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 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 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.