– 1 Regional Trauma Services, and the Departments of 2 Critical Care Medicine, 3 Surgery, and 5 Faculty of Medicine, Foothills Hospital, University of Calgary Calgary, Alberta, Canada; 4 Intensive Care Unit, Ghent University Hospital Gent, Belgium Address for correspondence: A.W. Kirkpatrick, MD, FRCSC Department of Surgery Foothills Medical Centre 1403 – 29th Street N.W. Calgary, Alberta T2N 2T9 Tel: +1 403 944 4262 Fax: +1 403 944 1277 E-mail: [email protected]
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which redevelop following the previous medical or surgical treatment of primary or SACS. Although there has been a diverse range of etiologies implicated, these cases seem to be linked by the common occurrence of severe shock requiring aggressive fluid resuscitation. The aim of this paper is to thus to review the historical background, awareness, definitions, pathophysiological implications and treatment options for SACS and RACS. Methods: This review will focus on the available literature regarding SACS and RACS. A Medline and Pubmed search was performed using the keywords; secondary abdominal compartment syndrome AND secondary AND tertiary AND recurrent AND abdominal compartment syndrome AND intraabdominal pressure AND intra-abdominal hypertension. Bibliographies of recovered papers were hand-searched for other appropriate references. The resulting references were included in the current review on the basis of relevance and scientific merit Results: There has been remarkably little specific study of these entities outside of specific groups such as those injured by thermal or traumatic injury. The epidemiology, risk factors for, treatment of and most importantly, strategies for prevention all remain scientifically unknown and therefore based on opinion. Notable, although small, studies suggest that specific resuscitation practices may avert these conditions. Conclusions: ACS can occur in any patient who is critically ill and subject to visceral and somatic swelling, regardless of whether the inciting pathology is extra-abdominal. The ACS may also reoccur with recurrent shock and swelling even
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if previous therapies had partially addressed IAH. Therefore IAP measurements should be considered a routine monitoring for the critically ill, especially those subjected to shock and requiring a subsequent resuscitation. Much further study is required to understand the differences in etiology, diagnosis, pathophysiology, and treatment for all cases of the ACS.
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INTRODUCTION The abdominal compartment syndrome (ACS) has generally been recognized as an adverse physiological state resulting from sustained increases in intra-abdominal pressure, that most obviously affects the cardiovascular, respiratory, and renal systems (1-4). The ACS has typically been recognized as a complication occurring in patients who have suffered either intraabdominal trauma or other intra-abdominal catastrophes such as ruptured aortic or other visceral aneurysm, mesenteric ischemia, and severe pancreatitis (1,2,5-8). The ACS independently predicts multi-system organ dysfunction and death (9). With greater attention and knowledge of the salient features of ACS, cases are being noted in those instances where there has been no direct abdominal injury. Cases of ACS without primary abdominal pathology or “secondary” ACS (SACS) have been reported to occur after vigorous resuscitation for burns, extra-abdominal injuries and systemic infections (10-12). A diverse range of inciting etiologies such as extraperitoneal trauma, severe burns, sepsis, and even unusual conditions such as hypothermia, lightning strikes, and pneumoperitoneum secondary to uncontrolled scuba diving ascents have been reported (3,5,13-16). These cases, termed secondary, appear to be related to resuscitation-induced bowel and abdominal wall edema and ascites (9,14,17-20). In this review, we will give an overview of the clinical conditions commonly associated with SACS and recurrent ACS (RACS), the presumed pathophysiological mechanisms involved, and potential strategies to prevent either condition.
CLINICAL CONDITIONS ASSOCIATED WITH SACS 1. Post-traumatic Secondary ACS The precise incidence of ACS in critically ill patients is unclear, but may occur in up to 1 to 14% of some high-risk populations (9,18,21). Clinicians are now preventing primary ACS after trauma or abdominal surgical diseases by prophylactically leaving the peritoneal cavity open after laparotomy (22,23). When the abdomen was closed after damage-control, high rates of primary ACS were reported. Offner reported on the outcomes of damage-control surgery, noting an 80% rate of ACS with primary fascial closure, 24% with skin closure only, and 18% with the Bogotá bag, despite an assumed bias for primary closure in more favorable patients (24). Now, in institutions that are familiar with, and which have a high degree of suspicion for, IAH, the incidence of secondary post-traumatic ACS may equal or exceed primary ACS. Balogh reported an incidence of secondary ACS of 8% compared to a 6% incidence of primary, in severely injured trauma patients presenting in shock with a mean ISS 28 in one cohort of patients (9), and 9% in another presenting in shock from severe injuries, which was 0.7% of all admissions to the shock trauma ICU (18). These patients all developed early SACS within the first 24 hours of hospital admission, and had severe shock from extra-abdominal bleeding from pelvic trauma, multiple long-bone fractures, or penetrating chest injuries (9). Balogh compared patients with primary and secondary ACS, and noted that the SACS patients tended to spend longer in the emergency department where they received significantly more crystalloid fluids (19). These patients often require aggressive fluid resuscitation and become grossly edematous. Rodas and colleagues also described a hyperacute subset of SACS that develops intra-operatively in settings requiring massive resuscitation for extra-abdominal injuries (25). 2. Secondary ACS and burns Thermal injury also induces the SACS, especially those with burns greater than 70% surface area or inhalational injury (26). Circumferential eschar is not required (26). Retrospective reviews have reported incidence of 1% of serious burns having required surgical decompression, when clinical monitoring was relied upon, potentially under-diagnosing this condition (27). SACS occurs either early during the acute burn resuscitation or during a later septic episode (26,27).
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3. Secondary ACS and Critical Illness Suggested markers of increased risk of the SACS essentially include anyone who is critically ill, and who requires fluid resuscitation in the setting of increased microvascular permeability (28). In a multi-institutional study of the point prevalence of IAH involving 6 countries, half of all patients were shown to have mild (> 12 mmHg) IAH, and 8% to have the ACS (IAH > 20mmHg and failure of 1 or more organs) (28). The volumes of fluid that have been noted to be associated with intra-abdominal hypertension are relatively modest considering current ICU practice. Malbrain considers the administration of as little as 3.5 liters of colloids or 10.5 liters of crystalloids in a 24 hour period as risk factor for IAH (29, M Malbrain, personal communication). Such volumes of fluid may be quite easily infused during aggressive resuscitation of the critically ill, especially in centres that rely primarily on crystalloid fluids. Malbrain and colleagues followed their single-day point prevalence study with a prospective study during which they followed 265 patients in six counties for a week or until death or discharge from the ICU with twice daily IAP measurements. They noted that 32% of all patents had IAH on admission, and 4.2% had ACS, although only one underwent a decompressive laparotomy (29). The mortality rate in those with IAH was significantly higher than in those without (29). They also found that the occurrence of IAH during the intensive care unit stay was an independent predictor of mortality, even using the modest threshold value of 12 mmHg (29). Although we suspect that IAH/ACS may frequently influence the outcome of the critically ill as either SACS or in a multi-factorial interaction, occurrences of the SACS after systemic sepsis, have only rarely been reported. When they have though, the outcomes have been markedly worse compared to post-surgical primary cases. This has been attributed to a lack of suspicion, leading to delayed recognition (5). We also speculate that this may relate to a lack of surveillance in non-surgical populations despite recommendations for screening available from other high risk patient groups. Such recommendations have noted thresholds of receiving 10L of crystalloid or 10 units of PRBC’s after trauma (14); or receiving 250 ml/kg of fluid after burns (15), or receiving 6L or more of crystalloids after being acutely resuscitated from shock (5). As essentially all critically ill patients are typically administered fluids and most suffer microvascular abnormalities, it is likely that almost all critically ill patients are at risk, although this has largely been overlooked by the medical community.
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This inattention is not limited though to any one institution or even nation. To date all commonly used organ dysfunction scoring systems to predict outcome in critically ill patients have disregarded the potential effects of IAH, including the APACHE II (30), SAPS II (31), SOFA (32), and MODS score (33).
PATHOPHYSIOLOGY OF THE SACS This ever increasing list of inciting conditions seems to have the unifying presence of a shock state requiring aggressive resuscitation with crystalloid fluids (34). The recognition that the shock state necessitated an obligatory loss of fluid to the intra-cellular space or “third space” has been recognized as a major advance in trauma care that has undoubtedly saved lives, and has all but eliminated renal failure as a complication of burn injury (35,36). It appears possible though, that “you can have too much of a good thing”, and that excess resuscitation with crystalloid fluids may be harming our patients and contributing to an increased occurrence of the ACS (9,20,37). Further, it appears that once IAH/ ACS is initiated that this may further potentiate systemic inflammation generating a vicious cycle culminating in multiple organ failure (34,38-40).
SACS: ARE WE CONTRIBUTING TO THE PROBLEM? The optimal fluid resuscitation strategy for the critically ill remains intensely controversial and unresolved (41,42). While some studies have identified a positive fluid balance as early as day 1 to 3 of an ICU admission as a marker of poor outcome (29,43,44), others have noted improved survival after the rapid and aggressive correction of the hemodynamic status with aggressive fluid resuscitation (45). Fluid resuscitation in these patients may influence IAP both by increasing intra-abdominal volume due to retroperitoneal and bowel wall edema, and the formation of ascites. Also ileus of the gastrointestinal tract may add to the observed increase in IAP. Often abdominal wall compliance is reduced which leads to a shift of the P/V curve of the abdomen upwards and to the left. Other current initiatives in critical care medicine may further increase the risk of the SACS. Severe sepsis (infection-induced organ dysfunction or hypoperfusion abnormalities) is a leading cause of death in critical care units through-out the world. The documented world-wide incidence is believed
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to be falsely low such that the estimated number of cases may be approaching 18 million, and is a leading cause of death worldwide (46,47). As it is acknowledged that the mortality rate of the most severe sepsis syndromes (severe sepsis or septic shock) remains unacceptably high, an international effort is underway dedicated to raising awareness of these syndromes and to promulgate guidelines intended to address severe sepsis (48,49). The first recognized priority in the subsequent “bundle” recommends fluid resuscitation to obtain a central venous pressure reading of between 8 – 12 mmHg, typically entailing aggressive fluid administration. If increased intra-thoracic or intra-abdominal pressure is recognized, even higher CVP’s will be targeted (48). These recommendations recognize that “large amounts of fluid may be administered over short periods of time” and with “venodilation and ongoing capillary leak, most patients require continuous aggressive fluid resuscitation during the first 24 hours of management” (48). Whether this increased emphasis on aggressive fluid resuscitation in the setting of sepsis induced microvascular “leakiness” will lead to an increased incidence of intra-abdominal hypertension, or even whether intra-abdominal hypertension influences outcomes in systemic sepsis, remains essentially unknown and must be studied.
THE RECURRENT ABDOMINAL COMPARTMENT SYNDROME Despite increasing use of abbreviated and decompressing abdominal closures, it has become apparent that protection from the adverse effects of IAH relies on documentation of the return to normal pressures. With marked progression in the swelling of the viscera and/or abdominal wall, cases of the abdominal compartment syndrome are being reported with increasing frequency. While the WSACS defines these cases as a condition in which the ACS redevelops following previous surgical or medical treatment of primary or SACS (3,50). Other synonyms have included the open abdomen compartment syndrome, or tertiary ACS (51,52). The important message is that an “open abdomen” in itself does not preclude the ACS, and that vigilant if not routine monitoring is required. Although the RACS has been described exclusively in a trauma population, it may also occur in the patient typically at risk for SACS. Especially in patients in the later stages after multiple surgical procedures for infectious problems or fistulas, also referred to as tertiary
peritonitis, the “frozen abdomen” that consists of a block of adherent, chronically inflamed bowel loops that cannot be mobilized, may lead to elevated IAP in patients with an open abdomen, and make abdominal decompression in these patients impossible. Often, extensive abdominal wall edema adds to the increased abdominal pressure.
PREVENTION OF SECONDARY AND RECURRENT ABDOMINAL COMPARTMENT SYNDROME At this point in time it remains truly unknown as to whether the SACS can be prevented in the most critically ill patients. The importance of early control of the inciting cause of shock is crucial, such as providing hemorrhage control for bleeding, or source control for sepsis. Despite this, some measure of fluid resuscitation is necessary to provide for tissue perfusion or to manage obligatory third-space fluid losses. Which is the correct fluid to use remains an intense debate and is beyond the scope of this review. The majority of critically injured patients will be adequately resuscitated with crystalloid fluid or blood (19). It has been suggested though that smaller volumes of higher-tonicity fluids may limit edema generation and secondary IAH (53). Small prospective trials of both a plasma-based (randomized) or a hypertonic saline (non-randomized) resuscitation strategy versus crystalloid fluids in severe burns have shown decreased intra-abdominal and ventilatory pressures, although survival advantages have not yet been demonstrated (37,54).
CONCLUSIONS The relative importance of SACS will undoubtedly increase significantly in the near future. The increased awareness of SACS in conditions associated with massive fluid resuscitation will coincide with the decreased incidence of primary ACS, as more preventive measures such as temporary abdominal closure devices are used in patients undergoing abdominal surgery. Primary ACS should be something that is rarely observed in the ICU, and that is dealt with promptly when it does occur. The true role of SACS however, in other than trauma associated conditions, remains to be elucidated and should be the focus of collaborative research efforts in the next few years. The secondary and recurrent ACS represent
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the worst case scenarios of IAH. These conditions are most related to edema of the viscera, retroperitoneum, and abdominal wall as well as intra-peritoneal ascites. When the ACS develops these conditions are potentially lethal unless dealt with urgently. What is currently unknown is to what extent lesser degrees of secondary IAH contribute in a multi-factorial way to the mortality and morbidity of the critically ill, and whether novel or modified resuscitation strategies might influence the outcome. Urgent study is currently required to evaluate the true incidence, outcomes of secondary ACS/IAH, and to consider strategies to avoid their occurrence.
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