Abdominal compartment syndrome associated with

endovascular and open repair of ruptured

abdominal aortic aneurysms
Chen Rubenstein, MD,a Gabriel Bietz, MBChB,b Daniel L. Davenport, PhD,c Michael Winkler, MD,c and
Eric D. Endean, MD,d Jerusalem, Israel; San Antonio, Tex; and Lexington, Ky

Background: Abdominal compartment syndrome (ACS) is a known complication of ruptured abdominal aortic aneurysm
(rAAA) repair and can occur with either endovascular (EVAR) or open repair. We hypothesize that the underlying
mechanism for the development of ACS may differ for patients treated with EVAR or open operation.
Methods: All patients who presented with rAAA at a tertiary care medical center between January 2005 and December
2010 were included in the study. Demographic factors, type of repair (open vs EVAR), development of ACS, intra-
operative and postoperative fluid requirements, estimated blood loss, length of stay, and morbidity and mortality were
recorded. Student t-test and Fisher exact test were performed. A P value < .05 was considered significant.
Results: Seventy-three patients, 62 men and 11 women with an average age of 70.5 years, were treated for rAAA. Forty-
four (60%) underwent open repair; 29 (40%) had EVAR. Overall mortality was 42% (31 of 73), with mortality being 31%
(9 of 29) in EVAR and 48% (21 of 44) in open repair. ACS developed in 21 patients (29%), more frequently in open repair
than in EVAR (15 of 44 [34%] vs 6 of 29 [21%]; P [ NS). Mortality was higher in patients who developed ACS
compared with those without ACS (13 of 21 [62%] vs 17 of 52 [33%]; P [ .022). This finding was especially pronounced
in the EVAR group, in which mortality in patients with ACS was 83% (5 of 6) compared with 17% (4 of 23) without ACS
(P [ .005). Intraoperative fluid requirements were significantly higher in EVAR patients who developed ACS compared
with those without ACS, including packed red blood cells (5600 mL vs 1100 mL; P < .0001), total blood products
(9300 mL vs 1500 mL; P < .001), crystalloid (11,200 mL vs 4500 mL; P < .001), and estimated blood loss (5000 mL vs
660 mL; P [ .006). In patients treated with open repair, there were no significant differences in intraoperative fluid
requirements between those who developed ACS and those without ACS. However, patients who developed ACS after
open repair required significantly more crystalloid on the first and second postoperative days (first postoperative day,
8300 mL vs 5600 mL [P [ .01]; second postoperative day, 6500 mL vs 3800 mL [P [ .004]).
Conclusions: This study demonstrates that the development of ACS after repair of rAAA is associated with increased
mortality, especially in EVAR-treated patients. The higher intraoperative blood and blood product requirements asso-
ciated with ACS in EVAR patients suggest that one potential cause of early ACS is continued hemorrhage from lumbar
and inferior mesenteric vessels through the ruptured aneurysm sac. Hence, open ligation of such vessels should be
considered in patients developing early ACS after EVAR for rAAA. (J Vasc Surg 2015;61:648-54.)

Abdominal compartment syndrome (ACS) develops as
a result of increased intra-abdominal pressure and is often
related to massive fluid resuscitation associated with either
hemorrhage or splanchnic reperfusion. Increased intra-
abdominal pressure has deleterious effects on multiple or-
gan systems. As intra-abdominal pressure rises, the inferior
vena cava is compressed, resulting in a decrease in venous
return that in turn leads to reduction in ventricular end-
diastolic volume, stroke volume, and cardiac output and
elevation of systemic vascular resistance. Elevated intra-
From the Department of Vascular Surgery, Hadassah Hebrew University,
Jerusalema; Peripheral Vascular Associates, San Antoniob; and the Depart-
ment of Radiologyc and Department of Surgery,d University of Kentucky
College of Medicine, Lexington.
Author conflict of interest: none.
Reprint requests: Eric D. Endean, MD, Department of Surgery, C-215,
800 Rose St, Lexington, KY 40536 (e-mail: edende0@uky.edu).
The editors and reviewers of this article have no relevant financial relationships
to disclose per the JVS policy that requires reviewers to decline review of any
manuscript for which they may have a conflict of interest.
0741-5214
Published by Elsevier Inc. on behalf of the Society for Vascular Surgery.
http://dx.doi.org/10.1016/j.jvs.2014.10.011
abdominal pressure also compresses the kidneys, and this
along with the adverse effects on cardiac function causes
a reduction in renal flow and a decrease in urine output.
Simultaneously, increased intra-abdominal pressure com-
presses the diaphragm, raising intrathoracic pressure with
an increase in airway pressures, pulmonary artery pressure,
and central venous pressure and a decrease in pulmonary
compliance. If ACS is left untreated, multiorgan failure
develops. Treatment is directed at relieving the intra-
abdominal pressure, often requiring a decompressive lapa-
rotomy. Failure to relieve the pressure is almost uniformly fatal;
surgical decompression demonstrates significant improvement
in mortality.1
Patients with ruptured abdominal aortic aneurysm
(rAAA) present with hemorrhagic shock. The hematoma
that forms in the retroperitoneum is a space-occupying
lesion that itself can contribute to a rise in intra-abdominal
pressure. In the perioperative period, these patients have
large fluid requirements from ongoing bleeding, co-
agulopathy, and third-space requirements that necessitate
resuscitation with blood, blood products, and fluids. This
resuscitation can lead to bowel edema and ascites that

648
JOURNAL OF VASCULAR SURGERY
Volume 61, Number 3
further increase intra-abdominal pressure and development
of ACS. Indeed, the development of ACS has been docu-
mented after both open and endovascular repair of
rAAA.2-7
We hypothesize that the underlying mechanisms for
the development of ACS after repair of rAAA may be
different for patients treated with an endovascular aneu-
rysm repair (EVAR) technique compared with those with
an open repair.
METHODS
A retrospective review of all patients treated for rAAA
between January 2005 and December 2010 at the Univer-
sity of Kentucky Chandler Medical Center was conducted.
The study was approved by the University of Kentucky
Institutional Review Board (IRB approval No. 10-0011-
P1H). Patient consent was not needed. Patients were
excluded if the aneurysm was an aortic dissection or if
the aneurysm was symptomatic but not ruptured. The
charts were reviewed to identify demographic information,
aneurysm size, and comorbid medical conditions. Opera-
tive details, including type of repair (open vs endovascular),
intraoperative fluid administration, operative time, aortic
cross-clamp time (open aneurysms), and need for suprare-
nal clamp (open aneurysms), were recorded. Available pre-
operative computed tomography scans were reviewed by a
vascular radiologist to identify the presence of patent
lumbar and inferior mesenteric arteries arising from the
aneurysm for patients treated with EVAR. Available intra-
operative completion studies after endograft placement
were reviewed for evidence of endoleaks. Postoperative
fluid resuscitation and urine output were recorded. The
diagnosis of ACS was made on the basis of a constellation
of clinical findings including increased airway pressures, oli-
guria, and physical examination revealing a tense abdom-
inal wall and (in some open cases) inability to close the
abdomen due to bowel edema. The development of com-
plications, including myocardial infarction, bowel ischemia,
pneumonia, renal failure, need for dialysis, number of days
on the ventilator, intensive care unit length of stay, total
hospital length of stay, and sepsis, were recorded. Final
outcome and disposition were noted.
Descriptive data are presented as mean 6 standard er-
ror. Comparisons were made by the unpaired t-test. Cate-
gorical data was compared with Fisher exact test or the
Mann-Whitney U test. P values of < .05 were considered
to be significant.
RESULTS
Between January 2005 and December 2010, 73 pa-
tients, 62 men and 11 women, were treated for rAAA.
The average age of patients was 70.5 years. Overall mortal-
ity for repair of rAAA was 31 of 73 (42%). ACS developed
in 21 patients (29%).
Twenty-nine patients (40%) had repair of rAAA with an
endograft, whereas 44 (60%) underwent an open repair.
Characteristics of patients undergoing EVAR or open
repair were not statistically significant except that patients
Rubenstein et al 649
undergoing EVAR were older and more patients in the
EVAR group had a history of cancer (Table I). Significantly
more patients undergoing open repair required dialysis
(P ¼ .009) than in the EVAR group. There was a trend
for lower morality, length of stay, and intensive care unit
length of stay in the EVAR group compared with the
open repair group, but statistical significance was not
reached.
ACS developed in 21 patients, including 6 of 29 pa-
tients (21%) who had an EVAR and 15 of 44 patients
(34%) who had an open repair. No differences were identi-
fied in patient characteristics whether or not they devel-
oped ACS in either the EVAR or open group (Table II).
In patients who underwent open repair, there were nine
deaths among the 15 patients who developed ACS (60%)
compared with 13 deaths in 29 patients (45%) who did
not develop ACS (P ¼ NS). However, in patients treated
with EVAR, 5 of 6 patients (83%) who developed ACS
died compared with four deaths among 23 patients
(17%) who did not develop ACS (P ¼ .005). In patients
who had an open repair, colon ischemia, multisystem organ
failure, and sepsis were significantly higher in patients who
developed ACS than in those without. No statistical signif-
icance was noted in these outcomes in the patients treated
with EVAR.
In patients who developed ACS, control of the aorta
was obtained in a suprarenal position in 11, infrarenal in
nine, and unknown in one. Patients who did not develop
ACS had control of the aorta suprarenally in 17, infrare-
nally in 31, and unknown in four. In the entire study
group, the location of aortic control was not significantly
associated with the development of ACS. Similarly, in pa-
tients treated with an open repair, suprarenal control of
the aorta was not associated with development of ACS.
However, in EVAR patients, balloon control of the aorta
was done in seven patients, whereas 20 did not have
balloon control, and in one, it was unknown. In this subset
of patients, ACS developed in six patients (five with balloon
control, one unknown) and was found to be significantly
associated with balloon control of the aorta (P < .001).
Because fluid resuscitation can play a key role in the
development of ACS, the amount and timing of fluids
given patients were evaluated comparing groups who
developed ACS and those who did not. In patients who
developed ACS with EVAR, the amount of blood products
(packed red blood cells, fresh frozen plasma, platelets, and
cryoprecipitate), colloid, and crystalloid given intraopera-
tively was significantly higher than in those who did not
develop ACS (Table III). Estimated blood loss was also
significantly higher in patients who developed ACS. In
comparison, in patients with an open approach, the only
significant difference seen in intraoperative fluid adminis-
tration between patients who developed ACS and those
who did not was that significantly more fresh frozen plasma
and platelets were given to patients who developed ACS.
In comparing intraoperative fluid administration to
patients who developed ACS between EVAR and open
repair, significantly more blood products and crystalloid
 JOURNAL OF VASCULAR SURGERY
650 Rubenstein et al March 2015

Table I. Patient characteristics and outcome for the entire cohort of patients

EVAR (n ¼ 29) Open (n ¼ 44) P value

Patient characteristics
Age 73.7 68.4 .04
Gender (male) 23/29 (74) 39/44 (89) NS
CAD 11/29 (38) 18/44 (41) NS
Current smoking 8/29 (28) 12/44 (27) NS
COPD 10/29 (35) 14/44 (32) NS
DM 5/29 (17) 11/44 (25) NS
Hypertension 15/29 (52) 25/44 (57) NS
Hyperlipidemia 1/29 (3) 7/44 (16) NS
History of CVA 1/29 (3) 5/44 (11) NS
History of cancer 4/29 (14) 0/44 .022
CRF 4/29 (14) 0/44 .022
BMI 27.8 28.1 NS
Outcome
MI 3 (10) 7 (16) NS
Pneumonia 8 (28) 9 (21) NS
CVA 1 (3) 1 (2) NS
Renal failure 9 (31) 13 (30) NS
Dialysis 0 9 (21) .009
Sepsis 3 (10) 7 (16) NS
Ischemic colon 1 (3) 8 (18) .078
Multisystem organ failure 0 4 (9.1) .147
Death 9 (31) 22 (50) .148
Median hospital length of stay, days 9 17 .212
Median intensive care unit length of stay, days 5 9 .051

BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular
accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant.
Fisher exact or Mann-Whitney U test as appropriate.

were given intraoperatively to patients who had EVAR. A
slightly higher estimated blood loss was recorded for
EVAR patients compared with open repair patients who
developed ACS (5000 mL vs 4400 mL; P ¼ .026). In mak-
ing a similar comparison between patients who underwent
EVAR and those who underwent open repair but did not
develop ACS, the opposite trend was seen: patients who
had EVAR had less blood, blood products, and crystalloid
than did patients with an open repair. Less blood loss was
observed in patients who did not develop ACS in those un-
dergoing EVAR compared with those with open repair
(660 mL vs 4000 mL; P < .0001).
The amount of fluids administered on the first and sec-
ond postoperative days was also evaluated (Table IV). Pa-
tients who had EVAR and developed ACS required more
blood on postoperative day 1 (7200 mL vs 600 mL; P ¼
.017). This is in contrast to patients with ACS who had
an open repair of the rAAA. These patients, compared
with those who did not develop ACS, required significantly
more crystalloid on postoperative day 1 (8300 mL vs
5600 mL; P ¼ .01) and day 2 (6500 mL vs 3800 mL;
P ¼ .004), with a trend of requiring more blood on post-
operative day 2.
DISCUSSION
In this retrospective review of patients undergoing
repair of rAAA at one institution, the overall observed mor-
tality of 42% is similar to that previously reported.7-11
Although it is not statistically significant in this report, there
was a trend for lower mortality when patients were treated
with an endograft compared with an open repair, consistent
with other reports.7-9,12-16 ACS developed in patients with
both endograft repair and open repair. The incidence for
the development of ACS is not known but is reported to
occur on average in 10% of patients.17 A systematic review
by Karkos et al8 reported that ACS occurred in 5.5% of pa-
tients treated with EVAR. A recent meta-analysis calculated
the rate as being 8% but suggested that the true incidence
could be >20% with increased awareness and vigilant moni-
toring.11 Interestingly, the occurrence of ACS in patients
treated with EVAR in the current series was 21%. Not sur-
prising, patients who develop ACS after repair of rAAA
have a higher incidence of colon ischemia, sepsis, and multi-
system organ failure. Treatment is directed at decreasing the
intra-abdominal pressure, often needing a decompressive
laparotomy.4,5 Failure to intervene can be fatal. Therefore,
early diagnosis and treatment are essential.
The death rate in patients who develop ACS after
EVAR for rAAA has been reported to be as high as
57%.18 The current study confirms that patients who
develop ACS after EVAR have a high mortality. It is of in-
terest that the meta-analysis conducted by Karkos et al11
did not find a statistically significant association between
ACS and mortality. Despite this lack of statistical signifi-
cance, they stated that “the development of ACS after
endovascular repair of RAAAs is an ominous scenario that
has a significant negative effect on survival.clearly, the
mortality rate is increased in patients with ACS.”11
JOURNAL OF VASCULAR SURGERY
Volume 61, Number 3 Rubenstein et al 651

Table II. Patient characteristics and outcome stratified by type of repair for ruptured abdominal aortic aneurysm (rAAA)
and the presence or absence of abdominal compartment syndrome (ACS)

EVAR Open

ACS No ACS ACS No ACS

(n ¼ 6) (n ¼ 23) P value (n ¼ 15) (n ¼ 29) P value

Gender (male) 6/6 17/23 NS 13/15 26/29 NS

CAD 2/6 9/23 NS 4/15 14/29 NS
Current smoking 1/6 7/23 NS 2/15 10/29 NS
COPD 2/6 8/23 NS 7/15 7/29 NS
DM 1/6 4/23 NS 5/15 6/29 NS
Hypertension 3/6 12/23 NS 9/15 16/29 NS
Hyperlipidemia 1/6 0/23 NS 3/15 4/29 NS
History of CVA 0/6 1/23 NS 1/15 4/29 NS
History of cancer 0/6 4/23 NS 0/15 0/29 NS
CRF 1/6 3/23 NS 0/15 0/29 NS
BMI d 27.8 NS 26.5 28.9 NS
Outcome
MI 1/6 2/23 NS 3/15 4/29 NS
Pneumonia 1/6 7/23 NS 3/15 6/29 NS
CVA 0/6 1/23 NS 0/15 1/29 NS
Renal failure 2/6 7/23 NS 5/15 8/29 NS
Dialysis 0/6 0/23 NS 3/15 6/29 NS
Sepsis 1/6 2/23 NS 5/15 2/29 .036
Ischemic colon 1/6 0/23 NS 6/15 2/29 .013
Multisystem organ failure 0/6 0/23 NS 4/15 0/29 .010
Death 5/6 4/23 .005 9/15 13/29 NS
Median hospital length of stay, days 10, n ¼ 3 9, n ¼ 23 .880 8.5 19 .117
Median intensive care unit length of stay, days 10, n ¼ 1 4.5, n ¼ 20 .571 11 8.5 .394

BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular
accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant.
Fisher exact or Mann-Whitney U test as appropriate.

Table III. Intraoperative fluid administration and estimated blood loss for open vs endovascular aneurysm repair
(EVAR)

EVAR Open ACS EVAR No ACS EVAR

vs open, vs open,
ACS No ACS P value ACS No ACS P value P value P value

Intraoperative fluids/blood
loss (volumes in milliliters)
PRBC 5600 1100 <.001 3200 3200 NS .002 <.001
FFP 27 220 <.001 1500 800 .027 .014 <.001
Platelets 730 70 .001 610 350 .013 .013 <.001
Cryoprecipitate 280 15 .016 180 82 NS .006 .002
Total blood products 9300 1500 <.001 5600 4100 NS .006 <.001
Colloid 1500 650 .032 760 1600 NS .015 <.001
Crystalloid 11,000 4500 <.001 10,300 8200 NS .027 .003
Estimated blood loss 5000 660 .006 4400 4000 NS .026 <.001

ACS, Abdominal compartment syndrome; FFP, fresh frozen plasma; NS, not significant; PRBC, packed red blood cells.
Mann-Whitney U tests.

The pathophysiologic mechanism in the development
of ACS is caused by intra-abdominal hypertension. In
patients treated for rAAA with an open operation, intra-
abdominal hypertension appears to be the result of resusci-
tation. An open operation and a shock state contribute to
third-space fluid requirements, often resulting in the need
for massive fluid administration. Shock and hypothermia
can result in coagulopathy, increasing the need for blood
and blood products. What is of particular interest in the
current study is that patients who developed ACS after
EVAR received significantly more blood, blood products,
colloid, and crystalloid intraoperatively compared with
either those patients who had EVAR without the develop-
ment of ACS or patients who developed ACS after open
repair. This implies that there was significantly more blood
loss occurring during the operation in the EVAR/ACS pa-
tients and is consistent with the higher estimated blood
loss in this subset of patients. This finding may further
 JOURNAL OF VASCULAR SURGERY
652 Rubenstein et al March 2015

Table IV. Fluid requirements for the first and second postoperative days

EVAR Open

ACS No ACS P value ACS No ACS P value

Fluids: postoperative day 1 (volumes in milliliters)

Blood 7200 600 .017 1300 600 .211
n¼2 n ¼ 14 n ¼ 12 n ¼ 11
Crystalloid 17,800 5200 .587 8300 5600 .010
n¼2 n ¼ 22 n ¼ 13 n ¼ 17
Fluids: postoperative day 2 (volumes in milliliters)
Blood 1900 470 .286 900 430 .081
n¼1 n¼6 n¼8 n¼6
Crystalloid 5200 2700 .116 6500 3800 .004
n¼2 n ¼ 22 n ¼ 12 n ¼ 17

ACS, Abdominal compartment syndrome; EVAR, endovascular aneurysm repair.

Mann-Whitney U tests.

suggest that these patients, despite a successful placement
of an endovascular graft, have continued blood loss. Such
bleeding can occur either while the endograft is being
placed or after successful placement, through a type II
endoleak that is open to the abdominal cavity through
the ruptured aneurysm sac as suggested by Mehta et al.18
If the latter situation were to be present, such patients
would be expected to have early development of ACS
with ongoing blood product requirements. Conversely, in
patients treated with an open approach, hemorrhage from
the rupture and patent vessels arising from the sac should
be controlled at the time of repair. It would be expected
that if these patients develop ACS, its etiology should be
related to fluid resuscitation. Consistent with this hypothe-
sis, we demonstrated that patients who had an open repair
and who developed ACS had increased crystalloid require-
ments during the first and second postoperative days.
We attempted to review the preoperative computed to-
mography scans to identify patent lumbar and inferior
mesenteric vessels and intraoperative completion angio-
grams to identify evidence for an endoleak through the
aortic wall tear. Unfortunately, the studies were either
not available or of insufficient quality to make an assess-
ment. Anecdotally, one patient in this series who was
treated with an endograft developed ACS in the operating
room and had a decompressive laparotomy. This patient
continued to have active bleeding from the laparotomy
wound, and because of his large habitus, access to his aortic
sac was not possible. Despite massive transfusion, he died
in the postanesthesia care unit. In retrospect, we suspect
that his ongoing blood loss was from patent vessels arising
from the aneurysm sac and bleeding into the abdominal
cavity through the ruptured aneurysm. It is likely that the
decompressive laparotomy, which treated his intra-abdominal
hypertension, facilitated the bleeding from a type II endoleak.
The mechanism for the development of ACS after
EVAR or open repair of rAAA is not limited to one or
the other mechanism and in an individual patient may be
multifactorial. It is of interest that balloon control of the
aorta in EVAR-treated patients was associated with the
development of ACS, although suprarenal clamping of
the aorta in open cases was not associated with ACS. These
findings should be viewed cautiously because of the small
numbers of patients. There are other factors that are likely
to contribute to the development of ACS. For example, pa-
tients who have undergone EVAR may have significant
fluid requirements postoperatively from the effects of
shock, have a mass effect from the retroperitoneal hema-
toma, and have a coagulopathy. Likewise, patients who
have had an open repair may have significant blood product
requirements from a coagulopathy or surgical bleeding in
addition to a retroperitoneal mass effect and bowel edema
from resuscitation.
Treatment of ACS, despite its cause, is directed at
lowering of intra-abdominal pressure. Whereas medical
treatment can be attempted, the ultimate treatment is a
decompressive laparotomy.19,20 We think that the results
of this report suggest that the underlying mechanism
believed to be responsible for the development of ACS af-
ter repair of rAAA should be evaluated in considering a
decompressive laparotomy (Fig). Early need for blood after
placement of an endograft should alert the surgeon to the
possibility of ongoing bleeding related to a type II endo-
leak. Such a situation would require consideration for the
evacuation of a space-occupying hematoma and opening
of the aneurysm sac to ligate bleeding vessels within the
aneurysm sac. Late development of ACS, with no evidence
of ongoing blood loss, whether after EVAR or open repair,
is likely to be due to aggressive fluid resuscitation, and
decompressive laparotomy would simply be needed. Early
development of ACS after open repair could be the result
of ongoing hemorrhage due to a coagulopathy or surgical
bleeding. Efforts should be made to correct any coagulop-
athy and to ensure normothermia before performance of a
decompressive laparotomy.
There are a number of limitations to this study. The
study is not randomized, is from a single institution, is
retrospective, and has a relatively small number of patients.
In addition, there was no standardization for measuring
intra-abdominal pressures or set criteria for determining
when to intervene for ACS. We were unable to correlate
either preoperative or intraoperative radiographic studies
JOURNAL OF VASCULAR SURGERY
Volume 61, Number 3
Fig. Proposed algorithm for treatment of abdominal compartment syndrome (ACS) after endovascular aneurysm
repair (EVAR) or open repair of ruptured abdominal aortic aneurysm (rAAA).
with the presence of patent lumbar or inferior mesenteric
artery vessels arising from the aneurysm that could have
been or were contributing to a type II endoleak. We
were unable to determine the exact time of onset of ACS
symptoms but surmise that because four of six deaths
that occurred in patients with ACS treated with EVAR
were within the first day, the ACS in these patients devel-
oped early.
CONCLUSIONS
This study demonstrates that ACS occurs with both
EVAR and open repair of rAAA and may be more common
than prior studies suggest after EVAR. The study high-
lights possible mechanisms for the development of ACS af-
ter either the open or EVAR approach for treatment of
rAAA. This has implications for treatment of ACS after
repair of rAAA. We would recommend that in patients
who develop early ACS after EVAR with evidence of
ongoing blood requirements, consideration be given to
exploring the aortic sac at the time of decompressive lapa-
rotomy. Further studies and reports are needed to confirm
that bleeding through the aortic tear occurs and causes
ACS.
AUTHOR CONTRIBUTIONS
Conception and design: EE, CR
Analysis and interpretation: EE, DD
Data collection: EE, CR, GB, MW
Writing the article: EE
Critical revision of the article: EE
Final approval of the article: EE
Rubenstein et al 653
Statistical analysis: DD
Obtained funding: Not applicable
Overall responsibility: EE
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Submitted Jul 17, 2014; accepted Oct 8, 2014.