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164
Abdominal Compartment Syndrome
Figure 4. Effect of ACS following HS/R on neutrophil priming and lung injury. A) Flow cytometry was used
to examine the time course of neutrophil CD11b expression in rats following hemorrhagic shock and
resuscitation (HS/R). Neutrophils were primed (increased CD11b expression) at 8 hours following HS/R
(* P <0.05 vs. baseline). B) Rats were then subjected to the abdominal compartment syndrome (ACS) at
various times following HS/R and lung injury was assayed by measuring Evans blue dye concentration in
brochoalveolar fluid. HS/R alone or followed by ACS at 2 hours or 18 hours did not result in lung injury;
however, ACS induced lung injury when it occurred at 8 hours following HS/R (+ P <0.05 vs. sham).
These investigators went on to demonstrate that the administration of either melatonin52 (a
free-radical scavenger and anti-oxidant) or octreotide
50,51
(a mesenteric vasoconstrictor) im-
mediately prior to decompression of ACS abrogated the increase in MDA and MPO, preserved
165Abdominal Compartment Syndrome Provokes Multiple Organ Failure
Figure 5. Enzyme-linked immunosorbent assay was used to measure serum tumor necrosis factor (TNF)-α
levels in rats (black bars) during (60 min at 20 mm Hg) and after decompression of the abdominal
compartment syndrome (ACS). The serum TNF level did not increase until after ACS was decompressed
(* P <0.05 vs. sham and ACS). Myeloperoxidase (MPO) activity was examined to determine the effect of
ACS and decompression on lung neutrophil accumulation (grey bars). Accumulation of neutrophils in the
lung paralleled TNF levels; no increase in lung neutrophils occurred until ACS was decompressed (* P <0.05
vs. sham and ACS).
tissue GSH levels and prevented the rise in serum AST, BUN and creatinine. These data suggest that the mechanism of remote organ injury following ACS and decompression is due to
ischemia and reperfusion and that interventions aimed at limiting the oxidative injury inherent
to reperfusion can limit organ injury. We have previously reported that blocking xanthine
oxidase prior to splanchnic ischemia/reperfusion (temporary occlusion of superior mesenteric
artery) attenuates oxidative injury in the liver and lung;
53
however, Sener and colleagues are the
first to report similar findings in ACS and decompression. The exact mechanism of octreotide
in protecting animals from the reperfusion injury is unclear; however, the authors speculate
that the one-time dose of octreotide may result in a more gradual return of mesenteric perfusion that is better tolerated.
Summary
It has been argued that MOF associated with ACS is a reflection of the global hemodynamic compromise precipitated by the initial insult and that ACS is merely the terminal manifestation of MOF. Indeed, it is difficult to discern a direct adverse effect of ACS on remote
organ function as ACS rarely occurs in the absence of hemodynamic instability. However, in
our in vivo work of HS/R followed by ACS, crystalloid infusion was used to maintain a MAP
of 75 mm Hg during ACS. Despite this intervention, ACS lead to both lung and liver injury as
well as increased 24 hour mortality when instituted at 8 hours following HS/R. Furthermore,
Diebel et al have demonstrated that increased IAP results in decreased mesenteric, hepatic, and
portal venous blood flow even when MAP
mal values with fluid resuscitation. Ivatury and colleagues
that increased IAP results in mesenteric ischemia (gastric mucosal acidosis) in the absence of
the classic signs of ACS (cardiac, pulmonary and renal dysfunction). These findings further
support the hypothesis that ACS is not merely a late manifestation but rather a cause of MOF.
8,36,54
and cardiac output
8,54
9
have also shown in a clinical study
are maintained at nor-
166
Figure 6. Mesenteric lymph is the conduit for gut-derived mediators of systemic hyperinflammation.
Hemorrhagic shock provokes mesenteric ischemia/reperfusion which results in failure of the gut barrier and
damage to the interstitial matrix of the bowel. Whether gut barrier failure results in bacterial translocation
in humans is controversial. Comparison of portal vein and systemic cytokine levels have failed to show a
consistent increase in portal vein levels following hemorrhagic shock. Toxic lipid moieties present in mesenteric lymph obtained from animals following hemorrhagic shock induce a systemic inflammatory response (SIRS). We hypothesize that the abdominal compartment syndrome, by causing further mesenteric
ischemia/reperfusion, serves as a second-event to exacerbate the systemic inflammatory response ultimately
leading to multiple organ failure.
Abdominal Compartment Syndrome
The advent of damage control surgery has undoubtedly increased the survival of severely
injured patients; however, in doing so it has also transformed the abdominal compartment
syndrome from an interesting laboratory phenomenon to a common, devastating clinical entity. Clinical studies have demonstrated a strong association between ACS and MOF, and clinically relevant animal models have provided convincing evidence that ACS plays a causal role.
Current investigation has identified several early independent variables that predict which patients develop ACS. The University of Texas-Houston group has demonstrated that the volume
of crystalloid used during the initial 24 hours of trauma resuscitation is an independent predictor for the development of ACS.
19,26
Therefore, further investigation of alternative strategies in
trauma resuscitation such as the use of colloids, blood substitutes and hypertonic saline may
prove to decrease the incidence of ACS by reducing the crystalloid volume requirement. Moreover, the potential benefits of blood substitutes such as polymerized hemoglobin
tonic saline
56
for the resuscitation of patients at high risk for the development of ACS may
55
and hyper-
extend beyond a simple reduction in the volume of crystalloid infusion.
We have reported that severely injured patients resuscitated with polymerized hemoglobin
have lower systemic cytokine levels
57
and do not undergo neutrophil priming58 compared to
similar patients resuscitated with red blood cell transfusions. Thus, polymerized hemoglobin as
a resuscitation fluid may decrease the inflammatory response and resultant MOF associated
with early transfusion of red blood cells. Similarly, we
59,60
and others
61,62
have demonstrated
that hypertonic saline inhibits neutrophil priming both in vitro and in vivo.
167Abdominal Compartment Syndrome Provokes Multiple Organ Failure
While decreasing crystalloid administration during resuscitation may reduce the incidence
of ACS, it will not entirely prevent it. Early recognition and prompt abdominal decompression
remain the mainstay of treatment for ACS. Monitoring of gastric mucosal pH may identify a
subset of patients with increased IAP and mesenteric ischemia without the classic signs of
9
ACS.
These patients might benefit from earlier abdominal decompression. Animal work has
suggested that anti-oxidant therapies initiated prior to decompression of ACS may also limit
remote organ injury. Specific identity of proinflammatory agents in mesenteric lymph may
provide additional therapeutic strategies. While we now recognize the adverse physiologic effects of intra-abdominal hypertension in the injured patient, we have only begun to elucidate
the fundamental mechanisms that will be key to ultimately reduce the life-threatening consequences of the abdominal compartment syndrome.
Commentary
Manu L. N. G. Malbrain
With the advent of new studies, the correlation between intra-abdominal pressure (IAP),
intramucosal pH (pHi) and increased gut permeability (as demonstrated by bacterial translocation) seems to become stronger and stronger every day. The association between increased gut
permeability and the subsequent development of multiple organ failure (MOF) and death has
also been recently demonstrated. With regard to the abdominal compartment syndrome (ACS)
the question still remains whether the intra-abdominal hypertension (IAH) is the cause of or
an epi-phenomenon in the emergence of MOF. What is the chicken and what is the egg?
Nonbelievers will indeed point towards increased IAP as a mere side effect of the resuscitative
strategies in trauma, septic or burn patients, whereas believers will point towards the direct
negative effects of IAH on organ perfusion increasing intestinal and capillary permeability, and
requiring further and ongoing resuscitation that will eventually lead to a vicious cycle with
ongoing IAH and ACS. This chapter will take the reader through some historical perspectives,
followed by the association between and the cause and effect of ACS and MOF.
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to abdominal compartment syndrome: Stage for multiple organ failure. J Trauma 2002; 53:1121-8.
33. Bongard F, Pianim N, Dubecz S et al. Adverse consequences of increased intra-abdominal pressure
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abdominal compartment syndrome. J Trauma 1997; 43:852-5.
37. Eleftheriadis E, Kotzampassi K, Papanotas K et al. Gut ischemia, oxidative stress, and bacterial
translocation in elevated abdominal pressure in rats. World J Surg 1996; 20:11-6.
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levels of intra-abdominal pressure. Arch Surg 1998; 133:1351-5.
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pressure on bacterial translocation. J Trauma 2002; 52:13-7.
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perspective with major torso trauma. J Trauma 1991; 31:629-36, discussion 636-8.
41. Hassoun HT, Kone BC, Mercer DW et al. Post-injury multiple organ failure: The role of the gut.
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169Abdominal Compartment Syndrome Provokes Multiple Organ Failure
42. Moore EE. Mesenteric lymph: The critical bridge between dysfunctional gut and multiple organ
failure. Shock 1998; 10:415-6.
43. Gonzalez RJ, Moore EE, Ciesla DJ et al. Mesenteric lymph is responsible for post-hemorrhagic
shock systemic neutrophil priming. J Trauma 2001; 51:1069-72.
44. Zallen G, Moore EE, Johnson JL et al. Posthemorrhagic shock mesenteric lymph primes circulating neutrophils and provokes lung injury. J Surg Res 1999; 83:83-8.
45. Gonzalez RJ, Moore EE, Ciesla DJ et al. Post-hemorrhagic shock mesenteric lymph activates human pulmonary microvascular endothelium for in vitro neutrophil-mediated injury: The role of
intercellular adhesion molecule-1. J Trauma 2003; 54:219-23.
46. Deitch EA, Adams C, Lu Q et al. A time course study of the protective effect of mesenteric lymph
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47. Sarin E, Moore EE, Ciesla DJ et al. Mesenteric lymph duct ligation protects against hemmorhagic
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51. Kacmaz A, Polat A, User Y et al. Octreotide improves reperfusion-induced oxidative injury in
acute abdominal hypertension in rats. J Gastrointest Surg 2004; 8:113-9.
52. Sener G, Kacmaz A, User Y et al. Melatonin ameliorates oxidative organ damage induced by acute
intra-abdominal compartment syndrome in rats. J Pineal Res 2003; 35:163-8.
53. Poggetti RS, Moore FA, Moore EE et al. Simultaneous liver and lung injury following gut ischemia is mediated by xanthine oxidase. J Trauma 1992; 32:723-7, discussion 727-8.
54. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intra-abdominal pressure on mesenteric
arterial and intestinal mucosal blood flow. J Trauma 1992; 33:45-8, discussion 48-9.
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by means of resuscitation with a red cell substitute. J Trauma 2003; 54:133-9, discussion 139-40.
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61. Angle N, Hoyt DB, Coimbra R et al. Hypertonic saline resuscitation diminishes lung injury by
suppressing neutrophil activation after hemorrhagic shock. Shock 1998; 9:164-70.
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development of lung inflammation following hemorrhagic shock. J Immunol 1998; 161:6288-96.
170
Abdominal Compartment Syndrome
CHAPTER 13
Postinjury Secondary Abdominal
Compartment Syndrome
Zsolt Balogh* and Frederick A. Moore
Definition and Historical Perspectives
ostinjury ACS is defined by the presence of intra-abdominal hypertension (IAH) with
intra-abdominal pressure (IAP) greater than 25 mm Hg accompanied by organ
dysfunction(s) such as cardiac, respiratory and renal.
P
when there are no intraperitoneal injuries. To avoid misclassification, several issues need to be
clarified. Patients whose abdominal parenchymal organ injuries are managed nonoperatively
should not be categorized as secondary ACS since they have intraperitoneal injuries. Pelvic
fracture related retroperitoneal hematomas without intraperitoneal injury are classified as secondary ACS. However, retroperitoneal vascular, renal, duodenal, pancreatic etc injuries requiring laparotomy with and without packing should not be classified secondary ACS group. Burrows et al reported the first trauma related secondary ACS case in his series of primary ACS
cases in 1998.
scribed 6 cases and mentioned the potential connection with massive resuscitation.
2
The terminology (“secondary ACS”) was attributed to Maxwell et al who de-
1
ACS is referred to as “secondary”
3
Epidemiology
Incidence
It is difficult to determine the true incidence of postinjury secondary ACS due to its elusive
nature. Maxwell et al reported 13% incidence among trauma patients who required abdominal
mesh closure.
dence of postinjury secondary ACS to be 0.09% of all trauma admissions, 0.7% of all trauma
ICU admissions, 8% of shock trauma patients requiring aggressive resuscitation [with ISS>15,
requiring more than 6 units of packed red blood cell (PRBC) transfusions during the first 12
hours and having initial base deficit (BD) greater than 6 mEq/L] and it represented 58% of all
cases of postinjury ACS.
Time to Develop Secondary ACS from Hospital Admission
The initial studies
sion (up to 108 hours from hospital admission). This may be related to the late recognition of
the syndrome and/or to futile attempts to overcome IAH related cardiac dysfunction with fluid
challenges, which was the recommended treatment at that time.
postinjury secondary ACS is a much earlier phenomenon. Among trauma patients requiring
massive resuscitation ACS typically manifest itself within 12 to 14 hours after hospital admis-
1,6
sion.
*Corresponding Author: Zsolt Balogh—Department of Traumatology, University of Szeged,
Szeged, Hungary. Email: zsoltbalogh@yahoo.com
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham,
Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
3
Based on a prospective shock trauma database, Balogh et al reported the inci-
1
3,4
describing secondary ACS reported long delays in surgical decompres-
5
More recent data suggest that
It is important to concentrate diagnostic, preventive and predictive efforts during this
171Postinjury Secondary Abdominal Compartment Syndrome
Table 1. Demographics, injury characteristics and outcome of patients with
and without ACS
Primary ACS Secondary ACS Non ACS
(n = 11) (n = 15) (n = 162)
Demographics:
Age (years) 36 ± 5 45 ±4 39 ±1
Gender (male %) 73 80 76
Injury mechanism (blunt %) 82 86 85
Severity of shock:
Initial ED BD (mEq/L) 11 ± 19 ± 29 ± 0.5
Lowest ED SBP (mm Hg) 79 ± 3
12 hrs PRBCs (Units) 14 ± 4
% of urgent interventions (IR/OR) 82 87 85
Injury severity and pattern:
ISS 29 ± 3 28 ± 2 27 ± 1
ATI 18 ± 1
GCS 13 ± 1 13 ±1 13 ± 0.2
AIS head 1.3 ± 0.4 1.2 ± 0.2 1.6 ± 0.05
AIS face 0.8 ± 0.1 0.7 ± 0.1 1 ± 0.01
AIS chest 2.7 ± 0.3 2.4 ± 0.2 2.8 ± 0.05
AIS abdomen 3.9 ± 0.2
AIS extremity 2.7 ± 0.1 4.1 ± 0.2
AIS external 1.1 ± 0.2 1.3 ± 0.3 1.3 ± 0.01
Times from ED admission:
ED discharge (hours) 0.9 ± 0.1
ICU admission (hours) 3.7 ± 0.5
Outcome:
Mechanical ventilation (days) 13 ± 3
ICU LOS (days) 14 ± 5 16 ± 3 12 ± 2
MOF (%) 55
Mortality (%) 64
ACS: abdominal compartment syndrome; ED BD: emergency department base deficit; ED SBP:
emergency department systolic blood pressure; PRBCs: packed red blood cells; IR/OR: interventional
radiology/operating room; ISS: injury severity score; ATI: abdominal trauma index; GCS: Glasgow
coma scale; AIS: abbreviated injury scale; ICU: intensive care unit; MOF: multiple organ failure; ICU
LOS: intensive care unit length of stay. Univariate comparisons: a p<0.05 ACS vs nonACS, b p<0.05
primary vs. secondary ACS
a
a
a,b
a
a,b
a,b
a
a
a
a
82 ± 4
11 ± 2
4 ± 2
a,b
0
a
a,b
a,b
93 ± 2
8 ± 1
10 ± 2
2.6 ± 0.05
2.8 ± 0.05
3 ± 0.3 2 ± 0.1
6.2 ± 0.6 7 ± 0.25
a
14 ± 3
53
53
a
a
8 ± 2
12
17
early timeframe parallel with resuscitation, hemorrhage control and completion of diagnostic
studies.
Distinct Characteristics Compared to Primary ACS
All case reports describing postinjury secondary ACS mention massive resuscitation. A prospective evaluation of primary and secondary ACS patients compared to non ACS patients is
depicted in Table 1. Patients who develop these syndromes have similar demographics, injury
severity, injury mechanism and initial base deficit.
initial systolic blood pressure (SBP). The lower SBP reflected in more aggressive resuscitation
in the ACS patients’ preICU course. By definition secondary ACS patients have no intraperitoneal injury thus abdominal abbreviated injury scale (AIS) is zero compared to 3.9 ± 0.2 in
primary ACS patients. Secondary ACS patients typically have multiple extremity injuries and
8
ACS patients differ from nonACS in their
172
Abdominal Compartment Syndrome
severe pelvic fractures or penetrating chest injuries or extremity vascular injuries. Patients with
major vascular injuries presenting in shock undergo massive resuscitation which is known to be
related to secondary ACS. Trauma patients with multiple pelvic and long bone fractures without obvious abdominal or chest injuries undergo extended diagnostic evaluations which may
include pelvic angiography which is reflected in their significantly longer preICU course.
82% of primary ACS patients had hemorrhage control in the OR and only 9% of them was
taken to interventional radiology (IR) while in secondary ACS patients hemorrhage control
was attempted in the IR in 47% and in the OR in 40% of the cases. The longer preICU course
(6.2 vs 3.7 hours) results in longer periods of less controlled resuscitation. Compared to primary ACS patients, secondary ACS patients received significantly more crystalloid infusion
(32 vs. 20 Liters in first 24 hours) and had a much higher ratio of liters of crystalloid/unit of
PRBCs (1.92 vs 0.55). Primary and secondary ACS patients are both decompressed within 14
hours of hospital admission, but because of longer pre ICU times secondary ACS is an earlier
ICU phenomenon (~6 hours) than primary (~10 hours). Another reason for the differences in
time is that primary ACS patients arrive from the OR after damage control and their temporary abdominal closure prevents the very early development of ACS. After decompression the
time to
definitive fascial closure is shorter in secondary ACS patients (3 ±0.8 vs. 9 ±2 days) and
they are less likely to develop abdominal abscesses. The outcome of both syndromes is poor.
Mechanism
The pathologic mechanisms of postinjury 2˚ ACS should be searched for in the early injury
response of patients arriving with exsanguinating hemorrhage (see Fig. 1). Traumatic shock
and subsequent standard of care resuscitation leads to whole body ischemia/reperfusion injury
due to effects of inflammatory cells and mediators. The hemodilution after massive crystalloid
resuscitation together with the increased permeability and hydrostatic pressure are the key early
driving forces for interstitial fluid accumulation. The edematous bowel (increasing peritoneal
content) and the retroperitoneal hematoma (decreasing peritoneal volume) are both important
elements of the intra-abdominal hypertension. The elevated intra-abdominal pressure impairs
venous and lymphatic outflow from the gut, and thus worsens gut edema by increasing capillary filtration pressure. Therapeutic interventions initiated to reverse organ dysfunction (further fluid resuscitation, increased positive pressure ventilation) can be added factors to the
already developed IAH. In secondary ACS patients pelvic fractures with significant blood loss
and retroperitoneal hematoma are common findings, these as major sources of hemorrhagic
shock and by decreasing peritoneal volume are contributors to IAH.
7
Outcome
The reported mortality of postinjury secondary ACS ranges between 38-67% (Table 2).
Early studies reporting later recognition and decompression had higher mortality.
studies concluded that earlier decompression improves outcome. More recent studies in which
all patients were decompressed within 16 hours of hospital admission found no significant
difference between survivors and nonsurvivors related to the time elapsed until decompres-
1,6
sion.
55% of secondary ACS patients develop multiple organ failure (MOF) which is defined after the first 48 hours so as to not confuse early organ dysfunctions related to inadequate
resuscitation and to the effects of IAH. Based on our studies postinjury ACS is a strong independent predictor of postinjury death and MOF.
research postinjury ACS appears to be a modifiable link between hemorrhagic shock and
8-12
MOF.
8
With the available basic science and clinical
3,4
These
Prediction
Risk Factors
Seminal case series during the late 1990s published risk factors based on expert opinion
without strong statistical background.
2-4
These included severe trauma, massive resuscitation,
173Postinjury Secondary Abdominal Compartment Syndrome
Figure 1. The proposed mechanism of postinjury secondary abdominal compartment syndrome. I/R=
ischemia/reperfusion; PMN= neutrophil leukocytes; PEEP= positive end-expiratory pressure; IAH=
inta-abdominal hypertension.
hemorrhagic shock and coexisting cirrhosis. These reports also empirically set up crystalloid
cut-points above which IAP monitoring is recommended.
Maxwell recommended 10 liters of crystalloid or 10 units of PRBCs. Ivy et al (10 postburn
secondary ACS patients) suggested >0.25 L/kg crystalloid resuscitation as the trigger.
3
Based on 6 secondary ACS cases
13
Biffl et
al (8 trauma, 6 general surgical secondary ACS patients) have found both cut-offs ineffective
and recommended 6 liters or more crystalloid or 6 units of PRBCs in a 6 hours period among
patients with base deficit >10 mEq/L especially if they are on vasopressors.
6
Independent Predictors
Given the early occurrence of postinjury secondary ACS we focused our prediction models
on the first 6 hours from hospital admission.
gency Department model (0-3 hours, all patients are over their initial diagnostic work-up,
completed their initial laboratory results and discharged from the emergency department) and
Intensive Care Unit model (0-6 hours, all patients admitted to ICU and their first physiologic
measurements and laboratory parameters on the resuscitation protocol are available). Although
primary and secondary ACS patients develop the same symptoms and predecompression physiology, their injury pattern, resuscitation and hospital times are different. We thus hypothesized
that their predictors would be different. The variables, which were entered into the multivariate prediction models included demographics, shock severity, injury severity, interventions,
hospital times, crystalloid and blood volumes, vital signs, initial pulmonary artery catheter
readings on the ICU, respiratory parameters, gastric tonometry data, blood gas results, laboratory and coagulation results. From these variables, the ones listed in Table 3 turned out to be
8
We developed two prediction models: Emer-
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