WTA 2014 PLENARY PAPER

Adult respiratory distress syndrome risk factors for injured patients

undergoing damage-control laparotomy:
AAST multicenter post hoc analysis
Martin D. Zielinski, MD, Donald Jenkins, MD, Bryan A. Cotton, MD, Kenji Inaba, MD,
Gary Vercruysse, MD, Raul Coimbra, MD, Carlos V.R. Brown, MD, Darrell E.R. Alley, MD,
Joseph DuBose, MD, Thomas M. Scalea, MD,
and the AAST Open Abdomen Study Group, Rochester, Minnesota

Severely injured patients undergoing damage-control laparotomy (DCL) have multiple risk factors for adult respiratory distress
syndrome (ARDS), making it challenging to differentiate the contributions of individual causative factors. We aimed to
determine the relative contributions of ARDS risk factors.
METHODS:
Analysis of the prospectively collected American Association for the Surgery of Trauma Multi-institutional Open Abdomen
Database was performed. Inclusion criteria were any patient, 18 years or older, undergoing DCL at 1 of 14 participating Level I
trauma centers. Univariable and multivariable Cox regression analyses were performed to determine the association of variables with the development of ARDS during hospitalization.
RESULTS:
A total of 563 patients (78% men; mean [SD] age, 40 [18] years) were identied, of whom 77 developed ARDS (14%). Overall
mortality was 23%, with a 39% mortality rate for ARDS patients. Univariable analysis demonstrated that Injury Severity Score
(ISS, 1.03; 95% condence interval [CI], 1.02Y1.05), intraoperative (IO) estimated blood loss (hazard ratio [HR], 1.09; 95%
CI, 1.04Y1.13), IO plasma transfusion (HR, 1.17; 95% CI, 1.10Y1.25), 24-hour colloid volume (HR, 1.07; 95% CI, 1.04Y1.10),
and 24-hour crystalloid volume (HR, 1.01; 95% CI, 1.00Y1.01) were associated with the development of ARDS. Cox
multivariable analysis demonstrated that ISS, IO plasma transfusions, and total uid balance through 23 hours all increased the
risk of ARDS development.
CONCLUSION:
Severity of injury, plasma transfusions, and greater uid administration by 24 hours were independently associated with ARDS
development. Judicious use of plasma and other uids may reduce rates of ARDS in this critically injured population. (J Trauma
Acute Care Surg. 2014;77: 886Y891. Copyright * 2014 by Lippincott Williams & Wilkins)
LEVEL OF EVIDENCE: Prognostic study, level III; therapeutic study, level IV.
KEY WORDS:
Damage control; open abdomen; adult respiratory distress syndrome; trauma; laparotomy.
BACKGROUND:

amage-control resuscitation (DCR) has been promoted as

the standard of care to reduce mortality in the most severely injured, hemorrhaging patients. Several points are critical to DCR: (1) high ratio transfusions of plasma and platelets
to packed red blood cell (PRBC) units via massive transfusion
(MT) protocols, (2) limited crystalloid administration, (3) abbreviated procedures, and (4) permissive hypotension.1 Incorporation of these practices has been associated with a 62%
mortality benet for patients requiring MT (Q10 PRBC units in
24 hours).2 Damage-control laparotomy (DCL) was the initial
procedure introducing the concept of DCR and remains the
Submitted: January 7, 2014, Revised: May 20, 2014, Accepted: May 21, 2014,
Published online: September 22, 2014.
From the Mayo Clinic (M.D.Z., D.J.), Rochester, Minnesota; University of Texas at
Houston (B.A.C.), Houston; University of Texas, Austin (C.V.R.B.), Austin; and
East Texas Medical Center (D.E.R.A.), Tyler, Texas; University of Southern
California (K.I.), Los Angeles; University of California, San Diego (R.C.), La
Jolla, California; University of Arizona (G.V.), Tucson, Arizona; University of
Maryland (J.D., T.M.S.), College Park, Maryland.
This study was presented in part at the 44th Annual Meeting of the Western Trauma
Association, March 2Y7, 2014, in Steamboat Springs, Colorado.
Address for reprints: Martin D. Zielinski, MD, Division of Trauma, Critical Care and
General Surgery, Mary Brigh 2Y810, St. Marys Hospital, Mayo Clinic, 1216
Second St. SW, Rochester, MN 55902; email: zielinski.martin@mayo.edu.
DOI: 10.1097/TA.0000000000000421

886

most commonly applied procedure within the DCR management scheme.3Y6 These abbreviated laparotomies allow trauma
surgeons to gain source control of life-threatening injuries
while allowing for the delay in denitive treatment until
physiologic stabilization and subsequent reexploration. This
approach, hand in hand with the other DCR elements, remains
the standard of care for critically ill, unstable patients with
abdominal injuries.7
Despite demonstrated mortality benets with DCR
techniques, controversy remains. Integral in the counter argument to DCR is the potential three times greater risk of adult
respiratory distress syndrome (ARDS).8,9 This syndrome,
characterized by a profound dysfunction of gas exchange at the
alveoli secondary to inammation, can occur in up to 8.4% of
patients undergoing MT, with an associated 17% mortality in
severely injured patients.2,9 The etiology of ARDS in this
critically ill patient population remains elusive and is likely
multifactorial.10 The combination of phenotypic, environmental, and clinical hits have been implicated in ARDS
development. These hits are both inherent to the patient (genetic predisposition, injury severity, preexisting lung disease,
advanced age, ischemia/reperfusion) and potentially modiable by the clinician (i.e., fraction of inhaled oxygen [FIO2],
J Trauma Acute Care Surg
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positive end-expiratory pressure, blood product age/volume,

limited crystalloid administration).9Y13 Severely injured trauma
patients universally have some, and potentially all, of these risk
factors. For this reason, it can be challenging to differentiate the
contributions each of these individual causal factors provides to
the development of ARDS. Depending on the factors identied,
alterations in the treatment of severe hemorrhage such as
whole-blood transfusion or elimination of crystalloid may be
entertained.14 In this study, we aimed to determine the risk
factors for the development of ARDS in severely injured
trauma patients undergoing DCL and to elucidate the specic
contributions of blood product and crystalloid volumes to the
overall risk of ARDS. Specically, we hypothesized that (1)
increasing crystalloid resuscitation volumes will increase the
risk of ARDS and (2) plasma will provide a benecial effect in
helping to prevent the development of ARDS.

PATIENTS AND METHODS

This was a post hoc analysis of the prospective observational multi-institutional study sponsored by the American
Association for the Surgery of Trauma (AAST). The AAST
Multi-Institutional Trials Committee approved the study protocol, and each participating center had previously obtained
institutional review board approval for the use of the
deidentied data. This database, previously described, included
a total of 563 patients represented by the combined efforts of 14
trauma centers throughout the country between 2010 and
2011.7 Inclusion criteria were any patient, 18 years or older,
undergoing DCL as a result of injury. During the data collection, acute lung injury (ALI) and ARDS were dened as the
ratio of the partial pressure of arterial oxygen (PaO2) divided by
the fraction of inhaled oxygen (FIO2; i.e., the P/F ratio) of less
than 300 mm Hg and 200 mm Hg, respectively, in the absence
of signs of heart failure. New expert opinion has broadened the
denition into mild, moderate, and severe ARDS (based on the
P/F ratio) and eliminated the term ALI.15,16 PaO2 and FIO2
variables, however, were not collected during the prospective
data collection. As a result, both ALI and ARDS terms were
considered equivalent without differentiation into mild, moderate, and severe categories. Nonblood colloid included any
colloid resuscitation (i.e., albumin, hydroxyethyl starch) uid

except plasma, PRBC, platelets, or cryoprecipitate. Total colloid uid refers to the combination of nonblood colloids plus
blood product.17Y19
Descriptive statistics are reported as n (%) or as mean (SD)
as appropriate. Patients were assessed for the development of
ARDS following up a patient to either the postoperative day
(POD) of ARDS diagnosis (event) or the POD of hospital discharge (censor). The Cox proportional hazards model was used to
assess risk factors for association with ARDS. Variables known at
baseline, patient characteristics, organ injury and operative
intervention pattern, and intraoperative (IO) resuscitation characteristics were examined in all 563 patients. Resuscitation
characteristics through 24 hours were examined in the 510 patients still followed up at the end of POD 1, excluding patients
who died through POD 1 or those who had ARDS diagnosed by
POD 1. Similarly, resuscitation characteristics through 48 hours
were examined in the 480 patients still followed up at the end of
POD 2. All models included a variable for the medical center in
the study; therefore, a univariate model is a model containing a
class variable for medical centers and one additional variable of
interest. The medical center was included to account for possible
differences in practice between medical centers. A multivariable
model was examined for the 510 patients still followed up at the
end of POD 1. Patient characteristics and resuscitation characteristics known through POD 1 with a univariate signicance of
0.2 or less were examined. A backward selection method was
used retaining variables with signicance less than 0.05. The
> level was set at 0.05 for statistical signicance.

RESULTS
In total, 563 patients were in the AAST Open Abdomen
Database, of whom 77 (14%) developed ARDS. There was no
signicant association of either age or sex with the risk of
developing ARDS (Table 1). Univariable analysis demonstrated that a greater Injury Severity Score (ISS), Abbreviated
Injury Scale (AIS) score, and lower pH value were associated
with an increased risk of ARDS development. In addition,
ARDS was associated with a prolonged intensive care unit stay
when all deaths were excluded (28.5 [17.7] days vs. 16.0 [14.0]
days, p G 0.001). The same held true for hospital length of stay
when excluding all deaths (41.5 [23.8] vs. 24 [24.8], p G 0.001).

TABLE 1. Patient Characteristics

Cox Model Including
Medical Center

Univariate Cox Model

Age, y
Male sex
ISS
Head AIS score
Abdomen AIS score
Chest AIS score
Hemoglobin, g/dL
Lowest pH
Hypothermia (G35-C)

No ARDS (n = 486)

ARDS (n = 77)

HR (95% CI)

HR (95% CI)

39.7 (17.4)
375 (77.2%)
27.9 (13.2)
1.1 (1.7)
3.5 (1.1)
2.2 (1.6)
11.5 (3.1)
7.1 (0.8)
161 (33.1%)

43.0 (18.9)
62 (80.5%)
35.1 (14.5)
1.8 (1.8)
3.8 (0.9)
2.8 (1.4)
11.6 (3.2)
7.1 (0.1)
28 (36.4%)

1.12A (0.99Y1.27)
1.09 (0.62Y1.92)
1.03B (1.02Y1.05)
1.26B (1.11Y1.43)
1.42B (1.12Y1.80)
1.26B (1.08Y1.47)
1.00B (0.92Y1.08)
1.00B (0.74Y1.35)
1.33 (0.84Y2.12)

0.062
0.765
G0.001
G0.001
0.004
0.004
0.942
0.988
0.225

1.09 (0.95Y1.24)
1.07 (0.60Y1.90)
1.03 (1.01Y1.05)
1.16 (0.996Y1.34)
1.28 (0.995Y1.65)
1.19 (1.01Y1.40)
0.98 (0.90Y1.06)
0.97 (0.65Y1.45)
1.34 (0.83Y2.18)

0.221
0.812
G0.001
0.056
0.055
0.041
0.629
0.885
0.230

Continuous variables are provided as HR with 95% CI for Cox regression and as means (SD) for the descriptive statistics.

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The rate of death was nearly double if a patient developed

ARDS (20.6% vs. 39.0%, p = 0.001).
Resuscitation volumes of crystalloid, colloid, and blood
products were substantially different between the patients who
developed ARDS from presentation throughout the rst
48 hours on univariable analysis (Table 2). Specically, crystalloid was associated with a signicant risk for ARDS with
greater volumes infused at both 24 hours and 48 hours after
injury. IO estimated blood loss and plasma resuscitation volumes
were greater in patients who developed ARDS. In addition, the
colloid volume transfused throughout the rst 48 hours of resuscitation continued to be greater in the patients who developed
ARDS. As a result, the total volumes of uid infused were also
greater in the ARDS population.
There was a broad range of injury patterns and other
procedures performed for patients undergoing DCL (Table 3).
The most common abdominal organ requiring intervention was
the liver, followed by major vascular interventions and the
spleen. A minority of patients underwent thoracotomy concurrent with the DCL procedure (n = 62). There were no differences between organs injured and thoracotomy procedures
for patients who did and did not develop ARDS.
Cox multivariable regression analysis showed a signicant increased risk of ARDS with increased IO plasma use
(hazard ratio [HR], 1.16; 95% condence interval [CI],
1.07Y1.25). Each liter of IO plasma was associated with a 3%
increased risk of developing ARDS (Table 4). For an additional
10 L of total uids, there was a 10 % increase in the rate of
ARDS (HR, 1.10 per 10 L; 95% CI, 1.05Y1.15). In addition,
each ISS unit increase was associated with a 3% increased risk
of ARDS. Alternatively, a 25-point gain in ISS nearly doubled
the ARDS risk (HR, 1.95; 95% CI, 1.24Y3.07). There were no

variables under study which conferred a benet to prevent

ARDS development. The primary fascial closure rate was 66%.

DISCUSSION
DCR techniques, despite their benecial associations
with mortality, have signicant limitations. Similarly, DCL, as
an integral portion of DCR, has substantial drawbacks including
enterocutaneous stulae, sepsis, and ARDS.2,8,20 These complications, however, can only develop if the patient survives the
initial hemorrhagic event. Therefore, the real risk of death
outweighs the theoretical risk of complications from DCL and
should be performed if indicated. Naturally, the intensive care
unit portion of the patients course is fraught with further
complications, stemming not only from the initial physiologic
insult but also from subsequent second hits, which have their
own associated complications.10 It is the summation of these
primary and secondary hits that place critically ill trauma patients at risk for ARDS.21,22
ARDS has its own related mortality independent of the
traumatic insult. In the current study, ARDS was associated
with a doubling in the risk of death. As such, the development
of ARDS should not be viewed as an inevitable disease process
but as a preventable complication with the use of risk mitigation strategies throughout the resuscitation phase. As demonstrated, increasing reliance on plasma and uids for
resuscitation promoted an increased risk of ARDS. The infusion of 10 L of uid (both crystalloid and blood products)
during the rst 24 hours after injury increased the risk of ARDS
development by an additional 10%.
This study is not unique in nding that uid administration
is associated with poor outcomes in signicantly injured patients.

TABLE 2. Resuscitation Characteristics

Cox Model Including
Medical Center

Univariate Cox Model

IO
Estimated blood loss, L
Nonblood colloid, L
Total uid balance, L
PRBC volume, L
Plasma volume, L
Platelet volume, L
Plasma/PRBC, U
C/PRBC, U
24 h
Total colloid, L
Total crystalloid, L
Total uids, L
48 h
Total colloid, L
Total crystalloid, L
Total uids, L

No ARDS (n = 485)

ARDS (n = 77)

HR (95% CI)

HR (95% CI)

2.38 (3.22)
0.57 (1.26)
6.68 (13.75)
2.84 (7.27)
1.63 (2.06)
0.44 (0.98)
0.7 (0.5)
4.5 (6.5)

3.83 (5.39)
0.32 (0.55)
8.10 (7.96)
3.90 (3.86)
2.91 (3.39)
0.62 (1.00)
0.7 (0.5)
3.5 (5.9)

1.09 (1.04Y1.13)
0.70 (0.44Y1.11)
1.00 (0.99Y1.02)
1.01 (0.99Y1.03)
1.17 (1.10Y1.25)
1.14 (0.96Y1.35)
0.88A (0.54Y1.42)
1.40A (1.13Y1.72)

0.398
0.128
0.395
0.191
0.001
0.001
0.585
0.002

1.10 (1.05Y1.16)
0.77 (0.50Y1.20)
1.00 (0.99Y1.02)
1.01 (0.99Y1.03)
1.21 (1.12Y1.31)
1.13 (0.92Y1.38)
0.76 (0.43Y1.32)
0.96 (0.91Y1.00)

G0.001
0.250
0.524
0.245
G0.001
0.254
0.325
0.072

1.36 (3.02)
6.33 (8.70)
7.69 (9.51)

3.80 (7.33)
15.36 (54.59)
19.16 (57.65)

1.09 (1.05Y1.13)
1.01 (1.00Y1.01)
1.01 (1.00Y1.01)

G0.001
G0.001
G0.001

1.10 (1.05Y1.15)
1.005 (1.00Y1.01)
1.005 (1.001Y1.01)

G0.001
0.057
0.022

1.01 (2.91)
6.85 (7.94)
7.86 (9.04)

2.05 (5.42)
8.60 (6.94)
10.64 (10.59)

1.06 (1.00Y1.12)
1.03 (1.00Y1.05)
1.03 (1.01Y1.05)

0.034
0.058
0.016

1.10 (1.02Y1.19)
1.02 (0.99Y1.05)
1.03 (1.002Y1.05)

0.014
0.206
0.036

Continuous variables are provided as HR with 95% CI for Cox regression as well as means (SD) for descriptive statistics.
A
= Hazard Ratio based on smoothing spline result where values greater than 3 reset as equivalent to 3.

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TABLE 3. Organ Injury and Operative Intervention Patterns

Cox Model Including
Medical Center

Univariate Cox Model

No ARDS (n = 485)

ARDS (n = 77)

HR (95% CI)

HR (95% CI)

178 (36.0)
140 (28.3)
115 (23.7)
109 (22.0)
77 (15.8)
57 (11.5)
57 (11.5)
33 (6.7)

36 (46.8)
19 (24.7)
20 (26.0)
11 (14.3)
13 (16.9)
14 (18.2)
8 (10.4)
3 (3.9)

1.46 (0.93Y2.29)
0.88 (0.52Y1.48)
1.10 (0.66Y1.84)
0.62 (0.33Y1.17)
1.01 (0.55Y1.83)
1.46 (0.82Y2.61)
0.86 (0.41Y1.79)
0.56 (0.18Y1.79)

0.097
0.624
0.705
0.142
0.984
0.198
0.684
0.331

1.37 (0.75Y2.52)
0.72 (0.34Y1.52)
1.49 (0.79Y2.80)
0.74 (0.33Y1.70)
0.87 (0.38Y1.96)
1.41 (0.62Y3.20)
1.57 (0.65Y3.78)
0.67 (0.16Y2.80)

0.304
0.381
0.218
0.482
0.732
0.417
0.318
0.585

5 (1.0)
30 (6.2)
15 (3.0)

2 (2.6)
8 (10.4)
2 (2.6)

3.29 (0.81Y13.42)
2.07 (1.00Y4.31)
1.25 (0.31Y5.11)

0.097
0.051
0.753

4.78 (0.63Y36.34)
1.64 (0.49Y5.44)
1.92 (0.25Y14.55)

0.131
0.421
0.527

Abdominal organ injuries, n (%)

Liver
Major vascular
Spleen
Small bowel
Colon
Diaphragm
Stomach
Kidney
Thoracotomy incision, n (%)
Posterolateral
Anterolateral
Resuscitative

Continuous variables are provided as HR 95% CI for Cox regression as well as means (SD) for descriptive statistics.

A greater crystalloid-to-PRBC (C/PRBC) ratio has been associated with multisystem organ failure, ARDS, and abdominal
compartment syndrome, although, interestingly, not death.11
This effect was dose responsive as a C/PRBC greater than 1.5:1
conferred a two times higher likelihood of developing ARDS.
Correspondingly, the PRospective Observational Multicenter
Major Trauma Transfusion (PROMMTT) study conrms that
chest injury severity, advanced age, and greater use of crystalloid
were independent risk factors for ARDS development.16 Our
study, however, also demonstrated that blood product administration, specically plasma, was associated with the ARDS risk
on multivariable analysis.
While transfusion-related ALI may no longer be a recognized entity, the risk of transfusion-associated ARDS cannot be
eliminated because of nomenclature alone. Previous reports in
similar patient populations have demonstrated an increased risk
of ARDS with blood product transfusions.23,24 These studies,
however, considered ARDS as an single end point rather than one
that evolves throughout hospitalization as a time-dependent
complication. More precisely, the current study allows for the
true analysis of ARDS risk factors over time. In addition, the
multi-institutional, prospective nature of the current study should
confer a wider applicability of these results.
The next evolution in hemorrhage resuscitation, representing the ultimate culmination of DCR techniques, is the
transfusion of whole blood. That crystalloid, rather than blood
products, increases the risk of ARDS makes intuitive sense.

Hemorrhaging patients are losing volume, but this volume is not

crystalloid. Rather, the uid being lost is whole blood. Recent
data suggest that warm fresh whole blood (WFWB) and modied
whole blood have signicant improvement in mortality but the
risk of ARDS after whole-blood transfusion is less clear. In a
retrospective analysis of military data, survival at 24 hours was
improved in the WFWB cohort when compared with component
therapy (96% vs. 88%, p = 0.018).25 The rate of ARDS, however,
was nonsignicantly greater (7% vs. 3%, p = 0.08). It should be
noted that neither component nor WFWB products were
leukoreduced, which potentially increased the risk for ARDS. In
a randomized clinical trial, Cotton et al.14 demonstrated similar
rates of both 24-hour mortality (16% vs. 12%, p = 0.58) and
ARDS (0.0% vs. 1.9%. p = 0.32) with the use of leukoreduced,
modied whole blood. Whether whole blood products will have a
demonstrable improvement in the rates of ARDS remains to be
elucidated.
Despite our hypothesis, plasma was identied as an independent ARDS risk factor. This correlates with the acknowledgement that blood products can cause ARDS. In all
likelihood, there are multiple hits that are associated with
ARDS development, particularly in severely injured trauma
patients.10,12,26 The number of individual risk factors that have
been associated with ARDS is substantial. A single blood
product unit may only cause 1:5,000 to 1:74,000 cases of
ARDS.27Y29 As a result, the inuence that blood products
contribute can easily be overwhelmed by additional risk factors

TABLE 4. Multivariable Features Associated With the Development of ARDS

Multiple Variable Cox Model

ISS, per 1 point

IO plasma volume, mean (SD), L
Total uids at 24 hours, mean (SD), L

Cox Model Including Medical Center

HR (95% CI)

HR (95% CI)

1.03 (1.01Y1.05)
1.16 (1.07Y1.25)
1.010 (1.005Y1.014)

0.004
G0.001
G0.001

1.02 (1.002Y1.04)
1.17 (1.06Y1.28)
1.005 (1.001Y1.010)

0.031
0.001
0.028

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including crystalloid resuscitation, lung injury, endothelial

damage, and coagulopathy. The patients included in the current
study should be considered as some of the most severely injured patients and therefore will have some, if not all, of these
identied risk factors for ARDS. Given that DCL was required
to be included in this study, we were able to effectively control
for severity of injury in the multivariable analysis.
Despite the multi-institutional design of this study, there
were signicant limitations encountered. Chief among these
limitations is the post hoc nature of our analysis because the
original study was designed to identify risk factors for the lack
of primary fascial closure after DCL for trauma.7 As a result,
the data points collected were not aimed directly for an end
point of ARDS. Signicantly, the P/F ratio, a major determinant for the diagnosis of ARDS, was not collected and therefore not analyzed. While the denitions of transfusion-related
ALI and ARDS were standardized, the ability to convert into
the new system of ARDS severity was limited. As a result,
ARDS was a binary variable for the purposes of this report. An
additional limitation was the uncertainty of the exact blood
product transfusion rates at 24 hours. Nonblood colloid and
blood products were combined into a single data point. This
ambiguity has limited impact, however, as the overall volume
of IO nonblood colloid was far less than IO blood product
transfusion rates. Another limitation to consider is the presence
of confounding variables we were unable to account for in our
model. Certainly, given the myriad risk factors for ARDS development, this is likely and may be represented by the greater
plasma requirements acting as a surrogate rather than the cause
of the ARDS. Similarly, the greater plasma use may result in
transfusion-associated circulatory overload, which is misdiagnosed as ARDS given the difculty in differentiating the two
entities. Finally, the lack of ventilator management standardization and data collection compromises our analysis. The ARDS
denition is primarily based on the P/F ratio, which can be affected by greater positive end-expiratory pressure and alternative
ventilator strategies such as airway pressure release ventilation.
This study demonstrates that higher volume plasma resuscitations were associated with a greater risk of ARDS in
signicantly injured patients. Given the limitations of the
current study, we believe that plasma remains the standard of
care for resuscitation of the severely injured patient but consideration to the limitation of plasma when the patient stabilizes
should be entertained to potentially avoid ARDS.
AUTHORSHIP
M.D.Z. contributed in the project idea development, study design, data
collection, data analysis, manuscript preparation, manuscript review, and
data interpretation. D.J. contributed in the project idea development,
study design, data collection, data analysis, manuscript review, and data
interpretation. B.A.C. contributed in the project idea development, data
collection, study design, manuscript review, and data interpretation. K.I.
contributed in the project idea development, data collection, study design,
manuscript review, and data interpretation. G.V. contributed in the data
collection, manuscript review, study design, and data interpretation. R.C.
contributed in the data collection, manuscript review, and critical revision,
C.V.R.B. contributed in the data collection, manuscript review, and critical
revision, D.E.R.A. contributed in the data collection, manuscript review,
and critical revision, J.D. was an originator of the AAST database and
contributed in the project idea development, data collection, manuscript
review, critical revision, and project liaison. T.M.S. was an originator of the

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AAST database and contributed in the project idea development, manuscript review, and critical revision.
ACKNOWLEDGMENT
The AAST Open Abdomen Study group thanks the following individuals,
without whom this study could not have been completed: Mohammad
Alzghari, MBBS; Mahmoud A. Amr, MBBS; Meghan Spencer; Rebecca
Grace Lopez MS4; Jinfeng Han, BSN; Judith S. Katzen, MS, RN; Terry
Curry, RN; Sadia Ali, MPH; and Mary Waage.
AAST Open Abdomen Study Group Authors
In addition, we would like to acknowledge all participating members
and institutions included as authors in the AAST Open Abdomen Study
Group; Binod Shrestha, MD, and John Holcomb, MD, from the University of Texas Houston Medical Center; Kenji Inaba, MD, Obi Okoye,
MD, and Agathoklis Konstantinidis, MD, from the Los Angeles County +
University of Southern California Hospital; Tom Scalea, MD, Jay
Menaker, MD, and Joe DuBose, MD, from the R Adams Cowley Shock
Trauma Center, University of Maryland Medical Center; James F.
Whelan, MD, Rao Ivatury, MD, and Stephanie R. Goldberg, MD, from
the Virginia Commonwealth University; Martin D. Zielinski, MD, Donald
Jenkins, MD, Karla V. Ballman, PhD, and William S. Harmsen, from the
Mayo Clinic Trauma Centers; Stephen Rowe, MD, Darrell Alley, MD,
John Berne, MD, and LaDonna Allen, RN, from the East Texas Medical
Center; Paola G. Pieri, MD, and Starre Haney, RN, MS, from the
Maricopa Integrated Health System; Jeffrey A. Claridge, MD, and
Katherine Kelly, MD, from the MetroHealth Medical Center; Tiffany Bee,
MD, and Timothy Fabian, MD, from the University of Tennessee Health
Science Center; Raul Coimbra, MD, PhD, and Jay Doucet, MD, from the
University of California San Diego School of Medicine; Ben Coopwood,
MD, David Keith, MD, and Carlos Brown, MD, from the University of
Texas Southwestern-Austin, University Medical Center Brackenridge;
James M. Haan, MD, and Jeanette Ward, BA, from the Via Christi Hospital, St. Francis Campus; Stuart M. Leon, MD, Evert Eriksson, MD, and
Debbie Couillard, RN, BSN, from The Medical University of Southern
Carolina; and Marc A. de Moya, MD, and Gwendolyn M. van der
Wilden, MSc, from the Massachusetts General Hospital.
DISCLOSURE
The authors declare no conflicts of interest.

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