World J Surg (2009) 33:1142–1149 DOI 10.1007/s00268-009-9995-4

Intraabdominal Hypertension and the Abdominal Compartment Syndrome in Burn Patients Andrew W. Kirkpatrick Æ Chad G. Ball Æ Duncan Nickerson Æ Scott K. D’Amours

Published online: 7 April 2009 Ó Socie´te´ Internationale de Chirurgie 2009

Abstract Severe burns represent a devastating injury that induces profound systemic inflammation requiring large volumes of resuscitative fluids. The consequent massive swelling and peritoneal ascites raises intraabdominal pressures (IAP) to supraphysiologic levels commensurate with intraabdominal hypertension (IAH) and with the abdominal compartment syndrome (ACS) if consistently associated with IAP [20 mmHg and associated with new organ failure. Severe burn injuries are an example of the secondary ACS (2° ACS), wherein there has been no primary inciting intraperitoneal injury, yet severe IAH/ACS develops, setting the stage for progressive multiorgan dysfunction. These definitions along with practice management guidelines have recently been promulgated by the World Society of the Abdominal Compartment Syndrome (WSACS) in an effort to standardize terminology and communication regarding IAH/ACS in critical care. It is

currently unknown whether these syndromes are iatrogenic consequences of excessive or poorly managed fluid resuscitation or unavoidable sequelae of the primary injury. It occurs frequently with burns of [60% body surface area, especially with associated inhalational injury, delayed resuscitation, and abdominal wall injuries. IAH/ACS is often a hyperacute phenomenon that occurs within the first hours of admission and thereafter with any complication requiring aggressive fluid resuscitation. Despite a number of noninvasive management strategies, interventions such as percutaneous peritoneal drainage and, ultimately, decompressive laparotomy are often required once the ACS is established. Whether novel resuscitation strategies can avoid or minimize IAH/ACS is unproven at present and requires further study. Truly understanding postburn ACS may require further insights into the basic mechanisms of injury and resuscitation.

A. W. Kirkpatrick Regional Trauma Services, Foothills Hospital, University of Calgary, Calgary, AB, Canada

C. G. Ball Department of Trauma, Grady Memorial Hospital, Emory University, Atlanta, GA, USA

A. W. Kirkpatrick Department of Critical Care Medicine, Faculty of Medicine, Foothills Hospital, University of Calgary, Calgary, AB, Canada

C. G. Ball Department of Critical Care, Grady Memorial Hospital, Emory University, Atlanta, GA, USA

A. W. Kirkpatrick (&)
D. Nickerson Department of Surgery, Faculty of Medicine, Foothills Hospital, University of Calgary, 1403 – 29th Street N.W., Calgary, AB T2N 2T9, Canada e-mail: [email protected]

S. K. D’Amours Department of Trauma Surgery, Liverpool Hospital Sydney South West Area Health Service, Sydney, NSW, Australia

C. G. Ball Department of Surgery, Grady Memorial Hospital, Emory University, Atlanta, GA, USA

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S. K. D’Amours The University of New South Wales South Western Sydney Clinical School Liverpool Hospital, Sydney, NSW, Australia

World J Surg (2009) 33:1142–1149

Introduction Severe, extensive burns result in profound physiologic disturbance and have been considered one of the ultimate insults that the human body can sustain [1]. Although burn care and survival from major burn injury have improved significantly, new challenges have emerged. One such challenge is massive systemic swelling that accompanies both the inciting injury and subsequent fluid resuscitation. This swelling commonly results in severe intraabdominal hypertension (IAH) and a secondary abdominal compartment syndrome (2° ACS). Physical edema of the abdominal viscera and wall, intra- and retroperitoneal ascites, and luminal distension all contribute to whole-body organ dysfunction most overtly recognized as cardiorespiratory and renal failure but often culminating in multiorgan failure [2]. This syndrome occurs frequently with severe burns treated according to traditional recommendations, even when there has been no primary injury to the peritoneal or abdominal cavity, defining both secondary IAH and 2° ACS [3, 4]. These conditions are now being described much more commonly as a result of increased awareness but also because their development requires a conscious decision to provide aggressive therapy to a severe burn rather than to just palliate. To date, though, it is uncertain whether IAH/ACS are unavoidable consequences of the inciting injury or iatrogenic complications of our still poorly refined understanding of the basic mechanisms of injury and inflammation at a cellular level. We are also unsure of the optimal therapies with which to combat them [5].

Definitions In healthy patients, the intraabdominal pressure (IAP) ranges from slightly subatmospheric to 5 mmHg [6, 7], and those with uncomplicated postoperative courses following abdominal surgery typically exhibit IAPs of \15 mmHg [8]. IAP regularly fluctuates with respiration, activity, reference position, and body mass index, emphasizing the importance of standardized measurement conditions for comparison [9]. Advancement in the understanding and especially the therapy of IAH/ACS has until recently been greatly handicapped by major variation and discrepancies in the definitions and terminology of IAH/ACS [10]. In an attempt to provide a common framework and language for scientific research, the World Society of the Abdominal Compartment Syndrome (WSACS) constructed a number of consensus definitions intended to serve as a practical, yet comprehensive framework for both interpreting previous research and conducting prospective study [3]. More

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specifically, the Society proposed the working definition of IAH as being sustained or repeated pathologic elevation of IAP [12 mmHg [3, 11]. These measurements should be made in a relaxed patient and recorded at end-expiration. IAH is tiered as grade I IAP, 12 to15 mmHg; grade II IAP, 16 to 20 mmHg; grade III IAP, 21 to 25 mmHg; and grade IV IAP, [25 mmHg. ACS was defined as the presence of both an IAP [20 mmHg, with or without abdominal perfusion pressure (APP) \50 mmHg (recorded by a minimum of three standardized measurements conducted 1 to 6 hours apart), and single or multiple organ system failure that was not present previously [3]. APP—defined as the mean arterial pressure (MAP) minus the IAP—is a physiologic endpoint that deserves further study. In a retrospective study of 144 critically ill surgical patients with intermittent IAP measurement, an APP threshold of 50 mmHg proved superior to either MAP or IAP alone in predicting patient survival from IAH/ACS [12].

Historical and epidemiologic considerations Despite the fact that the adverse consequences of excessive IAP had been appreciated by some authors well over 100 years ago [13], the first reported documented occurrence of ACS without a primary inciting abdominal injury was not until 1994, when it was reported by Greenhalgh and Warden in burned children [14]. Since this seminal report, it has become recognized that the larger the thermal injury the greater the incidence of both IAH and ACS. A number of small series have been reported (Table 1). In a prospective study of burned children, severe IAH ([30 mmHg) developed in 11 of 30 children with Foley catheters and a mean body surface area (BSA) burn of 67% [14]. Another prospective study noted that IAH ([25 mmHg) developed in 7 of 10 burn patients with BSA burned [20% [15]. Furthermore, two patients had secondary ACS requiring decompression. Both the cohort being studied and the vigilance in measuring IAP are important factors to consider when discussing the incidence of IAH/ACS. A retrospective review found that only 1% (10/1014) of burn patients were diagnosed and treated for 2° ACS in two centers that depended on monitoring based on clinical factors, thus presumably underdiagnosing IAH [16]. Despite an array of disease processes that may result in 2° IAH/ACS, its occurrence appears to be unified by a requirement for massive crystalloid fluid resuscitation [5, 17]. If standard resuscitative guidelines are followed, clinicians must be aware of a number of threshold values that warrant increased vigilance. Burns of 60% to 70% BSA appear to represent a general threshold for the development of ACS with resuscitation [2, 17–19]. As smoke inhalation

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Table 1 Reported series: burns-related secondary abdominal compartment syndrome Study type

Year

No. of patients

Burn severity

IAH (threshold)

ACS

ACS mortality

Treatment

Greenhalgh

1994

30

56% TBSA

11/30 (30 mmHg)

3/3

54%

PD/laparotomy

Ivy

1999

3

[70% TB

3/3 (25 mmHg)

2/10

100%

Escharotomy

7/10 (25 mmHg)

Observational

Ivy

2000

10

[46% TBSA

Corcos

2001

3

[40% TBSA

Latenser

2002

9

[40% TBSA

Hobson

2002

10/1014 burns

70% TBSA (mean)

Pirsen

2004

1

53% TBSA

22 mmHg

1/1

0/1

Laparotomy

Rodas

2005

5 (only 1 burn)

70% TBSA

Clinical–severe

1/1

0/1

Laparotomy

Oda

2005

36

[30% TBSA

8/36 ([30 cmH2O)

8/36

Escharotomy (8)

Oda

2006

48

[30%TBSA (mean 95.9% ± 21.8%)

30 cm H2O

8/48

Escharotomy

Kowal-Vern

2006

22

[45% TBSA

22 mmHg ([22 mmHg)

9/22

73%

PD (17)/laparotomy (3)

Jensen

2006

3

70% TBSA (mean)

30 cmH2O

3/3

2 (67%)

Laparotomy (3)

Parra

2006

1

60% TBSA

34 mmHg (max)

Ball

2006

1

52% TBSA

38 mmHg (max)

1/1

0/1

K}untscher

2006

16

46% TBSA (mean)

6/16 (37.5%)

Escharotomy

Hershberger

2007

25

65% ± 19% TBSA (mean)

20/25 ([12 mmHg), mean 57.0 ± 4.2

25/5

22 (88%)

Sedation/paralysis Escharotomy (16)/ laparotomy (25)

Burke

2007

5

[40% TBSA (mean 61% ± 21%)

36 ± 21 mmHg (mean)

Oda

2007

38

[40% TBSA

[30 cmH2O

14/38

Keramati

2008

6

78% TBSA (mean)

30 mmHg

6/6

4 (67%)

Laparotomy (6)

2005

31

[25% TBSA (with inhalation)

[25 mmHg

2/31

7/31 (23%)

Sedation

[30 cmH2O

13/36

11/13 (85%)

Sedation/paralysis/ escharotomy

9/13 (25 mmHg)

3/3

50%

Sedation/laparotomy

4/13

66%

PD

10

100%

PD/laparotomy

60%

PD/laparotomy

PD/escharotomy Escharotomy/ laparotomy

Laparotomy (2) Sedation/paralysis/ escharotomy

Interventional O’Mara

Oda

2006

36 14 (HTS) 22 Ringer’s

[40% TBSA (without inhalation) [40% TBSA (mean 65.2%)

2/14 HTS 11/22 Ringer’s

ACS abdominal compartment syndrome, TBSA total body surface area, IAH intraabdominal hypertension, PD percutaneous drainage, HTS hypertonic saline

increases the degree of systemic injury, it lowers the threshold for IAH/ACS [2, 15, 19], presumably by increasing the systemic inflammatory response, which in turn requires greater resuscitation. If cumulative resuscitative fluid volumes approach 250 ml/kg, severe IAH or ACS should be anticipated. Ivy and colleagues noted that this amount correlated with an IAP of 24.4 mmHg based on a linear regression analysis. Hobson et al. reported that 2° ACS developed in burn patients who had received fluid at

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237 ml/kg during the first 12 hours [16]. Oda et al. reported that most of eight burned patients with 2° ACS had received fluid at more than 300 ml/kg during the first 24 hours [2]. In a small group of children, Jensen et al. noted that all had at least 4 ml/kg/%BSA prior to requiring decompression [20]. Although abdominal eschar is not a prerequisite for 2°ACS, it is a likely contributor to early increased IAP by profoundly decreasing abdominal wall complicance. Tsoutsos found that every patient in a small cohort with full-

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The earliest effect of raising the IAP above normal levels is to reduce visceral perfusion to organs such as the gut, liver, and kidneys [23–25]. The resulting effects may occur before the presence of IAH is recognized if routine measurements are not conducted. Furthermore, subtle interactions with other noxious organ-damaging effects (e.g., contrast agents, prerenal ischemia, septic mediators) may be indistinguishable in a multifactorial setting. With higher IAP, more overt symptoms may be seen such as hypercarbic hypoxemic respiratory failure in which the lungs are physically embarrassed by abdominal expansion [26], compromised venous return and subsequent reduced cardiac output despite apparently ‘‘normal’’ measured pressures, and oliguric renal failure [27]. Strong correlations between peak inspiratory pressures required to ventilate burned patients and the intrabladder pressure have been demonstrated in severely burned patients [2]. As these overt organ failures progress, a classic multisystem organ dysfunction profile develops, with vasoactive mediator release. These effects occur throughout the body and negatively affect all organ systems [28, 29]. By the time the ACS becomes overt, the prognosis for survival is grim, with reported mortality rates between 70% and 100% [14, 17, 19, 20, 30, 31].

standard for intermittent IAP measurement is via the bladder with a maximal instillation volume of 25 ml sterile saline [3]. Although greater instillation volumes have been used in the past, large volumes have the potential to influence the numeric reading by distending the bladder [34, 35]. In our ICUs, we use a continuous monitoring technique employing a three-lumen bladder catheter that has been shown in two small series to correlate well, although not perfectly, with the intermittent technique [36, 37]. As this technique greatly reduces nursing workload, we recommend placing such a catheter early in the care of a severely burned patient to facilitate frequent measurement, as the massive swelling that so frequently accompanies resuscitation later precludes changing the bladder catheter. Adequate IAP measurements may also be obtained from either direct intraperitoneal drains, gastric pressure measurement devices that offer continuous readings, or the Foley manometer device, which offers simplicity as well [38, 39]. The optimal IAP measurement technique varies among critical care settings and ultimately depends on what method is preferred by the nursing staff to obtain consistent, reliable measurements. In the past, ACS has also been diagnosed clinically even without IAP measurements through the recognition of renal and cardiorespiratory failure in conjunction with a tense, distended abdomen that improves with emergency decompression of the peritoneal cavity. It must be emphasized that such overt findings are too late and that the presence of severe IAH should have been suspected long before such events unfold. We therefore recommend routine measurement through any standard technique for all patients critically ill enough to be admitted to an ICU or burn unit with a large burn. At a minimum, the WSACS recommends serial IAP measurements be made throughout the care of a major burn patient [40]. This has been further interpreted by other authors to refer specifically to those with [40% isolated total (T)BSA burns or a 20% TBSA burn with concomitant inhalation injury [17].

Diagnosis

Prevention of IAH/ACS

It has been shown that assessment of IAP through physical examination of the abdomen is inaccurate [32, 33]. Furthermore, as the measurement of IAP is implicit in the definitions of both IAH and the ACS, it is intuitive that an accurate, simple method must be used to measure the IAP. The current recommendation from the WSACS states that IAP should be expressed in millimeters of mercury (mmHg); and it should be measured at end-expiration in the completely supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the mid-axillary line. The reference

It is still unknown if secondary IAH/ACS is iatrogenic or truly unavoidable in the most seriously burned patient. This is related to our uncertainty regarding the basic pathophysiology of thermal injury and resuscitation [5]. Nonetheless, injudicious and excessive fluid resuscitation, at a minimum, exacerbates the degree of IAH hypertension for any degree of injury and in the worst case induces fatal ACS when it might have been avoided. Recognition that the shock state necessitates an obligatory loss of fluid to the intracellular compartment, or ‘‘third space,’’ represents a seminal advance in trauma care that

thickness burns affecting the anterior, lateral, and most of the posterior surface of the torso had IAH, with 90% having at least grade III [21]. Finally, Oda et al. speculated that older patients may be at greater risk of ACS due to thinner skin [2]. Because it is intimately linked to the resuscitative process, burn-related IAH/ACS most often occurs early after hospital admission (i.e., within the first 12–24 hours) [20] or thereafter during any serious septic or other critical complication or procedure requiring aggressive fluid resuscitation, including burn wound excision [14–16, 18, 22].

Clinical effects

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has saved numerous lives and has all but eliminated postburn renal failure [41, 42]. This success must be weighed in comparison, however, to the possibility that excessive crystalloid fluid administration might be harming patients by inducing iatrogenic IAH/ACS. Given the obvious association between large-volume crystalloid resuscitation and IAH/ACS, a number of alternate resuscitation strategies have been explored in relatively small trials. An animal model of severe thermal injury showed considerably less water content in the colon (28% reduction), liver (9% reduction), and pancreas (55%), with otherwise equally effective hypertonic saline dextran versus Ringer’s lactate-based fluid regimens [43]. A recent prospective human study comparing Ringer’s lactate versus a plasma-based burn resuscitation formula found significant differences in the postresuscitation peak IAP (26.5 vs. 10.6 mmHg; P \ 0.0002) [44]. Only 13% of equally matched burn victims sustained grade IV IAH, whereas 93% of the crystalloid controls did so, although there was no mortality difference. Similar findings were seen in a nonrandomized comparison of two matched cohorts of severely burned patients (mean 65% TBSA) treated with either Ringer’s lactate (RL) or hypertonic saline (HTS) solutions. In all, 14% of those treated with HTS demonstrated severe grade IV IAH, whereas 50% of those treated with RL did so [45]. Antioxidants and mast cell stabilizers have also been experimentally shown to reduce capillary permeability after burn injury. High-dose vitamin C has considerably reduced successful burn fluid resuscitation requirements in both animal models and patients [46, 47]. Evenly matched and randomly allocated burn patients had considerably reduced fluid volume requirements, body weight gain, wound biopsy edema, partial pressure of oxygen/fraction of inspired oxygen ratios, and days of mechanical ventilation with this regimen [46]. Given the promise of these small studies, large fully powered studies are needed to determine whether alternate fluids or resuscitation strategies could prevent or diminish the onset of IAH/ACS. Until such data are available, though, it behooves clinicians to avoid any possible delay in initiating fluid resuscitation as such delay can eventuate in larger volumes being required to catch up. Close monitoring of the resuscitation protocol and avoidance of overresuscitation is also crucial, as many clinicians display an evolving tendency to exceed greatly the standard Parkland formula guidelines [48–51].

Treatment of IAH/ACS The WSACS recently published best practice guidelines for the diagnosis, management, and prevention of IAH and

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ACS, noting that for many of these recommendations good quality evidence to justify firm decisions were lacking [52]. Nonetheless, these guidelines are applicable to the management of thermal injury and are described herein. Once IAH is identified, the IAP should be frequently measured, and the patient’s organ function must be frequently assessed in anticipation of a high risk of both subtle and overt dysfunction. Medical management of IAH should initially be pursued, although if the ACS is formally diagnosed (new organ failure is detected in conjunction with severe IAH [20 mmHg) more emergent measures are required. Medical management of IAH consists of endoscopic or rectal tube decompression of a distended colon and both decompressing and preventing further gastric distension with nasogastric drainage [17, 52]. The use of analgesia, sedation, and even neuromuscular paralysis have been reported to reduce the measured IAP, although the durability of such interventions is unknown [53]. It is unclear if these methods are as effective in burn patients with greatly reduced abdominal wall compliance as they are in other patient groups. Also, pharmacologic measures are typically considered temporary maneuvers to allow other interventions to be conducted [54]. Drainage of ascites through percutaneously placed drains may be highly effective if the patient is on a steep portion of the abdominal wall compliance curve [55–57]. Latenser et al. reported that percutaneous decompression was a safe, effective method of decreasing IAH and preventing ACS in patients with \80% TBSA thermal injury, although those with greater degrees of burn injury required formal laparotomy with associated dismal outcomes [56]. Although burns to the abdominal wall are not a prerequisite for the development of IAH/ACS in burn patients, restrictive eschar, if present, offers a therapeutic opportunity for release and potentially decompressing the abdomen [20, 21, 58]. If all of the preceding treatment options fail, formal surgical decompression of the peritoneal cavity is required [4, 54]. Unlike primary ACS, wherein serious pathology necessitating complex intraperitoneal surgery may be expected, IAH/ACS related to burn resuscitation can often be safely decompressed at the bedside in the critical care unit. This simplifies the logistics of caring for these patients and often saves time [59]. Formally opening the peritoneal contents introduces numerous new potential complications to the severely burned patient, such as increased insensible fluid losses, environmental contamination, heat loss, bacterial colonization, and the real possibility that formal fascial closure will never been attained on a short-term basis [4, 60]. Preliminary reports describing decompression of fascia only with a subcutaneous approach (i.e., preserving intact skin coverage) [61], as well as minimally invasive techniques demonstrated in animal models, remain novel but may have applicability in the future [62].

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Postoperative management If escharotomies have been performed, it is essential to ensure that they remain adequate for sufficient release of the constricting eschar. It must be noted, however, that constriction from an injured abdominal wall may be dynamic over time [17]. Once the abdomen has been formally opened, an initial improvement in cardiorespiratory parameters is typically expected if decompression has not been unduly delayed [63]. Unfortunately, severe IAH and ACS seem to initiate the multiple organ dysfunction syndrome by their very presence. If not promptly reversed, progressive organ failure after seemingly successful decompression may be observed in addition to higher cytokine levels in both laboratory and clinical settings [18, 64, 65]. Secondary ACS can be considered a ‘‘secondary hit’’ to the severely burned patient, although it is presently unclear whether this process results from IAH/ACSinduced ischemia or as a reperfusion injury after decompression, or both [18]. The decompressed severe burn patient with an open abdomen remains susceptible to numerous ongoing complications. Many of these unfortunately require fluid resuscitation and therefore induce tertiary or recurrent IAH/ACS despite previous decompression of the peritoneal cavity [59]. Thus, continued vigilance and frequent, if not routine, monitoring of the IAP is recommended [4]. The technique of temporary abdominal closure is a combination of science and art and is beyond the scope of this review (Fig. 1). Although we personally prefer vacuum-assisted

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methods, both home-made and commercial [66, 67], there is great controversy in this area regarding technique, timing, and outcomes [60]. Critical principles are (1) utilize a method that does not compromise the fascia for future potential definitive closure; (2) drain biologic fluids in a sterile fashion; and (3) reapproximate the parietal musculature without inducing recurrent IAH/ACS.

Conclusions IAH/ACS is currently expected as a life-threatening complication in severely burned patients, particularly if they have sustained an inhalation injury, undergone a delayed or poorly supervised fluid resuscitation strategy, or sustained full-thickness abdominal burns. These conditions may subtly affect every aspect of the burned patient’s physiology, culminating in overt multiorgan failure when fullblown ACS occurs. Further methodologically correct studies into the basic questions of prevention and management are crucial. Future advances may potentially arise from modulation of the inflammatory response through improved therapies and fluids or from new insights into the basic mechanisms of cellular injury and its treatment. Until further evidence-based results are available, careful attention to adequate but judicious fluid resuscitation remains a basic but potentially life-saving duty of all involved in the care of the severely burned patient.

References

Fig. 1 Severely burned patient who has been massively fluidresuscitated and subsequently developed abdominal compartment syndrome. This required multiple escharotomies and ultimately a bedside decompressive laparotomy in the burn intensive care unit as a life-saving measure. She has been left with an ‘‘open abdomen’’ that remains imperfectly closed and at risk of subsequent complications

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