An early study by Mehta et al. evaluated 30 patients who were treated with an endovascular repair for rAAA from January 2002 to December 2004 [6]. The researchers found that 6 of the 30 patients (20 %) developed ACS necessitating abdominal decompression based on an IAP ≥25 mmHg in conjunction with new onset end-organ dysfunction. Their investigation showed that there were no differences in the preoperative demographics and chronic comorbidities (age, coronary artery disease, hypertension, diabetes, renal insufficiency, smoking status, etc). However, the study did reveal: that the patients that developed ACS: (a) required increased perioperative volume resuscitation; (b) had significantly greater need of blood transfusion (8 ± 2.5 units vs. 2 ± 1.7 units, P = 0.08); (c) required increased use of an aortic occlusion balloon (67 % vs. 12 %, P = 0.01); (d) demonstrated markedly longer activated partial thromboplastin time (128 ± 84 s vs. 49 ± 31 s, P = 0.013); and (e) had a higher incidence of conversion to aorto uni-iliac devices. The overall mortality for this cohort was 23 % [6]. However, when stratified by the presence of ACS, the mortality for those patients with ACS was significantly higher (67 %) compared to (13 %) those without ACS (P = 0.01). The two surviving patients with ACS experienced considerable morbidity in their post-operative course. One patient developed permanent renal failure requiring dialysis and underwent multiple operations for definitive abdominal wall closure while the other developed bowel ischemia requiring resection and prolonged ventilator support with a tracheostomy. The 21 survivors that did not develop ACS had a more benign post-operative course, with only one occurrence of renal failure and one incidence of myocardial infarction. In addition, two patients in this cohort dealt with a prolonged ileus while another patient developed colonic ischemia necessitating resection. This study by Mehta et al. was significant because it was one of the early studies the demonstrated a lower incidence of ACS following EVAR compared to that previously reported following open aortic repair. It is estimated that ACS occurs in approximately 30 % of patients undergoing open repair for a rupture abdominal aortic aneurysm (rAAA) [14, 15]. However the mortality of patients with ACS in Mehta et al’ cohort (67 %) is not much different than the associated mortality (as high as 70 %) in this open surgical cohort with ACS [14, 15].

Building on this foundation, Mayer et al. subsequently published the largest cohort study focusing on ACS after EVAR. This retrospective cohort analysis examined the 10-year experience of 102 patients who underwent emergent endovascular repair for rAAA. The suggested threshold in this study for surgical decompression differed from that of Mehta et al work with broadened characteristics utilized to diagnose ACS. In the Mayer et al. study, surgical decompression was based on IAP >20 mmHg or an abdominal perfusion pressure <50–60 mmHg and new development of organ dysfunction or the presence certain predisposing risk factors of abdominal compartment syndrome. Those factors included deep shock (SBP < 70 mmHg), intra operative fluid resuscitation >5 L, transfusion >6 units of packed red blood cells, hypothermia (<35 °C), vast retroperitoneal hematoma, and/or massive bowel edema [16]. The utilization of broader indications for surgical intervention led to improved mortality rates but a higher incidence compared to previous literature [17–19]. The researchers found that the overall 30-day mortality for emergent EVAR was 13 % (13 of 102 patients) and the stratified mortality for patients without ACS was 8 % (7 of 82 patients) compared to 30 % (6 of 20 patients) for patients with ACS. Decompression was required in 20 patients (20 %), 14 of which were completed at the time of aneurysm repair and 6 later on while in the intensive care unit [16]. There were similar mortality rates between the two groups whether the decompression was done at the time of repair or in the post-operative period [20].