Because we had this graft available for emergent use, we were able to perform the first EVAR for a ruptured AAA on April 21, 1994, on a patient who was hypotensive and categorically unsuitable for an open repair for anatomical and systemic reasons [10]. The rupture was sealed and the patient survived for more than 3 years after which he died from his medical comorbidities. Another ruptured AAA patient, successfully treated by EVAR at a later date than our patient, was reported in 1994 by Yusuf, Hopkinson, and their colleagues [11].

Thereafter in 1994 and 1995, we performed EVAR treatment on 11 other ruptured AAA patients who were prohibitive risks for an open repair. The leaking AAA was excluded in all 12 patients, and ten survived over 2 months despite serious comorbidities. This prompted us to hypothesize that EVAR would be the preferential treatment for all ruptured AAA patients with suitable anatomy [12, 13]. This hypothesis was also supported by the intuitive superiority of EVAR over open repair. EVAR would minimize dissection and the need for deep anesthesia; it would also reduce blood loss and avoid hypothermia, coagulopathy, and large vein injury. On the other hand, EVAR would require special equipment and skills and had the potential to delay aortic control and repair of the AAA. However, it turned out that this latter potential problem could be offset in most (~75 %) cases by strictly restricting fluid resuscitation and inducing the patient’s arterial blood pressure to fall (hypotensive hemostasis) until endograft exclusion of the rupture site was obtained [7, 12–15]. Adequate circulation for short periods was deemed acceptable if the patient was moving and talking even if he or she was profoundly hypotensive. In addition, when hypotensive hemostasis failed and circulatory collapse occurred (arterial pressure <50 mm Hg), supraceliac aortic control could be achieved with appropriate rapid placement, over a previously placed guidewire, of a large hemostatic sheath and a large compliant balloon. The technique of balloon placement and use is complex, but is well described in a recent article [16] and in other chapters in this text.

Between 1994 and 2009, our group treated 57 consecutive patients with ruptured AAAs using EVAR whenever the anatomy was suitable even if the patient was in profound shock [14]. The determination of anatomic suitability was often made on the basis of an intraoperative catheter arteriogram if the patient was unstable or severely hypotensive, but was sometimes made on the basis of a contrast computerized tomographic scan if one could be obtained rapidly. EVAR was performed on 45 of the 57 patients, while open repair was required in 12 patients. Only seven of these 57 patients died within 30 days of their procedure, giving a surprisingly low periprocedural mortality of 12 %. Only 13 or 23 % of these 57 patients required balloon aortic control for circulatory collapse, and several required open abdomen treatment for abdominal compartment syndrome [14, 15].

We concluded from this and other similar collected experience from 12 other centers which also performed EVAR to treat ruptured AAAs, whenever it was feasible, that EVAR was a better way to treat these patients than open repair. This conclusion was based on superior 30-day mortality rates from these 13 preferential EVAR centers of 19.7 % after EVAR and 36.3 % after open repair. This conclusion was reinforced by the ~12 % of ruptured AAA patients who were prohibitive risks for open repair but who could be treated successfully by EVAR [14].

However, there were several groups who disagreed with this conclusion mostly on the basis of single-center or registry controlled trials showing no mortality benefit from EVAR compared to open repair for ruptured AAA treatment. These groups believed that the good results reported for EVAR were based on case selection rather than EVAR superiority, while we believed that the good EVAR results were based on the strategies, techniques, and adjuncts for performing EVAR [14, 15].

Nevertheless it is fair to say that EVAR remains controversial in this setting, and randomized controlled trials (RCTs) have been demanded by many. Three such RCTs have recently been completed and their results published [17–19]. All three of these RCTs concluded that there was no mortality benefit from EVAR when compared to open repair for ruptured AAAs. As discussed in Chapter XX and a recent article [20], it is our belief that all three of these trials were flawed in various ways and that these RCTs were either inconclusive or reached a conclusion that was misleading.