Abdominal compartment syndrome associated with endovascular and open repair of ruptured abdominal aortic aneurysms

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...

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Bibliographic Details
Published in:Journal of vascular surgery 2015-03, Vol.61 (3), p.648-654
Main Authors: Rubenstein, Chen, MD, Bietz, Gabriel, MBChB, Davenport, Daniel L., PhD, Winkler, Michael, MD, Endean, Eric D., MD
Format: Article
Language:English
Subjects:
Aged
Aortic Aneurysm, Abdominal - complications
Aortic Aneurysm, Abdominal - diagnosis
Aortic Aneurysm, Abdominal - mortality
Aortic Aneurysm, Abdominal - surgery
Aortic Rupture - complications
Aortic Rupture - diagnosis
Aortic Rupture - mortality
Aortic Rupture - surgery
Blood Vessel Prosthesis Implantation - adverse effects
Blood Vessel Prosthesis Implantation - mortality
Endovascular Procedures - adverse effects
Endovascular Procedures - mortality
Female
Humans
Intra-Abdominal Hypertension - diagnosis
Intra-Abdominal Hypertension - etiology
Intra-Abdominal Hypertension - mortality
Intra-Abdominal Hypertension - therapy
Kentucky
Male
Retrospective Studies
Risk Factors
Surgery
Tertiary Care Centers
Time Factors
Treatment Outcome
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Summary: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, intraoperative 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 associated with ACS in
ISSN:0741-5214
1097-6809
DOI:10.1016/j.jvs.2014.10.011