Complications
Rates of abdominal compartment syndrome (ACS) are estimated at about 20% after open repair of ruptured AAA.[3] A small retrospective review reported ACS in 34% of patients following open repair of ruptured AAA and 21% after endovascular aneurysm repair (EVAR).[262] A nationwide population-based study (Swedish Vascular Registry) found that after ruptured AAA repair, ACS developed in 6.8% following open repair compared with 6.9% after EVAR.[263] A systematic review of 46 studies, including 3064 patients, showed that the ACS affects an approximated 9% of patients following EVAR for ruptured AAA.[264] ACS is associated with significant increases in perioperative mortality.[264] All patients should be assessed for ACS if their condition does not improve after EVAR or open surgical repair of a ruptured AAA.[78] Patients with abdominal compartment syndrome after open or endovascular treatment of a ruptured AAA should be treated with decompressive laparotomy.[3]
Ileus has been reported in 11% of patients, with intestinal obstruction and colitis each occurring in 1% of patients undergoing open repair.[259][265] One review reported a prevalence of clinically relevant bowel ischemia of approximately 10% following surgery for ruptured AAA.[266] If colonic ischemia is suspected in patients undergoing open or endovascular treatment for AAA, flexible sigmoidoscopy should be considered to confirm the diagnosis.[3]
Ischemic colitis requiring colectomy is rare.
Following EVAR and open repair of AAA, there is a significant incidence of acute kidney injury (AKI).[267][268][269] In open repair, this seems to be transient. However, following EVAR the causes are multifactorial, and decline in renal function is significantly greater (especially with suprarenal fixation) than in open surgery.[270][271] AKI following EVAR is associated with medium-term increased morbidity and mortality.[267] A strategy to preserve renal function by dose reduction of iodine contrast media, withdrawal of nephrotoxic drugs and ensuring adequate hydration should be considered in patients undergoing EVAR of a complex AAA.[3] Preservation of large accessory renal arteries (4 mm) should also be considered.[3] Interventions that have been shown in studies to have some potential benefit at reducing the incidence of AKI after AAA repair include mannitol, antioxidant supplements, an extraperitoneal approach for open repairs, and human atrial natriuretic peptide.[272]
Postimplantation syndrome is a poorly understood complication of EVAR, which occurs in the early postoperative period and may last for up to 10 days following EVAR.[273] Fever, malaise, and back pain, which may be due to cytokine release, are typical. Early major cardiovascular events have been reported to be more common in patients who develop postimplantation syndrome, although one study reported that postimplantation syndrome was not associated with a statistically significantly higher risk of cardiovascular events and had no impact on mortality.[273][274]
Rates of amputation due to limb ischemia were very low (0.1% at 30 days) in a large series of patients (n = 1135) who underwent open repair.[259] Patients with new onset or worsening of lower limb ischemia should be evaluated immediately for graft related problems, such as limb kinking or occlusion.[3]
Spinal cord ischemia is rare after EVAR, with an incidence in the EUROSTAR collaborators registry of 0.21%.[275] In a retrospective analysis of emergency endovascular treatment for ruptured AAA, 4 of 35 patients (11.5%) developed spinal cord ischemia postoperatively.[276] Delayed spinal cord ischemia (developing 2 days after EVAR) has been reported.[277] Increased operative time, intravascular handling, and difficult anatomy all contribute to an increased risk of spinal cord ischemia.[278] Early recognition is essential, with treatment including spinal drains and administration of steroids. Only 25% of cases will recover, with 25% showing some improvement, and 50% no improvement.[278]
Damage to the autonomic nerves (present at the aorto-iliac bifurcation) during dissection in open repair, as well as reduction in pelvic blood supply, can result in impotence and retrograde ejaculation. EVAR can also result in significant erectile dysfunction, mainly due to internal iliac artery (IIA) occlusion. Studies comparing rates of erectile dysfunction after open repair versus EVAR have shown inconsistent findings. One review estimated incidence of new erectile dysfunction of between 20% and 83% in the first year after open repair (variation depended on trial type).[279] The estimated incidence of new erectile dysfunction was no greater than 14.3% following endovascular repair (and was worse after bilateral rather than unilateral IIA occlusion). However, one prospective single center study found no statistically significant difference in de novo erectile dysfunction between open repair and EVAR groups.[280] 27% of the patients reported erectile dysfunction before open repair increasing to 53% one year after surgery. The corresponding frequencies after EVAR were 43% and 59% respectively.[3][280] For patients treated for AAA who are distressed by postoperative new onset sexual dysfunction, referral to specialized teams should be considered.[3]
One case series reported para-anastomotic aneurysms in 10% of patients after aortic bypass grafting.[281] The rate of femoral anastomotic pseudoaneurysm may be as high as 20% at 10 years after aortobifemoral reconstruction for AAA.[282] Infection should be considered as an underlying cause of para-anastomotic aneurysm.[3] Graft infection may be the underlying cause of secondary aneurysm formation, particularly within the first years after repair.[3] For patients with noninfectious aorto-iliac para-anastomotic aneurysm formation after previous AAA repair, endovascular repair should be considered preferentially.[3]
Aortic neck dilation occurred in 24.6% of EVAR patients during 15 months to 9 years of follow-up.[182] A composite clinical event of endoleak, migration, and reintervention was significantly more common in this group than in those patients without aortic neck dilation.
Can result from infection during implantation, or hematogenous seeding following dental procedures or endoscopic procedures with biopsy. Incidence is low: a retrospective cohort study found that the 2-year rate of graft infection was 0.19% following open repair versus 0.16% with EVAR.[283] Surgical removal of the infected endograft is the optimum treatment; there is a high mortality rate with medical management alone.[3][284]
Ureteric obstruction is related to encasement of the ureters in an inflammatory perianeurysmal fibrosis of unresolved etiology, rather than secondary to aneurysm compression.[285] Most often, ureteral compression is associated with inflammatory aortic aneurysm. Extensive retroperitoneal adhesions may result in ureteral obstruction in 18% of patients. The inferior vena cava may become involved.[286]
Duodenal obstruction is a consequence of compression of the duodenum in its fixed retroperitoneal course between the aneurysmal aorta and the superior mesenteric artery.[285]
The incidence of graft limb occlusion up to 10 years after open AAA repair has been reported as being between 2.6% and 3.0%.[287][288] The risk of graft occlusion is greater with EVAR, with a reported incidence of up to 7.2% in follow-up studies.[289] Kinking is a risk factor for graft limb occlusion following EVAR.[290]
Incidence is 3% to 29%, most commonly affecting the digits (blue toe syndrome). There is a 5% incidence of distal embolization resulting in limb-threatening ischemia, digital ischemia, and calf myonecrosis.[291]
Patients with aneurysmal disease have a high prevalence of abdominal wall hernias and 11% to 37% have postoperative incisional hernias following abdominal surgery.[292] Mesh augmentation during closure of the incision for open AAA repair can help reduce the occurrence of incisional hernias.[3][292]
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