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Complications of endovascular abdominal aortic repair

Complications of endovascular abdominal aortic repair
Literature review current through: Jan 2024.
This topic last updated: Mar 09, 2022.

INTRODUCTION — Endovascular grafts are used to exclude the native aortic (figure 1) and iliac artery (figure 2) wall from blood flow and pressure and in the abdominal aorta are used primarily for the management of abdominal aortic aneurysm (AAA). Endovascular repair involves the insertion of endovascular graft components, usually via a femoral artery approach. The endovascular graft is constructed by the delivery and deployment of these components in vivo.

The technical success rate for abdominal aortic endografting is high, and the overall rate of systemic perioperative complications is lower for endovascular compared with open surgical repair of the abdominal aorta. However, the endograft remains a dynamic entity, and late graft-related complications are likely.

The complications associated with abdominal aortic endografting are reviewed. The indications for abdominal aortic endografts, technical aspects of endograft placement, and specific endografts devised are discussed elsewhere. (See "Management of asymptomatic abdominal aortic aneurysm" and "Endovascular repair of abdominal aortic aneurysm" and "Endovascular devices for abdominal aortic repair".)

ENDOGRAFT-RELATED COMPLICATIONS — Complications associated with endovascular abdominal aortic repair are usually related to some technical aspect of endograft placement. Technical complications associated with endografts include vascular injury (eg, iliac, femoral) during access or device deployment; endoleak from inadequate fixation, sealing of the graft to the vessel wall, or breakdown of the graft material; stent fractures; component separations; and endograft collapse. Some reported endograft complications are device specific and have led to device modifications by manufacturers and, in some cases, to public health notifications in the United States and the United Kingdom and withdrawal of several devices from the market [1,2]. (See "Endovascular devices for abdominal aortic repair", section on 'Withdrawn/investigational devices'.)

Incidence and associated factors — Although the technical success rate for abdominal aortic endografting is high (99 percent), endograft-related complications are common, with an incidence that ranges from 11 to 30 percent [3-9]. In an analysis of 22,830 matched Medicare beneficiaries who underwent endovascular or open AAA repair, reintervention related to the aneurysm repair was significantly more likely with endovascular compared with open repair (9 versus 1.7 percent) [10].

The incidence of complications appears to be higher with larger-diameter aneurysms [11] but also depends upon many factors, including anatomic suitability for endograft placement, graft choice, and proper measurement for the specific device chosen. The importance of strict adherence to anatomic suitability in preventing complications during endovascular repair of abdominal aortic aneurysm (EVAR) was evaluated in a series of 10,228 patients treated with a variety of endografts who underwent pre-EVAR and at least one post-EVAR computed tomography scan [12]. This multicenter observational study found a low compliance with manufacturer's instructions for device use and a high rate of post-EVAR aneurysm sac enlargement, raising concern for an increased long-term risk of aneurysm rupture when adherence to device-specific criteria is not strict. The manufacturer's most conservative indications for anatomic suitability were met in 42 percent of patients, but 31 percent did not meet the manufacturer's most liberal criteria. The rate of aortic sac enlargement was 41 percent at five-year follow-up. Independent predictors of AAA sac enlargement included endoleak, age ≥80 years, aortic neck diameter ≥28 mm, aortic neck angle >60°, and common iliac artery diameter >20 mm. Anatomic suitability and endograft choice are discussed elsewhere. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability' and "Endovascular devices for abdominal aortic repair", section on 'Choice of device'.)

Timing of complications — Endograft-related complications occur with varying frequency and timing relative to endograft placement. Endograft-related complications rarely lead to a need to convert to open surgery at the time of placement and, when they occur late, can usually be managed using endovascular means [13]. Endograft-related complications are the main reason for reintervention (including late conversion), which is required in up to 30 percent of patients. The overall incidence of conversion is approximately 2 percent [14].

Immediate — Immediate problems during endograft placement are common and are often not predictable. In most cases, these issues are corrected at the initial procedure and initial technical success rates are high, typically approximately 99 percent. In a survey that included data from 1696 procedures from 11 centers, between 2.7 and 69 percent of cases were reported to have immediate technical issues [15]. Problems related to insertion of the delivery system were the most common, occurring in 7.7 percent of patients. Arterial rupture (eg, aorta, iliac artery) occurred in 0.7 percent and arterial dissection in 0.9 percent. Problems related to endograft deployment occurred in approximately 0.4 percent of patients, and retrieval was a problem in another 0.4 percent. Visceral vessels were unintentionally covered in 0.8 percent, and the hypogastric artery required exclusion in 2.7 percent, despite efforts to preserve it. Atheroembolism occurred in 0.5 percent. Lower limb ischemia was due to graft limb kinks in 0.7 percent and to graft limb occlusion in 0.9 percent.

The risk of systemic perioperative complications increases with more complex endovascular repairs. Ischemic complications are often related to embolism but may also be due to positioning the endograft and can affect the extremities, intestine, pelvic organs, spinal cord, or kidneys. Renal insufficiency can also be caused by the administration of intravenous contrast (eg, allergic reaction, contrast-induced nephropathy).

Delayed — Following endovascular aortic aneurysm repair, the aneurysm sac typically thromboses, and approximately 50 percent of aneurysm sacs have decreased in diameter at one-year follow-up. However, the endograft remains a dynamic entity and may respond to the new mechanical stresses and the changing configuration of the aorta. Late endograft complications develop and require reintervention in up to 30 percent of cases. As examples, changes in the aneurysm sac may lead to endograft angulation, kinking, migration, or thrombosis (image 1 and image 2A-B). EVAR in patients with large-diameter necks also appears to be associated with neck-related adverse events in midterm follow-up [16,17]. As an example, in a series of 118 patients who underwent EVAR for AAA with large (≥28 mm) infrarenal neck, there was significant infrarenal aortic neck enlargement at 24 months as well as proximal type I endoleak and proximal neck-related reintervention [16]. (See 'Device migration' below.)

Changes in endograft configuration can be detected with abdominal plain films or surveillance duplex ultrasound. The identification of any abnormalities should prompt follow-up evaluation with computed tomography [18-20]. The importance of ongoing surveillance following endograft placement to detect and correct endograft problems cannot be overstressed. Endograft surveillance is discussed in detail elsewhere. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Endograft surveillance'.)

The ability of anatomic criteria to predict future EVAR complications was evaluated in a study using the ENGAGE (Endurant Stent Graft Natural Selection Global Postmarket) registry [21]. Preoperative aneurysm morphology obtained from the database was used to calculate the St George's Vascular Institute (SGVI) score. Freedom from reintervention and freedom from a composite outcome measure of reintervention or endograft complications were significantly higher for patients with a low-risk SGVI score versus a high-risk SVGI score (91 versus 79 percent and 75 versus 66 percent, respectively).

Access site complications — Access site complications are among the most common problems after endovascular aortic repair, occurring in 9 to 16 percent of patients following endovascular AAA repair [15,22]. Access site complications including hematoma, acute thrombosis of the accessed vessel, distal embolization, dissection, pseudoaneurysm, and arteriovenous fistula have all been reported. The management of arteriovenous fistula and acute limb ischemia due to thrombosis, dissection, or embolization is discussed elsewhere. (See "Acquired arteriovenous fistula of the lower extremity".)

Percutaneous access — Percutaneous access for abdominal aortic endografting eliminates the groin incision that is used to access the femoral vessels. Percutaneous access for endovascular repair of the abdominal aorta has become the norm with an improved learning curve in using preclosure techniques as well as the availability of later-generation collagen-based technology designed to close large-bore arteriotomies created by devices with an outer diameter ranging from 12 to 25 F [23].

Early attempts at percutaneous access for endovascular abdominal aortic repair using various techniques were disappointing, but improvements in percutaneous device delivery systems have reduced complication rates [24]. A systematic review identified one randomized trial and seven studies that compared complications associated with percutaneous access with open access. Access-related complications occurred in 4.4 percent of patients, a rate that was significantly lower compared with open femoral access (relative risk [RR] 0.47, 95% CI 0.28-0.78). (See "Endovascular repair of abdominal aortic aneurysm", section on 'Vascular access'.)

Endoleak — Endoleak is defined as persistent flow of blood into the aneurysm sac after device placement and indicates a failure to completely exclude the aneurysm [25]. The types of endoleak (figure 3 and table 1) are discussed in detail separately [26,27]. Following completed endovascular repair, the diagnosis of endoleak is made either with completion arteriography or on follow-up imaging, usually computed tomography (CT), that demonstrates blood outside the bounds of the endograft. For some types of endoleak, the source can be difficult to determine. Color flow duplex or selective arteriography may be needed to establish the diagnosis. Endoleak is associated with a continued risk for aneurysm expansion or rupture. The most common types of endoleak (I and II) are usually managed successfully with the placement of additional stents or embolization techniques, but sometimes open surgery is needed. Type III endoleaks may be more commonly seen with certain endografts and require either relining with another graft or open surgical conversion to prevent rupture [28]. (See "Endoleak following endovascular aortic repair".)

Device migration — Device migration is one of the major causes of secondary intervention after endovascular aneurysm repair [29]. Device migration is due to proximal aortic neck dilation, which may be related to continued aneurysmal degeneration of the aortic wall or possibly a consequence of excessive oversizing of the main body graft diameter. There are no data to suggest that aortic dilation is device dependent [30]. If untreated, potential complications include endoleak, aneurysm expansion, and rupture.

A case series illustrates typical findings. The incidence of migration was evaluated for two different endografts (AneuRx and Zenith) in 130 patients treated for AAA [31]. Migration was defined as caudal movement of the endograft ≥10 mm or any migration distance associated with a related clinical event.

With AneuRx, device migration was identified in 14 of 130 patients. Freedom from device migration was 96, 90, 78, and 72 percent at one, two, three, and four years, respectively. The initial neck length was shorter in patients with migration compared with patients who did not demonstrate migration (22 versus 31 mm). Aortic neck dilation (≥3 mm) occurred in 22 percent of patients. Twelve of the 14 patients underwent 14 secondary procedures (13 endovascular, 1 open conversion).

With Zenith, freedom from device migration (≥10 mm or a clinical event) was 100, 98, 98, and 98 percent at one, two, three, and four years, respectively. The single patient with stent migration did not require treatment.

The authors concluded that careful surveillance for stent migration is an essential component of follow-up in patients receiving stent-grafts. Data regarding stent-graft migration for devices approved for use in the United States (eg, Zenith, Excluder, AFX2, Alto, Endurant, Aorfix, Incraft, Treo) can be found on respective manufacturer websites based on the initial device approval trials (table 2).

In a series of 229 patients who underwent open conversion or major endovascular intervention (relining, cuff/limb extension, parallel graft), failure modes after EVAR differed for various endografts (whether commercially available or not), and the presentation could be delayed [32]. This review and others have noted the important of targeted interrogation of surveillance studies and follow-up schedules by device, even for discontinued devices, as well as ongoing comparisons and estimation of EVAR failure rates [32,33].

Separation of components — Endograft component separation is a consequence of modular endograft design and was more prevalent with earlier-generation endografts. Component separation can be due to inadequate overlap of the components during placement or may be a problem of device integrity. Component separation can also be related to shrinking of the aneurysm sac over time, producing new forces that can pull the iliac limbs apart. Component separation can result in type III endoleak and is important to identify on routine post-EVAR surveillance imaging. Component separation is repaired by using a bridging stent-graft or performing an aorto-uni-iliac conversion [34]. (See 'Endoleak' above and "Endovascular repair of abdominal aortic aneurysm", section on 'Endografts' and "Endoleak following endovascular aortic repair", section on 'Type III endoleak'.)

Limb kinking and occlusion — Endograft limb kinking and occlusion were more commonly seen following endovascular aneurysm repair of AAA (2.3 versus 0.2 percent) compared with open repair in the EVAR trial 1 [35]. In a review of the EUROSTAR registry, postoperative endograft kinking was seen in 3.7 percent of cases and was significantly associated with type I endoleak (table 1), type III endoleak (table 1), graft thrombosis, graft migration, and conversion to open repair [36]. Graft kinking and occlusion can cause acute limb ischemia. (See 'Extremity ischemia' below and "Endoleak following endovascular aortic repair", section on 'Endoleak management after EVAR'.)

Graft limb stenosis or kinking may be diagnosed with duplex ultrasound. One study suggested a peak systolic velocity (PSV) threshold of 300 cm/second [37]. In this study of 479 graft limbs, none of the limbs with PSV <300 cm/sec occluded, whereas 7 out of 17 with PSV >300 cm/second occluded.

Symptomatic patients with kinked grafts that remain patent can usually be treated with additional stenting, whereas an occluded endograft limb will typically require surgical bypass (femorofemoral crossover). Standard mechanical balloon thrombectomy is less likely to be successful with EVAR limb occlusion, but percutaneous catheter-directed thrombolysis followed by stenting can be considered based on the anatomy and clinical presentation.

Postimplantation syndrome — Between 13 and 60 percent of patients experience a transient acute flu-like inflammatory syndrome following aortic endograft placement that can delay the usually quick recovery following EVAR. Factors associated with postimplantation syndrome include new-onset thrombus and possibly the material composition of the stent-graft [38-40].

This acute inflammatory syndrome is characterized by fever, leukocytosis, elevated serum C-reactive protein (CRP) concentration, and perigraft air during the first week to 10 days after implantation [41-45]. Elevated levels of endotoxin, interleukin-6, and platelet activation have also been demonstrated [43,44]; procalcitonin levels were demonstrated in one study to remain low [46]. The etiology of the postimplantation syndrome has not been definitively determined, but it does not appear to be due to infection and is not specific to any particular endograft. When this syndrome accompanies endograft placement, treatment consists of aspirin and surveillance [47]. Antibiotic therapy is not indicated. Whether specific pharmacologic therapy can prevent this syndrome is the subject of ongoing investigation. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Prophylaxis for postimplantation syndrome'.)

Endograft infection — The incidence of endograft infection (image 3) ranges from 0.4 to 3 percent, with associated mortality rates of 25 to 50 percent [48-57]. In one study, 42 percent of patients diagnosed with graft infection presented within three months of aortic endografting, suggesting contamination during endograft placement [49]. In another review, the mean time from endograft placement to diagnosis was 20 months; 6 of the 26 cases presented with aortoenteric fistula [57]. Graft explantation can be challenging and associated with increased morbidity and mortality, and the need for supraceliac clamping during endograft removal was associated with higher mortality compared with infrarenal clamping (71 versus 36 percent).

Treatment strategies for the management of endograft infection are like those used to manage graft infection following open aneurysm repair. Both aggressive and conservative strategies have been applied in the treatment of infected endografts. General considerations for the management of infected aortic aneurysm and infected grafts are discussed elsewhere. (See "Overview of infected (mycotic) arterial aneurysm" and "Aortoenteric fistula: Recognition and management".)

SYSTEMIC COMPLICATIONS — The incidence of systemic complications for endovascular abdominal aortic repair ranges from 3 to 12 percent, including cardiopulmonary complications, ischemic complications, and renal issues, which can be related to intravenous contrast or embolism. Compared with open surgical repair of abdominal aortic aneurysm (AAA), endovascular repair is associated with a lower overall incidence of systemic complications [3,35,58-61].

Complication rates in high-risk patients were evaluated from data taken from the Swedish Vascular Registry from 2000 to 2006 [62]. Patients were defined as high risk for age ≥60 years, American Anesthesiologists Association (ASA) class ≥3, and if at least one comorbidity (cardiac, pulmonary, renal) was present. Using these criteria, 217 of 1000 patients undergoing endovascular aneurysm repair (EVAR) and 483 of 2831 patients undergoing open surgical repair were deemed high risk. EVAR patients were approximately two years older, and renal insufficiency and diabetes mellitus were more common compared with the open surgical patients. Significantly more bleeding complications occurred in the EVAR group, but more pulmonary complications occurred in the open surgical group; there were no differences in cardiac, cerebrovascular, or renal complications at a mean follow-up of 3.4 years.

Older adults and females appear to have at higher risk for complications after endovascular aortic repair. In older patients, the occurrence of in-hospital complications impacts short- and long-term survival, with the greatest reductions on long-term mortality seen with in-hospital renal dysfunction (2.4 percent), blood transfusion (3.4 percent), and the need for reintubation (2.4 percent) [63].

In separate systematic reviews, compared with male sex, female sex was associated with an increased risks for perioperative (30 day) death, limb ischemia, renal complications, cardiac complications, and long-term all-cause mortality following infrarenal EVAR [64,65]. Females also had a higher incidence of transfusion and pulmonary and bowel complications after EVAR.

Cardiopulmonary complications — Patients with AAA are at risk for cardiovascular events such as myocardial infarction, and, based upon established guidelines, patients with AAA are considered to have a coronary heart disease equivalent. Patients with AAA should have their risk factors (ie, blood pressure, lipids) controlled before undertaking AAA repair to reduce the risk for cardiovascular complications [66]. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Medical risk assessment'.)

Cardiovascular events are a common cause of morbidity and mortality following AAA repair. The incidence of perioperative cardiac complications ranges from 1.8 to 5.3 percent [3,58,67]. Significant differences in clinically relevant perioperative cardiac complications are not consistently found when comparing endovascular and open AAA repair [3,67]; however, in one trial, myocardial ischemia (observed by electrocardiogram [ECG] and transesophageal echocardiography [TEE]) was observed less frequently in the endovascular patients (26 versus 53 percent). Randomized trials have not found any significant differences in long-term cardiovascular morbidity and mortality between open surgical and endovascular repair of AAA [3,58,59,68].

The incidence of pulmonary complications with endovascular repair of AAA ranges from 2.9 to 3.3 percent [3,60]. The need for postoperative mechanical ventilation is low following endovascular repair of AAA and in one trial was required in 3.5 percent of patients [3]. In the Dutch Randomized Endovascular Aneurysm Management (DREAM) trial, the risk for pulmonary complications was significantly lower for EVAR compared with open surgical repair of AAA [3].

Older patients, as a subgroup, are more likely to be offered endovascular aneurysm repair. One study that evaluated complication rates in patients >80 years old found that octogenarians had a significantly higher rate of pulmonary complications (5.1 versus 1 percent) compared with patients <80 years of age [69]. In this study, octogenarians more often had a history of chronic obstructive pulmonary disease (44 versus 30 percent), among other medical conditions.

Intravenous contrast complications — Intravenous contrast is required during the placement of endografts to assist in proper endograft positioning and to make certain that no endoleaks are present at the completion of the procedure. Complications associated with intravenous contrast include contrast-induced nephropathy and contrast allergy.

Contrast-induced nephropathy — The incidence of severe renal dysfunction after elective endovascular repair of AAA is 0.7 to 2 percent, which may be related to renal ischemia or the administration of intravenous contrast [3,59,60,70]. (See 'Renal ischemia' below.)

The clinical features, diagnosis, and indications for treatment to prevent contrast-induced nephropathy are discussed in detail elsewhere. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management" and "Prevention of contrast-associated acute kidney injury related to angiography".)

Repeated administration of intravenous contrast agents for endograft surveillance and reintervention to manage technical issues may impair renal function in the long term [71-73]. A retrospective review of 223 consecutive patients compared renal function of 103 endovascular and 120 open surgical patients undergoing AAA repair [71]. Renal function was reduced at 30 days postoperatively in open surgical patients, but at a mean follow-up of 23 months there were no differences in mean glomerular filtration rate between the endovascular and open surgical groups. Deterioration of renal function was seen in both groups over a mean of 24 months and was independently associated with age >70 years for both groups and performance of endovascular compared with open surgical repair. A separate review of patients with preoperative chronic renal insufficiency found that serum creatinine and creatinine clearance were not significantly different between the open and endovascular groups at any time over the study period, which averaged 15.6 and 19.8 months for the endovascular and open groups, respectively [74].

For patients at high risk for contrast nephropathy, the judicious use of dilute contrast along with carbon dioxide (CO2) angiography and intravascular ultrasound can minimize renal injury. In addition, surveillance protocols that reduce or eliminate the need for exposure to intravenous contrast may help reduce the risk for long-term renal dysfunction. (See "Endovascular repair of abdominal aortic aneurysm", section on 'Endograft surveillance'.)

Allergy — Intravenous contrast allergy is rare but should be suspected in patients with prior reactions to iodinated contrast agents. Whether or not to proceed with endovascular repair after contrast reaction is suspected depends upon the clinical presentation. Clinical evidence of significant hemodynamic or respiratory alterations should abort the endovascular repair. Milder reactions such as a rash may allow continuation of the procedure after medicating the patient (eg, antihistamines, glucocorticoids). Intravenous contrast reactions are discussed in detail elsewhere. (See "Allergy evaluation of immediate hypersensitivity reactions to radiocontrast media" and "Diagnosis and treatment of an acute reaction to a radiologic contrast agent" and "Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography", section on 'Patients with past reactions to contrast'.)

Allergy to the metal components of the endograft is rare but should be considered and tested in patients with certain metal allergies. Allergy to nickel, stainless steel, or nitinol is a contraindication to EVAR and may require explantation if diagnosed after device implantation.

Ischemic complications — Ischemic complications are frequent after endovascular aortic repair. One retrospective review of 311 patients reported ischemic complications in 9 percent of patients following endovascular aortic repair [75]. This incidence of ischemia overall exceeds that following open surgical repair and may be driven by endograft limb occlusion. The majority of patients (78 percent) in this review had lower extremity ischemia. Ischemia may also be due to arterial thrombosis, embolism, arterial dissection, or arterial obstruction as a result of the endograft positioning. Ischemia may affect any arterial bed in the immediate vicinity of the endograft or distal to it, including the kidneys, intestines, pelvic muscles or organs, and lower extremities.

It is unclear whether the incidence of ischemic complications has been diminished by the use of low-profile new-generation endografts, and the use of percutaneous EVAR.

Extremity ischemia — Lower extremity ischemia is most often a result of endograft limb occlusion, but other etiologies can also occur. One retrospective review of 311 patients reported lower extremity ischemic complications in 9 percent of patients following endovascular aortic repair [75]. Of the 21 patients with lower extremity ischemia, 70 percent had endograft limb occlusions, 15 percent were due to embolization, and 15 percent had common femoral artery thromboses.

Endograft limb occlusion has been reported in up to 7 percent of patients following endograft placement [75,76]. Most limb occlusions occur within six months after endovascular repair. In one multivariate analysis using ENGAGE registry data, the following factors were associated with graft limb occlusion: placement of the distal end of the device in the external iliac artery, diameter of the external iliac artery <10 mm, maximum diameter of aneurysm <59 mm, correction of endoleak, and presence of stent-graft kinking [76]. Other factors from other studies have included excessive iliac artery tortuosity, endograft oversizing, increased body mass index, and flexibility of the device that is used [77,78]. Nongraft factors that could impact iliac limb patency include worsening occlusive disease in the ipsilateral iliac artery or femoral outflow. (See 'Limb kinking and occlusion' above.)

Endograft limb occlusions manifest as acute limb ischemia in most patents. In the review, acute limb ischemia occurred in 40 percent, rest pain in 20 percent, intermittent claudication in 33 percent, and decreased femoral pulse in 7 percent [75]. Due to the presence of chronic component, endograft limb occlusion cannot usually be managed successfully using interventions commonly used in native vessels or with open aortofemoral grafts, such as mechanical thrombectomy or thrombolysis. Endograft occlusions usually require a cross-over femoral bypass. In this study, limb occlusions were managed with femorofemoral bypass in 47 percent, thrombectomy and stent placement in 27 percent, and expectant management in 20 percent (all with intermittent claudication), and one patient required endograft explantation because of persistent endoleak.

For patients with lower extremity ischemia due to embolization or common femoral artery injury, the presentation is typically acute. The management of acute limb ischemia is discussed elsewhere.

Intestinal ischemia — Intestinal ischemia following endovascular aneurysm repair may affect the small or large intestine. Colonic ischemia is the predominant form of intestinal ischemia and is thought to be related to endograft coverage of the inferior mesenteric artery, particularly in the setting of prior hypogastric embolization, but thromboembolism may also contribute. Colonic ischemia occurs in 1 to 3 percent of patients following endovascular aneurysm repair [75,79-83]. Ischemia in the distribution of the superior mesenteric artery is rare and likely due to atheroembolism or thromboembolism from manipulation of wires and catheters in the suprarenal aorta. The diagnosis and management of mesenteric ischemia is discussed elsewhere. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)" and "Thromboembolism from aortic plaque" and "Overview of intestinal ischemia in adults" and "Colonic ischemia".)

In a later review of 7312 patients undergoing intact or ruptured AAA repair from the Vascular Study Group of New England (VSGNE), the overall incidence of bowel ischemia after intact endovascular AAA repair was 0.6 percent and 6.4 percent after ruptured AAA repair [81]. While the dataset did not distinguish small-bowel ischemia from colonic ischemia, bowel ischemia was presumed to be in the colon. Overall, patients experiencing bowel ischemia had a significantly higher perioperative mortality (intact AAA: 34.6 versus 0.9 percent; ruptured AAA: 30.8 versus 21.1 percent). Risk factors for bowel ischemia included rupture (odds ratio [OR] 6.4, 95% CI 4.5-9.0), which was the most important determinant, followed by open repair (OR 2.9, 95% CI 1.8-4.7). Other factors included advanced age, female sex, hypertension, heart failure, current smoking, unilateral interruption of the hypogastric artery, prolonged operative time, blood loss >1 L, and for open repair, a distal anastomosis to the femoral artery.

Pelvic ischemia — Pelvic ischemia can be a complication of coil embolization of the internal iliac artery (hypogastric artery), a technique that is used to extend the application of endovascular aneurysm repair to those with iliac artery aneurysm or other challenging anatomy. The need for hypogastric embolization is reserved for selected indications, given the availability of approved branched iliac devices, which allow the preservation of pelvic perfusion on long-term follow-up [84]. (See "Surgical and endovascular repair of iliac artery aneurysm", section on 'Internal iliac artery embolization'.)

The incidence and severity of pelvic ischemia related to coil embolization is variable, and its significance is debated [85-91]. Pelvic ischemia can also be due to atheroembolism or thromboembolism despite preservation of the hypogastric arteries.

Buttock claudication or erectile dysfunction occurs in up to 40 percent of patients who have undergone hypogastric artery embolization prior to endovascular repair of abdominal aortic aneurysm. A systematic review identified 18 studies involving 634 patients [92]. Buttock claudication occurred in 31 percent of patients following unilateral embolization and 35 percent after bilateral embolization. New erectile dysfunction occurred in 17 percent of unilateral embolizations and 24 percent of bilateral embolizations. In a separate review involving embolization of 2748 internal iliac arteries in 2671 patients, buttock claudication occurred in 27.9 percent of patients, and erectile dysfunction occurred in 10.2 percent [85]. Buttock claudication rates were 32.6 percent using coils, 23.8 percent with plugs, and 12.9 percent with coverage alone. The incidence of buttock claudication was lower with unilateral compared with bilateral internal iliac artery treatment (26.7 versus 38.3 percent). Coverage only versus coiling, and more proximal treatment, were associated with lower rates of buttock claudication.

Symptoms tend to improve over time but persist in approximately 10 percent of patients. In a systematic review, claudication resolved in 48 percent after 21.8 months [85]. Patients undergoing bilateral hypogastric embolization have a slightly higher incidence of persistent symptoms.

Renal ischemia — Renal ischemia may be due to renal artery embolism, thrombosis, dissection, or impingement of the origin of the renal artery by the endograft [93,94]. The diagnosis and management of renal artery thromboembolism leading to renal infarction are discussed elsewhere. Ischemic renal complications related to the endograft are discussed below. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli" and "Renal infarction".)

The incidence of renal complications following elective endovascular repair of abdominal aortic aneurysm ranges from 0.7 to 18 percent [3,59,60,95]. A retrospective study evaluated acute kidney injury in 6516 patients using the 2002 Nationwide Inpatient Sample (NIS) following endovascular versus open surgical repair of abdominal aortic aneurysm [96]. Postprocedure acute kidney injury developed in 6.7 percent of patients overall. Compared with open surgical repair, endovascular repair was associated with lower risk of acute kidney injury (OR 0.42, 95% CI 0.33-0.53) and lower risk of acute kidney injury requiring dialysis (OR 0.30, 95% CI 0.15-0.63).

Inadvertent coverage of the origin of the renal arteries is most likely to occur with endograft placement in the setting of a short aortic neck. If the kidney is not visualized on completion arteriography, renal salvage can be attempted by repositioning the graft inferiorly. Stenting the occluded renal artery may be possible from a femoral or a brachial approach if the graft cannot be repositioned, but surgical bypass may be needed if renal function deteriorates. The mid-to-distal renal artery often remains patent. (See "Renal artery aneurysm".)

Proximal endograft migration or unrecognized partial renal artery coverage may lead to delayed deterioration in renal function. Although rare, renal artery occlusion has been reported in the first week following endovascular aneurysm repair in spite of a completion aortogram demonstrating patent bilateral renal arteries [97]. A high index of suspicion and urgent intervention are warranted to identify and treat this unusual cause of renal ischemia.

Whether suprarenal fixation is associated with deterioration of renal function has been debated [98]. Suprarenal bare stents may limit endograft migration, particularly in patients with short or flared proximal aortic necks, but a disadvantage may be worsening renal function, particularly in patients with preexisting renal insufficiency. In a study that reviewed 705 patients who underwent endovascular repair of AAA, patients with infrarenal fixation devices were compared with suprarenal fixation devices [99]. Although mean serum creatinine and creatinine clearance did not change in the immediate postoperative period, with longer follow-up, a mild decrease in renal function developed for either type of fixation. There were no significant differences in serum creatinine, creatinine clearance decrease, or incidence of small renal infarcts between the groups. The risk for worsening renal insufficiency and need for dialysis was only slightly but not significantly greater in patients with baseline renal dysfunction compared with patients with normal renal function. Other studies have reported transient renal dysfunction with EVAR using devices with suprarenal fixation, with stabilization or improvement within one to two years postrepair [98,100]. A later review of 3587 patients from the Targeted Vascular Module of the National Surgical Quality Improvement Project compared renal complications between 2263 endografts with suprarenal and 1314 grafts with infrarenal fixation [101]. Suprarenal fixation had a higher risk of renal complications (1.1 versus 0.1 percent) and prolonged length of stay. The authors attributed these complications to deployment techniques or the presence of a bare stent overlying the renal arteries but acknowledged that despite risk adjustment, this may represent a selection bias.

Spinal ischemia — Spinal cord ischemia after EVAR for AAA is very rare [75,102,103]. In the EUROSTAR database, an incidence of 0.21 percent was reported [104]. The incidence of spinal cord ischemia is much lower for endovascular repair of the abdominal aorta compared with the thoracic aorta, for which the incidence can be as high as 12 percent [105].

The mechanism is not completely understood, but atheromatous embolization and interruption of collateral circulation from lumbar and internal iliac arteries together with a variable anatomy of the artery of Adamkiewicz seem to be the most common contributing factors [104].

Abdominal compartment syndrome — Abdominal compartment syndrome refers to organ dysfunction caused by intra-abdominal hypertension. The diagnosis and management of abdominal compartment syndrome and management of the open abdomen are discussed in detail elsewhere. (See "Abdominal compartment syndrome in adults" and "Management of the open abdomen in adults".)

Abdominal compartment syndrome has been reported following both open and endovascular repair of abdominal aortic aneurysm [106]. The risk of abdominal compartment syndrome is increased in patients with ruptured abdominal aortic aneurysm (AAA) due to the extent of fluid resuscitation and the volume effect of the retroperitoneal hematoma. In one study, abdominal compartment syndrome developed in 10 percent of patients following endovascular repair of ruptured abdominal aortic aneurysm [106]. Abdominal compartment syndrome can also theoretically occur following elective endovascular aneurysm repair (EVAR).

CONVERSION TO OPEN REPAIR — Despite advances in endovascular salvage techniques for endograft failures, certain circumstances (eg, persistent endoleak, late rupture) require conversion to open abdominal aneurysm repair.

When open conversion is performed, suprarenal or supraceliac aortic control is often needed depending upon the location of the endograft and whether or not the graft has suprarenal fixation. Replacement of the clamp to an infrarenal position is performed as soon as possible to reduce complications related to intestinal and renal ischemia. Explantation of the endograft, complete or partial, with in situ aortic replacement is performed. The degree to which the graft is adherent to surrounding structures determines if complete or partial removal of the endograft is undertaken. Portions of the graft that are adherent to surrounding structures are best left in place. A poorly adherent graft may be infected.

The perioperative morbidity and mortality associated with conversion of endovascular to open abdominal aortic aneurysm (AAA) repair appears to be increased in both the emergency and elective setting, particularly if the patient was originally deemed high risk for open surgery. In retrospective reviews, the mortality rate for open conversion is 10 to 13 percent [55,107,108]. In a review of the National Surgical Quality Improvement Program, 300 patients underwent open conversion, which was associated with a significantly higher 30-day mortality compared with standard open repair (10.0 versus 4.2 percent; odds ratio [OR] 2.4, 95% CI 1.6-3.6) and endovascular aneurysm repair (EVAR; 10.0 versus 1.7 percent; OR 7.2, 95% CI 4.8-10.9). Conversion surgery also increased risk for any complication compared with open surgery (OR 1.5, 95% CI 1.2-1.9) or EVAR (OR 7.8, 95% CI 6.1-9.9) [108]. However, others have reported lower mortality rates comparable to open AAA repair [109].

The mortality rates for emergency conversion related to ruptured aneurysm were similar to open repair of ruptured AAA not related to endograft conversion at approximately 50 percent [107]. In addition, the outcomes and mortality for patients undergoing nonelective EVAR conversion were compared to nonelective primary aortic repair in the Vascular Quality Initiative (VQI). Urgent/emergency EVAR conversion was found to have a significantly higher risk of 30 day mortality compared with nonelective primary aortic repair (37 versus 24 percent) [110].

Open conversion is performed using standard open aneurysm surgical techniques via a transperitoneal or retroperitoneal approach. (See "Open surgical repair of abdominal aortic aneurysm".)

Early — Open conversion during the initial endograft placement is rare but may be needed if a type I endoleak (table 1) cannot be resolved by endovascular means. (See 'Endoleak' above and "Endovascular repair of abdominal aortic aneurysm", section on 'Handling immediate endoleak' and "Endoleak following endovascular aortic repair", section on 'Etiology and classification'.)

In a systematic review, the overall rate of early (<30 days) conversion among 12,235 endovascular abdominal aortic aneurysm repairs was 1.5 percent, ranging from 0.3 to 5.9 percent [14]. The overall mortality associated with early conversion was 12.4 percent, ranging from 0 to 29 percent.

Late — The etiologies and outcomes of late conversion from endograft to open surgical repair are reported in retrospective reviews [14,55,107,109]. In one systematic review, the overall incidence of late conversion in 14,289 patients who underwent endovascular repair of AAA was 1.9 percent, ranging from 0.4 to 22 percent [14]. The overall mortality of late conversion was 10 percent. One study found that the need for reintervention increased the risk for late conversion by a factor of 16 [107].

The indications for conversion included the following (in descending order of frequency), in a study that followed patients over a seven-year period [109]:

Type I endoleak (table 1)

Graft migration with aneurysm expansion

New aneurysm in the visceral segment

Type II endoleak (table 1) with aneurysm expansion

Aortic rupture

Aortic infection

No endograft is immune, and late conversions have been reported for approved (table 2) or discontinued devices. (See "Endovascular devices for abdominal aortic repair", section on 'Withdrawn/recalled devices'.)

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

Endovascular repair and timing of complications Endovascular grafts are predominantly used to treat infrarenal abdominal aortic aneurysm (AAA). Complications associated with endovascular abdominal aortic repair are commonly related to some technical aspect of endograft placement. Immediate graft-related complications are managed when they are identified. However, the endograft remains a dynamic entity, and late endograft-related complications can occur. Compared with open surgical repair, the overall incidence of severe perioperative systemic complications is generally lower. (See 'Introduction' above and 'Incidence and associated factors' above.)

Endograft complications – Endograft-related complications are common, occurring in 16 to 30 percent of patients following endovascular repair of AAA. Technical complications associated with endografts include vascular injury during access or device deployment; endoleak from inadequate fixation, poor sealing of the graft to the vessel wall, or breakdown of the graft material; stent fractures; component separations; and endograft kinking or collapse. These problems occur with varying frequency and timing relative to endograft placement. Their occurrence depends upon many factors, including anatomic suitability for endograft placement and proper measurements for the chosen device. (See 'Endograft-related complications' above.)

Endoleak – Endoleak is a term that describes the presence of persistent flow of blood into the aneurysm sac after endograft placement. Endoleaks are associated with a continued risk for aneurysm expansion or rupture. Five types of endoleaks (figure 3 and table 1) are described. The diagnosis and management of endoleak is reviewed separately. (See 'Endoleak' above and "Endoleak following endovascular aortic repair".)

Endograft infection – Endograft infection is an uncommon complication of abdominal aortic aneurysm repair and has been reported with an incidence that ranges from 0.4 to 3 percent following endovascular repair. As with infected aneurysm or graft infection associated with open surgical repair of abdominal aortic aneurysm, the mortality rate is high at approximately 25 percent. (See 'Endograft infection' above.)

Systemic complications – The incidence of systemic complications (cardiopulmonary, ischemia-related, renal) following endovascular aneurysm repair ranges from 3 to 12 percent, which is lower than open surgical repair of AAA. (See 'Systemic complications' above and 'Intravenous contrast complications' above.)

Other complications – Other complications related to endovascular repair of abdominal aortic aneurysm include abdominal compartment syndrome and postimplantation syndrome. Abdominal compartment syndrome is more likely following endovascular repair of ruptured abdominal aortic aneurysm but can theoretically occur following elective aneurysm repair. Postimplantation syndrome was a transient condition of unknown etiology associated with earlier endografts. (See 'Abdominal compartment syndrome' above and 'Postimplantation syndrome' above.)

Conversion to open surgery (early, late) – Despite advances in endovascular salvage techniques for endograft complications, some circumstances require conversion to open repair. The overall incidence of conversion (early or late) is approximately 2 percent. Elective open surgical conversion following failed endovascular repair may be associated with increased morbidity and mortality, particularly if the patient was deemed at high risk for open surgery, but some studies have reported mortality rates comparable to open AAA repair. (See 'Conversion to open repair' above.)

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Topic 16918 Version 20.0

References

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