Surgical and endovascular repair of ruptured abdominal aortic aneurysm

INTRODUCTION — Rupture is a fatal complication of abdominal aortic aneurysm (AAA). An aneurysm is defined as ruptured when bleeding is present outside of the wall of the aneurysm. Elective aneurysm repair is associated with low rates of morbidity and mortality in properly selected individuals, but in spite of advances in intensive care unit management and techniques for repair, mortality following repair of ruptured AAA remains high [1]. Surgical outcomes may be improved using endovascular aortic repair (EVAR), but as promising as EVAR may be for the treatment of ruptured AAA, logistical and practical barriers need to be overcome [1]. Increasing numbers of institutions have initiated protocols for endovascular repair of ruptured AAA, with lowered perioperative morbidity [2], but not all institutions are equipped to treat ruptured AAAs using minimally invasive technology. Moreover, interfacility transfer that delays definitive management increases length of stay, cost, and overall mortality [3,4]. Thus, many ruptured AAAs will still be repaired using open surgical techniques.

Specific considerations for the surgical and endovascular repair of emergency AAA repair will be reviewed here. General techniques for AAA repair are discussed elsewhere. The diagnosis and management of AAA and ruptured AAA are discussed in separate topic reviews. (See "Endovascular repair of abdominal aortic aneurysm" and "Open surgical repair of abdominal aortic aneurysm" and "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction' and "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Introduction'.)

OPEN SURGICAL VERSUS ENDOVASCULAR REPAIR — For patients with anatomy suitable for an endovascular approach, we suggest an endovascular rather than open surgical approach. This recommendation is in agreement with guidelines from the Society for Vascular Surgery (SVS) guidelines for the care of the patient with abdominal aortic aneurysm (AAA), which also include rapid transfer to a vascular center when appropriately experienced personnel and equipment are not immediately available, providing that transfer can be accomplished expeditiously (ie, emergency department presentation to surgical intervention <90 minutes) [5]. However, overall mortality is increased for patients with ruptured AAA (17 to 19 percent) who are transferred for repair compared with those who can be repaired expeditiously at the institution to which they presented [3,4]. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Decision for patient transfer'.)

Although significant differences in mortality rates for open compared with endovascular repair for ruptured aneurysm have not been demonstrated in a randomized trial, there is evidence to suggest that perioperative (30 day) outcomes for endovascular aneurysm repair (EVAR) following ruptured AAA may be better than for open AAA repair [6-13]. Mortality rates associated with open versus endovascular repair of ruptured AAA remain disputed, but perioperative morbidity is generally lower for EVAR compared with open repair [14-21]. The apparent advantage of EVAR in the setting of ruptured AAA likely relates to its minimally invasive nature, which minimizes physiologic stress and decreases the risk of subsequent cardiovascular, pulmonary, and renal morbidity. In a matched cohort study comparing open versus endovascular repair following rupture in patients from the Vascular Quality Initiative, perioperative morbidity and mortality was significantly lower for endovascular repair and length of hospital stay was reduced [22]. All-cause survival was higher at one year for endovascular repair (73 versus 59 percent) in the propensity-matched cohort.

The main criticism of early observational studies, which have associated endovascular repair with lower mortality, is that hemodynamically stable patients with ruptured AAA are more often selected for EVAR, and hemodynamically unstable patients tend to be treated with open repair [7,8,12,23-34]. Some have suggested that such patient selection biases the comparison, and that the mortality rates for EVAR and open repair for ruptured AAA are actually similar [35,36]. In addition, patients treated with EVAR for ruptured AAA may be more likely to be treated in higher volume, more advanced centers that have dedicated vascular surgeons and operative teams compared with patients treated in lower-volume centers. In support of this idea was a comparison of morphologic variables among 458 patients in the Immediate Management of the Patient with Rupture: Open versus Endovascular Repair (IMPROVE) trial [12,37,38] (discussed in the next paragraph) who underwent open or endovascular repair [39]. Short aneurysm neck length adversely affected mortality after open repair of ruptured AAA (an exclusion criterion for EVAR), which may help explain why observational studies, and not randomized trials [12,33,37,38,40-44], show an early survival benefit. A meta-analysis that included four trials found no difference in perioperative (30-day) mortality comparing endovascular with open repair for ruptured AAA (odds ratio [OR] 0.88, 95% CI 0.66-1.16) [16]. For complications, including myocardial infarction, renal complications, and respiratory failure, no differences were seen, though the quality of the evidence was low. Endovascular repair may reduce the incidence of bowel ischemia, but very few events were reported (OR 0.37, 95% CI 0.14-0.94). Six-month mortality was likewise no different (OR 0.89, 95% CI 0.40-1.98) [15].

The largest of the trials included in the meta-analysis was the IMPROVE trial [12,37,38,45]. The trial, which used a "real-world" study design, randomly assigned 613 patients with suspected ruptured AAA (based upon clinical history or examination but prior to definitive imaging) to open repair or EVAR. Patients assigned to a particular group underwent the assigned treatment, underwent the other treatment, or did not undergo either treatment due to death prior to repair or establishment of an alternative diagnosis. As assigned, no difference in perioperative (30 day) mortality was seen between the groups. As treated, the mortality for patients who underwent EVAR was 25 percent compared with 38 percent for those who underwent open repair. Patients assigned to EVAR were significantly more likely to be discharged directly to home compared with those assigned to open repair (94 versus 77 percent). At one-year follow-up, all-cause mortality rates were also not significantly different for endovascular compared with open surgical repair [37]. At three years, mortality was lower in the endovascular strategy group (42 versus 54 percent; OR 0.62, 95% CI 0.43-0.88), but after seven years there was no clear difference between the groups (hazard ratio [HR] 0.86, 95% CI 0.68-1.08) [45]. Reintervention rates up to three years were not significantly different between the groups (HR 1.02, 95% CI 0.79-1.32). The initial rapid rate of reintervention was followed by a much slower mid-term reintervention rate in both groups.

The IMPROVE trial shows that for patients suspected but not proven to have ruptured AAA, an open surgical or endovascular strategy for repair may be equally valid. However, most facilities in developed countries will, at a minimum, be able to exclude other confounding diagnoses (present in 8.9 percent of the patients in this study) given the general availability of computed tomography (CT). Where this is not possible, transfer to a facility that can perform either type of AAA repair seems prudent. The determination of anatomic suitability for EVAR may be best determined at the treating facility, commonly made preoperatively using multidetector CT angiography. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Decision for patient transfer' and 'Endovascular repair' below.)

Although attempts have been made to quantify the risk of mortality with ruptured AAA, no variable or classification has proven reliable for predicting mortality with certainty [46]. Factors on admission that have been associated with increased mortality following open repair of ruptured AAA are discussed elsewhere. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Risk assessment'.)

CRITERIA FOR ENDOVASCULAR REPAIR — Several anatomic factors must be satisfied to undertake endovascular abdominal aortic aneurysm (AAA) repair under elective circumstances and also for ruptured AAA. Anatomic suitability is determined through vascular imaging in hemodynamically stable patients and for hemodynamically unstable patients, it can be determined intraoperatively. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability'.)

Although early work described that up to 50 percent of patients with ruptured AAA do not have anatomy suitable for endovascular aneurysm repair (EVAR) [10], increased experience with EVAR and new grafts have undoubtedly decreased this proportion. Aortic anatomy, aortic measurements, and criteria for elective endovascular graft placement are reviewed in detail elsewhere.

Contraindications — Endovascular repair is contraindicated in the circumstances listed below. These contraindications (absolute and relative) are discussed in more detail elsewhere. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability' and "Endovascular repair of abdominal aortic aneurysm", section on 'Contraindications'.)

●An aortic neck diameter more than 32 mm at the renal arteries should not be treated with endovascular aneurysm repair (elective or emergency). The largest available endograft is 36 mm in diameter (Zenith) (table 1). With 10 percent oversizing as recommended by most endograft manufacturers, an aortic neck diameter more than 32 mm will not have an adequate proximal seal. (See "Endovascular devices for abdominal aortic repair".)

●A ruptured AAA with an aortic neck length <7 mm should not be treated with EVAR, as this is the shortest neck length that can be treated by any device that is approved in the United States (Ovation) (table 1). At least 15 mm of undilated aorta (ie, aortic neck) below the renal arteries is ideal to achieve an adequate seal between the endograft and aortic neck; between 7 and 10 mm is the minimum neck length, depending upon the amount of aortic neck angulation that is present. When neck angulation is more than 30 degrees, a longer neck length should be present to provide an adequate proximal endograft seal. Adherence to these criteria may help reduce the incidence of endoleak. (See 'Complications' below and "Complications of endovascular abdominal aortic repair", section on 'Endoleak'.)

Relative contraindications to EVAR include the following:

●More than 40 percent of the aortic neck diameter occupied with thrombus

●Circumferential calcification at the level of the aortic neck

●Aortic neck angulation >60 degrees

●Bilateral iliac arteries <6.5 cm in diameter

PREPARATION — Standard laboratory testing (basic metabolic panel, complete blood count, coagulation profile, and liver function tests) should be obtained in preparation for surgery. The patient should have at least 10 units of packed red blood cells (pRBCs) and fresh frozen plasma (FFP) or similar products (eg, PF24) available for transfusion. The blood bank should be alerted to the potential need for massive transfusion. Similar to trauma patients with severe ongoing hemorrhage, patients with ruptured abdominal aortic aneurysm (AAA) who require massive transfusion may benefit from a pRBC to FFP ratio ≤2:1 rather than higher ratios [47]. (See "Clinical use of plasma components" and "Initial management of moderate to severe hemorrhage in the adult trauma patient" and "Massive blood transfusion", section on 'Trauma'.)

Antimicrobial prophylaxis is recommended prior to the placement of prosthetic material (table 2). (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Vascular surgery'.)

Permissive hypotension — During imaging and transfer to the operating room, the patient is allowed to have relatively low blood pressure (permissive hypotension), with a goal systolic blood pressure of 80 to 100 mmHg, which may prevent further tearing of the aorta and decrease blood loss [9,38,48]. Pain control is an important part of management. It is important to keep the patient comfortable, but consciousness should be maintained. (See "Treatment of severe hypovolemia or hypovolemic shock in adults" and "Pain control in the critically ill adult patient".)

Preoperative balloon occlusion — For hemodynamically unstable patients or in those with difficult anatomy, placement of a standard aortic occlusion balloon via the femoral artery into the suprarenal aorta and held into position using a long sheath can help stabilize the patient prior to either open or endovascular repair (figure 1) [26,49]. In addition, with the increased experience using the resuscitative endovascular balloon occlusion of the aorta (REBOA) technique for managing trauma, REBOA may become useful for managing ruptured AAA. The REBOA balloon is a partially occlusive aortic balloon, which can compress the area(s) of aortic wall disruption while still allowing blood to flow through a central chamber. For aneurysm rupture, the REBOA can be deployed in any area of the aorta that will provide the best control or hemodynamic effect. When placed early and properly positioned, REBOA can improve blood pressure and reduce mortality [50]. More study is needed to clarify the role of REBOA for patients with aortic rupture. (See "Endovascular methods for aortic control in trauma".)

Anesthesia — For patients undergoing endovascular repair, local anesthetic is generally adequate [51]. Some work has found lower mortality with this approach, but this benefit may be a marker for institutions that have a higher comfort level with endovascular aneurysm repair (EVAR) for ruptured aneurysm [52]. Patients undergoing open repair will require general anesthesia. (See "Anesthesia for open abdominal aortic surgery".)

Regardless of whether open or endovascular repair is performed, we prepare the patient from the chest to the knees. Access to the abdomen may be needed if EVAR becomes complicated or is unsuccessful, necessitating conversion to an open procedure. In addition, clot evacuation via laparotomy may be needed in the event of large volume during EVAR to avoid abdominal compartment syndrome. Access to the groin is necessary for EVAR and may be needed for femoral thromboembolectomy during open surgery. The patient should be prepared and draped prior to induction of general anesthesia. The surgical team should be ready to begin the procedure immediately after induction in anticipation of hemodynamic collapse.

OPEN SURGICAL REPAIR — Open surgical repair of ruptured abdominal aortic aneurysm (AAA) is similar to elective AAA repair with modifications in technique that reflect the urgency of the repair and the pathophysiology of rupture. The discussion below is focused on the essential differences. (See "Open surgical repair of abdominal aortic aneurysm".)

Incision — Open surgical AAA repair can be performed through a midline abdominal or left retroperitoneal incision [53]. For infrarenal ruptured AAA, a midline approach is preferred because it is expedient and exposure of the right iliac artery is better, which is important if an iliac aneurysm is present or there are signs of thromboembolism on that side. In patients who are known to have a ruptured juxtarenal aneurysm, a retroperitoneal approach may provide better proximal exposure. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Incision and aortic exposure'.)

Aortic control — The first priority after entering the abdomen should be control of hemorrhage. Bleeding from the rupture site can usually be controlled with direct pressure (manual or sponge stick) prior to aortic clamping. Direct pressure allows filling of the heart and facilitates resuscitative efforts by the anesthesia staff.

The location of initial aortic clamping depends upon the location of the rupture and retroperitoneal hematoma. Opening a pararenal hematoma without adequate vascular control can result in hemorrhage that may be difficult to control, and although some surgeons may enter a pararenal retroperitoneal hematoma directly, we suggest controlling the aorta using a supraceliac aortic clamp prior to entering the hematoma. When the hematoma is located in the mid- to distal aorta, the infrarenal aorta can often be clamped without the need for supraceliac clamping. If there is any question, we suggest placing a suprarenal clamp, having it ready to clamp should it become necessary.

To perform supraceliac clamping, an incision should be made up to the xiphoid process and the patient placed in reverse Trendelenburg position. The left triangular ligament attaching the left lobe of the liver to the diaphragm should be divided, and the lesser sac can be entered by dividing the gastrohepatic ligament. Exposure of the supraceliac aorta is facilitated by retraction of the rib cage using a self-retraining retractor (eg, Thompson, Bookwalter, upper hand). The aorta is then palpated, and the medial and lateral aspects of the aorta are cleared to the spine using finger dissection. The right crus of the diaphragm should be divided with electrocautery to aid exposure. A long aortic clamp is then placed on the aorta and closed to the degree that is needed to control bleeding from the aortic rupture site. Supraceliac aortic clamping can often be accomplished in less than five minutes but may take longer. Once the supraceliac clamp is in place, it is usually necessary to adjust the retractors to facilitate exposure of the infrarenal aorta.

In hemodynamically stable patients with an infrarenal rupture, it may be possible to open the retroperitoneum, dissect the infrarenal aorta, and obtain aortic control below the renal arteries without closing the supraceliac clamp. Once the aorta is controlled at the level of the renal arteries, the supraceliac clamp, if closed, can be opened to minimize visceral ischemia. Prolonged supraceliac aortic clamping >30 minutes significantly increases morbidity due to hepatic, mesenteric, and renal ischemia [54]. (See 'Complications' below and 'Mortality' below.)

Once vascular control is achieved, aortic replacement proceeds in a manner similar to elective open abdominal aortic aneurysm repair with a tube or bifurcated graft (figure 2). If the aortic neck is short, it may be necessary to perform the proximal anastomosis with the suprarenal or supraceliac clamp in place, releasing the supraceliac clamp after the proximal aortic graft has been clamped. Once the graft is in place, the aneurysm sac and retroperitoneal tissues should be reapproximated over the graft to cover the proximal and distal suture lines to minimize the potential for aortoenteric fistula. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Incision and aortic exposure' and "Open surgical repair of abdominal aortic aneurysm", section on 'Anticoagulation and reversal'.)

Systemic anticoagulation — Systemic anticoagulation (typically heparin) is commonly administered during the course of elective AAA repair, but we prefer to administer heparin on a case-by-case basis during repair of ruptured AAA. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Anticoagulation and reversal'.)

Once the infrarenal aorta has been clamped and hemorrhage is under control, we generally anticoagulate the patient. However, in patients with obvious coagulopathy, those at risk for coagulopathy (eg, massive transfusion), or in patients for whom supraceliac clamping was prolonged, proceeding without anticoagulation is an acceptable option. Reassessing coagulation parameters is often indicated at this point.

Handling the inferior mesenteric artery — Colonic ischemia is commonly observed following ruptured AAA with approximately 35 percent of ruptured AAA patients suffering some degree of ischemia, an incidence that is higher compared with elective AAA repair [55,56]. We prefer to reimplant the origin of the inferior mesenteric artery (IMA) into the distal aortic graft, whenever possible, to minimize the potential for colonic ischemia, unless backbleeding from the IMA orifice within the aneurysm sac is vigorous, indicating adequate collateral flow, or the vessel is occluded (no back bleeding). However, because reimplantation of the IMA prolongs the operation, the IMA is reimplanted less frequently for ruptured AAA than with elective AAA repair [46,57].

Thromboembolectomy — In our experience, thromboembolism is also a more common sequela of ruptured AAA compared with elective aneurysm repair. All aortic aneurysms have some degree of mural thrombus and cholesterol plaque, which have the potential to dislodge and embolize during the course of aortic dissection and clamping. Fresh thrombus can also form in situ in the iliac and femoral arteries in patients who have not been anticoagulated. Diminished back bleeding from the iliac arteries just prior to the completion of the distal anastomosis should prompt Fogarty catheter embolectomy. (See "Embolism to the lower extremities", section on 'Open embolectomy'.)

Distal perfusion should be assessed by palpating the pedal vessels or by using a handheld Doppler prior to removing the surgical drapes and comparing the quality of the pulse or Doppler signal with the preoperative examination. If the distal pulses are absent or diminished by comparison, embolization to the infrainguinal vessels may have occurred, and embolectomy is indicated.

ENDOVASCULAR REPAIR — Endovascular repair of ruptured abdominal aortic aneurysm (AAA) is limited to endovascular centers with a defined program for emergency endovascular surgery. Some centers have adapted an "endovascular aneurysm repair (EVAR) first" approach to ruptured AAA, in which endovascular repair is attempted first and conversion to an open repair is made if the attempted EVAR is not successful [17,26,58,59].

Aortic control and graft placement — Endovascular repair is largely limited to patients who are at least transiently hemodynamically stable and can undergo CT of the abdomen and pelvis prior to consideration for EVAR to determine the anatomic suitability of EVAR. The anatomic requirements for endovascular repair are discussed elsewhere. (See 'Criteria for endovascular repair' above and "Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability'.)

For hemodynamically unstable patients, bleeding from the aortic rupture site can be controlled using an aortic occlusion balloon that is advanced through the femoral access site to the area of aortic rupture and stabilized with a long sheath (figure 1) [49,60-65]. Once the balloon is inflated and the patient has been fluid resuscitated by the anesthesia staff, an aortogram below the level of the aortic occlusion balloon can be performed to evaluate the diameter, length, and morphology of the aorta to determine if endovascular repair is possible if CT scan was not performed. Alternatively, the aorta can be imaged using intravascular ultrasound (IVUS), if available.

Once it has been determined that endovascular repair is appropriate, endograft positioning and deployment proceed in a manner that is similar to elective endovascular aneurysm repair. For infrarenal aortic rupture, the balloon should be repositioned just distal to the renal arteries to preserve renal blood flow while the stent-graft is positioned and deployed. Intermittent deflation of the balloon is required during the course of endograft placement. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Endograft placement'.)

A completion aortogram should be obtained to evaluate for endoleak (figure 3). Although reasonable efforts should be made to minimize the volume of contrast used during the procedure, it is important to get an adequate final study demonstrating that no endoleaks are present. As with elective repair, type I and type III endoleaks are repaired when identified. During elective EVAR, type II endoleak (backbleeding into the aneurysm sac) can be observed initially since the majority will resolve over time. However, following endovascular repair for ruptured AAA, type II endoleak will not tamponade spontaneously, and thus, when type II endoleak is identified, open surgical ligation of the backbleeding vessel may be necessary. (See "Complications of endovascular abdominal aortic repair", section on 'Endoleak'.)

Conversion to open surgery — Conversion from EVAR to open repair is uncommon for elective AAA repair and is, as yet, undefined with ruptured AAA. Conversion of EVAR to open repair is generally associated with higher mortality rates compared with primary open repair. There are no comparable studies for ruptured AAA. In one study of elective EVAR, early conversion to open surgery was associated with a mortality rate of 12.4 percent [66], which contrasts to the approximately 3 percent mortality for the initial open AAA repair [23]. Late conversions had a 10 percent mortality rate [66]. (See "Complications of endovascular abdominal aortic repair", section on 'Conversion to open repair'.)

Early conversion from EVAR to open repair may be needed following EVAR for ruptured AAA for the following reasons:

●Bleeding cannot be controlled with endovascular balloon occlusion

●The graft cannot be positioned or deployed

●Large endoleaks or continued bleeding are evident after graft deployment

When EVAR cannot be accomplished, open repair is performed in the manner described above. (See 'Open surgical repair' above.)

FOLLOW-UP IMAGING — Following aortic repair, imaging of the aorta should be tailored to the clinical needs of the patient. It is common to have some degree of postoperative renal dysfunction following ruptured abdominal aortic aneurysm (AAA), and thus, imaging in the immediate postoperative period using intravenous contrast should be limited to concerns for bleeding or other ongoing abdominal pathology such as intra-abdominal infection or suspected ischemic bowel. Following endovascular aneurysm repair (EVAR), CT should be performed to evaluate the endograft once renal function has stabilized. Thereafter, follow-up is similar to elective aneurysm repair. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Postoperative care' and "Open surgical repair of abdominal aortic aneurysm", section on 'Follow-up'.)

COMPLICATIONS — Complications of ruptured abdominal aortic aneurysm (AAA) repair are similar to those of elective aneurysm repair, but there is a higher incidence of complications such as myocardial infarction, respiratory failure, and acute kidney injury compared with elective AAA repair [58,67].

Prolonged operating time, increased blood loss, increased fluid administration, and intraoperative hypotension are predictive of postoperative bowel ischemia, which has a nearly 60 percent mortality rate in patients undergoing open ruptured AAA repair [57]. In a systematic review that included 101 studies involving over 50,000 patients, the prevalence of clinically relevant bowel ischemia after repair of ruptured AAA was 10 percent [68]. In one small review, 22 percent of patients had some degree of colonic ischemia following repair of ruptured AAA [69]. (See "Colonic ischemia".)

The risk of abdominal compartment syndrome is also increased in patients with ruptured AAA due to the magnitude of the fluid resuscitation and the volume effect of the retroperitoneal hematoma. Abdominal compartment syndrome can occur as a sequela of open or endovascular repair of ruptured AAA. In a systematic review of endovascular repair of ruptured AAA, the pooled incidence was 8 percent [70]. Importantly, the incidence was similar for open surgical repair and endovascular repair (6.8 and 6.9 percent, respectively, in one review [71]). Following open surgical repair, prophylactic open abdomen may be selected. For those in whom the abdomen is closed, routine measurement of bladder pressure and peak inspiratory pressures following repair of ruptured AAA is advocated. The diagnosis and management of abdominal compartment syndrome and the open abdomen are discussed in detail elsewhere. (See "Abdominal compartment syndrome in adults", section on 'Measurement of intra-abdominal pressure'.)

Late complications such as aortic graft infection, aortoenteric fistula, and graft occlusion do not appear to be significantly different between ruptured and elective aneurysm repair in the short term to mid-term [72]. In a meta-analysis of midterm results of several ruptured AAA trials, there were no differences in overall intervention rates, but endovascular repair patients were more likely to have interventions for life-threatening complications, whereas open repair patients were more likely to have amputations [73]. (See "Complications of endovascular abdominal aortic repair".)

MORTALITY — With improvements in prehospital care, cardiovascular anesthesia, and critical care, postoperative mortality following repair of ruptured abdominal aortic aneurysm (AAA) remains high, but has improved with time [28,74-79]. Mortality after repair was near 50 percent prior to 2000 [76], and has been reported to be closer to 30 percent in an analysis using the National Surgical Quality Improvement Program (NSQIP) database [79]. The mortality associated with ruptured AAA may be as high as 90 percent when patients who die at home or upon arrival to the hospital are taken into account [77].

Factors that decrease survival during open surgical repair of ruptured AAA include supraceliac aortic clamping >30 minutes, volume of blood administered >3500 mL, intraoperative urine output <200 mL, thrombosis of other vascular beds, and intraoperative hypotension [38,54]. Endovascular aneurysm repair (EVAR) has the potential to minimize these variable complications and may improve survival following ruptured AAA, but this has not been definitively established. In one review, open surgery was an independent risk for perioperative (30 day) death compared with endovascular repair for both hemodynamically unstable patients (odds ratio [OR] 1.74, 95% CI 1.16-2.62) and hemodynamically stable patients (OR 1.64, 95% CI 1.10-2.43) [80]. (See 'Open surgical versus endovascular repair' above.)

Long-term (five-year) survival following repair of ruptured AAA is 41 to 64 percent, in contrast to survival rates following elective repair, which range from 65 to 74 percent [54,81-83]. Factors associated with poor long-term survival include advancing age, renal dysfunction, respiratory failure, and myocardial infarction.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic and other peripheral aneurysms".)

SUMMARY AND RECOMMENDATIONS

●Ruptured abdominal aortic aneurysm – Rupture is a fatal complication of abdominal aortic aneurysm (AAA) without treatment. With improvements in prehospital, operative, and postoperative care, overall mortality following repair of ruptured AAA has improved but remains high with mortality rates about 30 percent. It is estimated that approximately half of patients with AAA rupture do not get to a hospital for treatment, resulting in an estimated overall survival less than 25 percent. (See 'Introduction' above and 'Mortality' above.)

●Approach to repair – For patients with ruptured AAA, where appropriate facilities, personnel, equipment, and expertise are available for endovascular aneurysm repair (EVAR), we suggest EVAR rather than open AAA repair, provided it is anatomically feasible (Grade 2C). Although significant differences in mortality rates for open compared with endovascular repair for ruptured aneurysm have not been demonstrated in randomized trials, perioperative morbidity for EVAR appears to be lower compared with open repair, although there may be a selection bias in the available studies. (See 'Open surgical versus endovascular repair' above.)

•Endovascular repair is largely limited to patients with ruptured AAA who remain hemodynamically stable, most of whom will have undergone CT to determine the anatomic suitability for EVAR. However, suitability can be determined intraoperatively in hemodynamically unstable patients. An aortic neck diameter more than 32 mm at the renal arteries, or an aortic neck length less than 5 mm, contraindicates endovascular repair. If anatomy is unsuitable, an abdominal incision is made for open surgical repair. (See 'Criteria for endovascular repair' above.)

•Logistical and practical barriers need to be overcome to uniformly offer EVAR for repair of ruptured AAA. Thus, ruptured AAA is often repaired with open surgical techniques, particularly in smaller hospitals, due to the lower number of centers capable of performing urgent or emergency EVAR.

•For hemodynamically stable patients with ruptured AAA, particularly those who are poor candidates for open surgical repair, transfer to a vascular center is appropriate for possible EVAR, and for the recognized benefits of repair of ruptured AAA when performed at a tertiary center. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Decision for patient transfer'.)

●Techniques – Repair of ruptured AAA using an open or endovascular approach is similar to elective AAA repair with modifications in technique that reflect the urgency of the repair and the pathophysiology of rupture.

•If endovascular repair is feasible, endograft positioning and deployment proceeds in a manner that is like elective endovascular aneurysm repair. Surgical preparation should include the possibility for open repair. (See 'Endovascular repair' above.)

•During open repair of ruptured AAA in patients with retroperitoneal hematoma that obscures the proximal infrarenal aorta, we suggest placement of a supraceliac clamp rather than opening the hematoma to place an infrarenal clamp (Grade 2C). Opening the hematoma without adequate vascular control can result in hemorrhage that may be difficult to control. (See 'Open surgical repair' above.)

●Complications – Complications of ruptured AAA repair are similar to those occurring after elective aneurysm repair, but there is a higher incidence of complications such as myocardial infarction, respiratory failure, bowel ischemia, peripheral ischemia, and acute kidney injury. (See 'Complications' above.)