Abdominal aortic aneurysm

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Patients presenting with a ruptured aneurysm require emergent repair.

For patients with symptomatic aortic aneurysms, repair is indicated regardless of diameter.[5][78]

For asymptomatic AAA detected as an incidental finding, surveillance is preferred to repair until the theoretical risk of rupture exceeds the estimated risk of operative mortality. Generally, repair is indicated in patients with large asymptomatic AAA (e.g., with a diameter exceeding 5.5 cm in men or 5.0 cm in women in the US, although treatment decisions based on greater size may differ in other countries).[1][5][76][78][103][104][105][106]

Repair of asymptomatic, symptomatic, and ruptured aneurysms can be accomplished using either an endovascular or open surgical technique; the selection of surgical technique should take account of patient preference, patient age, sex, perioperative risk factors, and anatomic factors. A shared decision making approach taking into account the risks and benefits of the procedures is recommended.[5]

Ruptured AAA

Patients with the triad of abdominal and/or back pain, pulsatile abdominal mass, and hypotension warrant immediate resuscitation and surgical evaluation as repair offers the only potential cure.[76][107] However, most patients with rupture will not survive to reach the operating suite.[Figure caption and citation for the preceding image starts]: Computed tomography scan of a ruptured AAAUniversity of Michigan, specifically the cases of Dr G.R. Upchurch reflecting the Departments of Vascular Surgery and Radiology [Citation ends]. com.bmj.content.model.Caption@3716b368

The American College of Cardiology/American Heart Association (ACC/AHA) recommend computed tomography (CT) imaging in patients presenting with ruptured AAA who are hemodynamically stable to evaluate whether the AAA is amenable to endovascular repair.[5] This recommendation is supported by results from the IMPROVE multicenter randomized controlled trial, which suggest that for most patients, confirmatory CT did not add significant delays to treatment and facilitated appropriate preoperative planning.[108]

If the anatomy is suitable, the ACC/AHA recommend endovascular repair over open repair to reduce the risk of morbidity and mortality.[5]

In patients with confirmed ruptured AAA, 3-year mortality was lower among those randomized to endovascular aneurysm repair (EVAR) than to an open repair strategy (48% vs. 56%; hazard ratio [HR] 0.57, 95% CI 0.36 to 0.90).[109]
The difference between treatment groups was no longer evident after 7 years of follow-up (HR 0.92, 95% CI 0.75 to 1.13). Re-intervention rates were not significantly different between the randomized groups at 3 years (HR 1.02, 95% CI 0.79 to 1.32).[109]
There is some evidence to suggest that an endovascular strategy for repair of ruptured AAA may reduce mortality more effectively in women than in men.[109][110]

There is some evidence to suggest that mode of anesthesia for operative repair of AAA affects outcomes.[5][111] In 2024, the European Society for Vascular Surgery (ESVS) issued a weak recommendation favoring local anesthesia over general anesthesia in elective settings, based on potential reduction in procedure time, ICU admissions, and postoperative hospital stay.[3][112][113][114]

The IMPROVE (Immediate Management of Patients with Rupture: Open Versus Endovascular Repair) multicenter randomized controlled trial detected a significantly reduced 30-day mortality in patients who had EVAR under local anesthesia alone compared with general anesthesia (adjusted OR 0.27, 0.1 to 0.7).[108]
A separate meta-analysis comparing mode of anesthesia for endovascular repair of ruptured AAA replicated these findings or improved outcomes with EVAR under local anesthesia.[115] However, another systematic review did not show any mortality benefit with local anesthesia, but did demonstrate shorter hospital stays.[116]
Data from the UK’s National Vascular Registry (9783 patients who received an elective, standard infrarenal EVAR; general anesthetic, n = 7069; regional anesthetic, n = 2347; local anesthetic, n = 367) showed a lower 30 day mortality rate after regional versus general anesthesia.[117]
The international multicenter Endurant Stent Graft Natural Selection Global Post-Market Registry (ENGAGE) study examined the outcomes of 1231 patients undergoing EVAR under general (62% of patients), regional (27%), and local (11%) anesthesia.[118] The type of anesthesia had no influence on perioperative mortality or morbidity but the use of local or regional anesthesia during EVAR appeared to be beneficial in decreasing procedure time, need for ICU admission, and duration of postoperative hospital stay.[118]

Supportive treatment of ruptured AAA

Standard resuscitation measures should be initiated immediately. These include:

Airway management (supplemental oxygen or endotracheal intubation and assisted ventilation if the patient is unconscious).
Intravenous access (central venous catheter).
Arterial catheter; urinary catheter.
Hypotensive resuscitation: aggressive fluid replacement may cause dilutional and hypothermic coagulopathy and secondary clot disruption from increased blood flow, increased perfusion pressure, and decreased blood viscosity, thereby exacerbating bleeding.[119][120] A target systolic blood pressure (SBP) of 50 to 70 mmHg and withholding fluids is advocated preoperatively.[119][120] The ACC/AHA guidelines recommend permissive hypotension to reduce bleeding.[5] However, recommended targets vary and there is no consensus among global guideline groups.
- The IMPROVE multicenter randomized controlled trial found that lowest SBP was significantly and independently associated with 30-day mortality in patients with ruptured AAA, and that a target SBP below 70 mmHg in older patients may have contributed to worse outcomes.[108] In people with ruptured AAA with a recorded preoperative SBP less than 70 mmHg, mortality at 30 days was higher (51.0%) compared with those with SBP above 70 mmHg (34.1%).[108]
- One Cochrane review of controlled (permissive) hypotension versus normotensive resuscitative strategy for people with ruptured AAA, which included the IMPROVE trial, noted that people with ruptured AAA are usually older and more likely to have coronary and renal atherosclerotic disease. These patients are also at greater risk of myocardial infarction and renal insufficiency if submitted to low SBP levels compared with younger people with trauma.[121]
Blood product (packed red cells, platelets, and fresh frozen plasma) availability and transfusion for resuscitation, severe anemia, and coagulopathy.
Notifying anesthetic, intensive care unit (ICU), and operating teams.

Tracheal intubation: animated demonstration

How to insert a tracheal tube in an adult using a laryngoscope.

Bag-valve-mask ventilation: animated demonstration

How to use bag-valve-mask apparatus to deliver ventilatory support to adults. Video demonstrates the two-person technique.

Symptomatic but not ruptured AAA

In patients with symptomatic aortic aneurysm, urgent repair is indicated regardless of diameter.[5][78][102] The development of new or worsening pain may herald aneurysm expansion and impending rupture. Symptomatic, nonruptured aneurysm is, therefore, best treated urgently.[76] Under some circumstances, intervention may be delayed for several hours to optimize conditions to ensure successful repair; these patients should be closely monitored in the ICU.[76]

EVAR is increasingly used in the management of patients with symptomatic AAA.[125][126] In observational studies, short-term all-cause mortality rates did not differ between endovascular and open repair of symptomatic AAA.[125][126][127]

Data from the 2011-2013 American College of Surgeons National Surgical Quality Improvement Program suggest that 30-day mortality risk after repair of symptomatic AAA was approximately double that following asymptomatic AAA repair, regardless of surgical approach (EVAR: symptomatic 3.8% vs. asymptomatic 1.4%, P=0.001; open surgery: symptomatic 7.7% vs. asymptomatic 4.3%, P=0.08).[128] Smaller patient numbers likely contribute to the non-statistically significant finding reported for open repair.

Incidental finding of small asymptomatic AAA

For AAA detected as an incidental finding, surveillance is preferred to repair until the theoretical risk of rupture exceeds the estimated risk of operative mortality.[4] Early surgery for the treatment of smaller AAAs does not reduce all-cause or AAA-specific mortality.[4][129] [ ] One systematic review (4 trials, 3314 participants) found high-quality evidence to demonstrate that immediate repair of small AAA (4 cm to 5.5 cm) did not improve long-term survival compared with surveillance (adjusted HR 0.88, 95% CI 0.75 to 1.02, mean follow-up 10 years).[129] The lack of benefit attributable to immediate surgery was consistent regardless of patient age, diameter of small aneurysm, and whether repair was endovascular or open.[129]

Surgical referral of smaller AAA is usually reserved for rapid growth, or once the threshold diameter for aneurysm repair is reached on repeated ultrasonography.[4]

However, in patients with an underlying genetic cause or connective tissue disorder, the threshold diameter for considering repair should be individualized, depending on:[3]

Anatomic features
Underlying genetics: rupture risk is higher at smaller aortic diameters in some conditions, and surgical repair is more challenging in certain disorders owing to the increased arterial wall fragility and anatomy[3]

Medical goals for asymptomatic small aneurysms include:

1. Surveillance:

American College of Cardiology Foundation/American Heart Association guidelines recommend that infra-/juxtarenal AAAs measuring 4.0 to 4.9 cm in diameter by ultrasound/CT should be monitored every 6-12 months.[5] Once larger than 4.5 cm in women and 5 cm in men, these guidelines recommend surveillance every 6 months.[5] AAAs <3.9 cm can be monitored with ultrasound every 2-3 years.[5]
The UK National Health Service recommends that annual screening intervals are employed for 3.0 to 4.4 cm AAAs and 3-month intervals for 4.5 to 5.4 cm AAAs.[130]
One systematic review and meta-analysis of individual patient data concluded that surveillance intervals of 2 years for 3.0 to 4.4 cm AAA, and 6 months for 4.5 to 5.4 cm AAA, are safe and cost-effective.[131]
Analysis of AAA growth and rupture rates indicated that in order to maintain a AAA rupture risk <1%, an 8.5-year surveillance interval is required for men with baseline AAA diameter of 3.0 cm.[131] The corresponding estimated surveillance interval for men with an initial aneurysm diameter of 5.0 cm was 17 months. Despite having similar small aneurysm growth rates, rupture rates were four times higher in women than in men.[131] Surveillance programs and criteria for considering surgery need to be tailored for women with opportunistically detected AAA.
Most AAAs show linear growth; modeling based on this suggests that smaller AAAs (<4.25 cm) could be followed up every 2 years, with minimal chance of exceeding interventional thresholds within that time.[132][133]
Aneurysmal growth of ≥0.5 cm in 6 months may be an indication for repair, to reduce the risk of rupture.[5]
The ESVS recommends incorporation of subaneurysmal aortas (2.5 to 2.9 cm) into AAA surveillance recommendations since long-term cohort studies show that most subaneurysmal aortas eventually progress to an AAA of which a substantial proportion will reach the diameter threshold for consideration of repair.[3] Surveillance decisions should take into account life expectancy, suitability for future repair, and patient preferences.[3]

2. Control of modifiable risk factors for expansion and rupture:

Smoking cessation - nicotine-replacement therapy, nortriptyline, and bupropion, or counseling.[1][5][13][15][22][23][134][135][136] [ ]
Short-term treatment with beta-blockers does not appear to reduce the rate of AAA expansion.[4][137] Trials in which patients with small AAAs were randomized to propranolol, and other beta-blockers, with the intention of reducing the rate of aneurysm expansion failed to demonstrate significant protective effects.[137][138] Propranolol was poorly tolerated in these studies.[138]

3. Aggressive management of other cardiovascular disease:

Modifiable cardiovascular risk factors such as hypertension and hyperlipidemia should be treated.[5][78] Statins should be started at least 1 month before surgery to reduce cardiovascular morbidity and mortality, and continued indefinitely.[3][139]
There is limited evidence, but in the absence of any contraindication, patients with AAA should receive single antiplatelet therapy (aspirin or clopidogrel).[3][5][140]

Incidental finding of large asymptomatic AAA

Generally, repair is indicated in patients with large asymptomatic AAA (e.g., with a diameter exceeding 5.5 cm in men or 5.0 cm in women in the US, although treatment decisions based on greater size may differ in other countries).[5] Repair of aneurysms ≥5.5 cm offers a survival advantage.[1][76][78][104][105][106]

Decisions regarding repair should be individualized, taking account of patient preference, patient age, sex, perioperative risk factors, and anatomic risk factors. Care should be taken to evaluate patient quality of life, and careful counseling undertaken regarding the risks of surgery (e.g., informing patients of their Vascular Quality Initiative perioperative mortality risk score) and subsequent quality of life. A shared decision making approach taking into account the risks and benefits of the procedures is recommended.[5] EVAR should be considered in patients who are unfit for open surgery.[5][76][78][129]

Data suggest that in patients with large AAAs (ranging from 5.0 to 5.5 cm) undergoing elective repair, EVAR is equivalent to open repair in terms of overall survival, although the rate of secondary interventions is higher for EVAR.[141][142] EVAR reduces AAA-related mortality (but not longer-term overall survival) in patients with large AAA (≥5.5 cm) who are unsuitable for open repair.[143] Post-repair, larger AAAs appear to be associated with worse late survival than smaller aneurysms (pooled HR 1.14 per 1-cm increase in AAA diameter, 95% CI 1.09 to 1.18; 12.0- to 91.2-month follow-up).[144] The association is more pronounced with EVAR than with open repair.

Elective repair in asymptomatic patients allows for preoperative assessment, cardiac risk stratification, and medical optimization of other comorbidities. Coronary artery disease remains the leading cause of early and late mortality after AAA repair.

Endovascular aneurysm repair (EVAR)

EVAR involves the transfemoral endoluminal delivery of a covered stent graft into the aorta, thus sealing off the aneurysm wall from systemic pressures, preventing rupture, and allowing for sac shrinkage. The endograft can be deployed percutaneously through low-profile devices, or after exposing the femoral arteries surgically. A Cochrane review found no difference between the techniques after short follow-up (6 months), except that the percutaneous approach may be faster.[145] [ ] Long-term data for the durability of low-profile devices are lacking.[Figure caption and citation for the preceding image starts]: Various endovascular stent grafts used for endovascular aneurysm repair (EVAR)University of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends]. com.bmj.content.model.Caption@6992968b [Figure caption and citation for the preceding image starts]: Endovascular aneurysm repair (EVAR)University of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends].

Assessment of suitability for EVAR should be through the use of 0.5 mm-slice CT angiography.[79] It is essential that the operator is familiar with the specific instructions for use of the endograft to be used.

Lifelong, annual surveillance with ultrasonography or CT is recommended following endovascular repair of AAAs to detect late complications and identify late device failure and disease progression.[3][76]

Open repair

Open repair may be transperitoneal or retroperitoneal. With proximal and distal aortic control obtained, the aneurysm is opened, back-bleeding branch arteries are ligated, and a prosthetic graft is sutured from normal proximal aorta to normal distal aorta (or iliac segments). Once flow is restored to the bilateral iliac arteries, the aneurysm sac is closed over the graft.[146] A retroperitoneal approach should be considered for patients with aneurysmal disease that extends to the juxtarenal and/or visceral aortic segment, or in the presence of an inflammatory aneurysm, horseshoe kidney, or hostile abdomen.[76][147]

Straight tube grafts are recommended for repair in the absence of significant disease of the iliac arteries.[76] The proximal aortic anastomosis should be performed as close to the renal arteries as possible.[76] It is recommended that all portions of an aortic graft should be excluded from direct contact with the intestinal contents of the peritoneal cavity.[76] Re-implantation of a patent inferior mesenteric artery (IMA) should be considered under circumstances that suggest an increased risk of colonic ischemia (i.e., associated celiac or superior mesenteric artery occlusive disease, an enlarged meandering mesenteric artery, a history of prior colon resection, inability to preserve hypogastric perfusion, substantial blood loss or intraoperative hypotension, poor IMA backbleeding when graft open, poor Doppler flow in colonic vessels, or should the colon appear ischemic).[76][148]

Fenestrated EVAR (FEVAR) and branched endografts (bEVAR)

For patients with a complex AAA and standard surgical risk, open or EVAR should be considered based on fitness, anatomy, and patient preference. For patients with a complex AAA and high surgical risk, EVAR with fenestrated and branched technologies should be considered as first-line therapy. Fenestrated and branched endografts have become the treatment of choice of complex AAAs in most high volume centers.[3] These procedures are viable alternatives to open repair for juxtarenal and suprarenal AAA, or for those with AAA where a short or diseased neck precludes conventional repair.[3][149] FEVAR endografts have holes that correspond to the position of branching arteries within the aorta, and permit endovascular repair of complex aneurysms. One pooled analysis of 7 retrospective studies (including 772 patients) suggested favorable mortality and target visceral vessel patency rates of 8.0% and 95.4% at 1 year, respectively.[150] However, other meta-analyses looking at FEVAR for complex aneurysms and juxtarenal abdominal aortic aneurysms (including 7061 patients and 2974 patients respectively) suggest no mortality difference with FEVAR, but a potential increased re-intervention hazard.[151][152] The procedure is performed routinely in some centers.[150][151][153] Branched devices either with inner or outer branches involve more extended aortic coverage compared with fenestrated devices.[3] The ESVS states these should be reserved for type 4 thoracoabdominal aortic aneurysms (these involve entire abdominal aorta from the level of the diaphragm to the aortic bifurcation).[3]

Choice of elective repair

EVAR accounts for more than 70% of all AAA repairs in the US.[154] In the UK, 61% of elective infrarenal AAAs and 89% of complex AAAs were treated with EVAR during 2018-2020.[155] However, not all patients are suitable candidates for EVAR. Guidelines therefore recommend an individualized approach to surgical choice.[5][76][78][156] Factors that will influence the decision include: anatomic determinants (e.g., aneurysm diameter, neck length, neck diameter); life expectancy, sex, comorbidities; and perioperative risk.[157][158] A shared decision making approach taking into account the risks and benefits of the procedures is recommended.[5]

EVAR may be preferred in patients who:

Have high perioperative risk, and
Have anatomy that is congruent with the relevant stent-graft manufacturer's eligibility criteria as determined in the instructions for use, and
Are able to satisfy the mandatory surveillance regimen following surgery.

Patients with lower perioperative risk and favorable anatomy may nonetheless also be candidates for EVAR, but consideration should be given to safety and durability of repair (need for re-intervention), and open repair may be preferred in patients who are relatively younger.[159][160]

Elective repair outcomes

Data regarding the comparative safety and efficacy of EVAR and open repair differ depending on the outcome of interest. Evidence to date suggests that:

Short-term all-cause postoperative mortality (≤30 days) is lower for endovascular than open repair
Long-term (5-10 year) survival is similar among patients who underwent EVAR versus open repair[142][161][162]
Operative, perioperative, and postoperative mortality (≤30 days) is greater among women than men for both open repair and EVAR[163][164]
Overall rates of re-intervention are more common following EVAR than open repair.[165][166][167]

Six-month postoperative mortality appears to be lower among patients with AAA who undergo EVAR than those who have open surgery, but this is primarily attributable to lower 30-day operative mortality.[168] Pooled analysis of data from four high-quality randomized trials (that enrolled patients with AAA diameter >5 cm) found that short-term mortality (30-day or in-hospital mortality) was significantly lower among those randomized to EVAR than among those who underwent open repair (1.4% vs. 4.2%, odds ratio [OR] 0.33, 95% CI 0.20 to 0.55; P <0.0001).[169] However, the early benefit of EVAR is diminished with follow-up.[168][169][170] Open repair was significantly associated with lower all-cause mortality than EVAR, after more than 8 years of follow-up, in data from the UK endovascular aneurysm repair trial 1 (46% vs. 53%, P=0.048) and a further meta-analysis.[171][172] One meta-analysis identified a survival curve crossover point at 1.8 years post repair, whereafter patients undergoing EVAR had lower survival compared with those undergoing open repair.[173]

The same trend is seen in aneurysm-related mortality. One meta-analysis found 3-year aneurysm-related mortality to be significantly higher following EVAR repair than after open repair (pooled hazard ratio [HR] 5.16, 95% CI 1.49 to 17.89; P=0.010).[168] Data from the UK endovascular aneurysm repair trial 1 indicate that, after more than 8 years of follow-up, aneurysm-related mortality is greater among EVAR patients than open repair patients (5% vs. 1%, P=0.0064).[171] Aneurysm rupture was more common in patients after EVAR than open repair (5.4% vs. 1.4%, P <0.001) in a large cohort study with 8 years of follow-up.[174] Another systematic review that included more than 30,000 patients in 22 observational studies found no significant difference in aneurysm-related mortality with EVAR compared with open repair.[175]

Extenuating factors have been proposed to account for the worse late-phase mortality reported in EVAR patients compared with those who undergo open repair. One systematic review concluded that long-term postoperative survival in patients undergoing EVAR had improved in trials published after 2005, and attributed this to a possible improvement in EVAR techniques and perioperative care.[176]

Perioperative and short-term mortality is higher among women than among men.[163][164] During elective AAA repair, operative mortality among women exceeds that of men for both open (7.0% vs. 5.2%) and endovascular approaches (2.1% vs. 1.3%).[177] In the UK, women undergoing elective AAA repair were found to have increased short-term mortality compared with men for open repair (30-day mortality: OR 1.39; 95% CI 1.25 to 1.56) and EVAR (30-day mortality: OR 1.57; 95% CI 1.23 to 2.00), despite having fewer preoperative cardiovascular risk factors.[178] Female sex was an independent risk factor for all-cause mortality among women who had an open repair at 1 year (crude cumulative all-cause mortality 15.9% vs. 12.1%, P <0.001) and at 5 years (22.2% vs. 19.6%, P <0.001).[178] Long-term all-cause survival did not differ significantly between women and men in the EVAR group (P=0.356). One review concluded that the morphological criteria for diagnosing aneurysms and offering EVAR did not take sex-related variations in aortic size into account: women are less likely to be offered intervention because they have smaller aortas.[179]

Overall rates of re-intervention are higher with EVAR than with open surgery; however, rates have been reported heterogeneously in clinical trials.[165][166][168][169] In pooled analysis of individual-patient data, re-intervention was reported in 65.8% of EVAR patients with type I endoleak (79 of 120) and 22.8% of EVAR patients with type II endoleak (99 of 435) over 5 years of follow-up.[168] Observational data suggest that interventions related to the management of aneurysm or its complications are more common following EVAR than open surgery (18.8% vs. 3.7%, P <0.001) over 8 years of follow-up.[174]

Meta-analysis found no significant difference between EVAR and open surgery in the incidence of myocardial death (OR 1.14, 95% CI 0.86 to 1.52; P=0.36), fatal stroke (OR 0.81, 95% CI 0.42 to 1.55; P=0.52), or nonfatal stroke (OR 0.81, 95% CI 0.50 to 1.31; P=0.39).[169] Patients with moderate renal dysfunction or cardiovascular disease do not appear to derive an early survival benefit (to 6 months) from EVAR, while those with peripheral arterial disease may benefit from open repair.[168] In another meta-analysis, long-term survival following elective AAA repair (EVAR or open) was worst among patients with end-stage renal disease (HR 3.15, 95% CI 2.45 to 4.04) and COPD requiring supplementary oxygen (HR 3.05, 95% CI 1.93 to 4.80).[180]

Low-quality evidence from four small randomized controlled trials suggests that elective open repair performed retroperitoneally can reduce blood loss and hospital stay compared with a transperitoneal approach.[181] However, there was no difference in mortality between retroperitoneal and transperitoneal elective open AAA repair (very low-quality evidence). Moreover, the retroperitoneal approach may increase the risk of hematoma, chronic wound pain, and abdominal wall hernia compared with transperitoneal.[181]

Adverse effects

Complications of EVAR may include endoleak, graft occlusion, and graft migration with aortic neck expansion. A systematic review reported aortic neck dilation in 24.6% of EVARs (9439 men included), which led to higher rates of type I endoleak, graft migration, and re-intervention.[182] Such complications are typically detected on completion angiography or postoperative imaging, though studies suggest that intraoperative CT angiography may be a more sensitive method of detecting complications of EVAR.[183]

As an adjunct to EVAR, either unilateral or bilateral internal iliac artery (IIA) occlusion may be acceptable in certain anatomic situations for patients at high risk for open surgical repair. Buttock claudication will occur in 27.9% of patients following IIA occlusion, although this resolves in 48% of cases after an average of 21.8 months. It is less likely to occur following unilateral occlusion (OR 0.57, 95% CI 0.36 to 0.91). Erectile dysfunction occurred in 10% to 14% of men following IIA occlusion.[76][184]

IIA revascularization techniques, involving specialized iliac branch devices, have high technical success rates (up to 97.5%) and are associated with low morbidity (e.g., buttock claudication rate of 2.15% to 4.1%).[185] The effects of IIA occlusion versus IIA revascularization have not been well compared.[186]

In patients with synchronous intra-abdominal malignancy, EVAR reduces mortality and delay between the treatment of the two pathologies despite a significant risk for thrombotic events.[187][188]

Complications of open repair include cardiac and pulmonary events, mesenteric ischemia, renal failure, bleeding, wound and graft infection, spinal cord ischemia/paraplegia, embolization/limb ischemia, and late graft complications (i.e., aorto-enteric fistula and aortic pseudoaneurysm).[1][189]

Perioperative management

Treatment of co-existing cardiac disease:

Cardiovascular risk prevention should be prioritized in patients in AAA screening programs.[78][190]
Noninvasive stress testing should be considered for patients with a history of three or more clinical risk factors (i.e., coronary artery disease, congestive heart failure, stroke, diabetes mellitus, chronic renal insufficiency) and an unknown or poor functional capacity (MET <4) if it will change management.[76]
Coronary revascularization is indicated for those patients who present with acute ST elevation myocardial infarction, unstable angina, or stable angina with left main coronary artery or three-vessel disease, as well as those patients with two-vessel disease that includes the proximal left anterior descending artery and either ischemia on noninvasive testing or an ejection fraction <0.5.[76]

Regarding blood transfusion:[76]

Preoperative autologous blood donation may be beneficial for patients undergoing open aneurysm repair.
Cell salvage or an ultrafiltration device is recommended if large blood loss is anticipated or the risk of disease transmission from banked blood is considered high.
Blood transfusion is recommended if the intraoperative hemoglobin level is <10 g/dL in the presence of ongoing blood loss. Consider use of fresh frozen plasma and platelets in a ratio with packed blood cells of 1:1:1.[3][76][191]

Pulmonary artery catheters should not be used routinely in aortic surgery, unless there is a high risk for a major hemodynamic disturbance.[76] Central venous access is recommended for all patients undergoing open aneurysm repair.[76] Prophylaxis for deep venous thrombosis consisting of intermittent pneumatic compression and early ambulation is recommended for all patients undergoing open repair or EVAR.[76][192]

Avoiding hypothermia during open repair and EVAR can reduce hospital length of stay, length of stay in the ICU, and rates of organ dysfunction.[193]

Preoperative cardiovascular risk reduction:

Addressing modifiable cardiovascular risk factors preoperatively improves long-term survival after AAA repair.[194]
Preoperative exercise training reduced postsurgical cardiac complications in a small randomized controlled trial of patients undergoing open or endovascular AAA repair, though a Cochrane review and a separate systematic review of prehabilitation (exercise training) prior to AAA surgery did not show any outcome benefit.[195][196][197] While preoperative exercise training may be beneficial for patients undergoing AAA repair, further investigation with RCTs is needed before it can be recommended more widely.[198]
Perioperative statin use slows aneurysm growth, reduces risk of rupture, and reduces mortality from AAA repair or ruptured AAA.[5] Statins should be started at least 1 month before surgery to reduce cardiovascular morbidity and mortality, and continued indefinitely.[3][139]
Patients with AAAs are at increased risk of major adverse cardiovascular events. There is limited evidence, but in the absence of any contraindication, patients with AAA should receive single antiplatelet therapy (aspirin or clopidogrel).[5][140] This should be continued during the perioperative period.[3]
Hypertension should be controlled to reduce cardiovascular morbidity and mortality.[3][5]
Initiation of beta blockers is not recommended prior to AAA repair.[3] However, a beta-blocker can be continued if a patient is already taking this at an appropriate dose.[3] Large trials where beta-blockade was started a few days before surgery have indicated no benefit, or even harm, from perioperative beta-blockade.[199][200][201]

Antibiotic cover:

Antibiotic therapy is indicated for patients undergoing elective repair of AAA or emergent repair of ruptured AAA to cover gram-positive and gram-negative organisms (i.e., Staphylococcus aureus, Staphylococcus epidermidis, and enteric gram-negative bacilli) and prevent graft infection.

Broad-spectrum antibiotic coverage is tailored to patient clinical presentation and cultures, and in accordance with local protocols.

Treatment of infectious/inflammatory cause

Once the patient is stable and urgent surgical repair, if indicated, has been prioritized, infectious or inflammatory etiology should be addressed.

Infectious AAA

If the patient has a suspected infectious aneurysm, early diagnosis, prompt treatment with antibiotics and urgent surgical repair is essential to improve outcomes.[3] Open surgical repair has traditionally been considered gold standard for infectious aneurysms, though more recent data suggests that EVAR may be associated with equal or superior outcomes.[3][5][202] Extensive debridement is often needed. There is a high risk of secondary infective complications and further surgery may be needed for new infectious lesions.

Intraoperative cultures should be taken to accurately guide subsequent antibiotic therapy; however, empirical antibiotics are often administered, as peripheral blood cultures and surgical specimen cultures are negative in a large proportion of patients.[5]

Prolonged antibiotic therapy (from 4-6 weeks duration to lifelong) may be indicated depending on the specific pathogen, the type of operative repair, and the patient's immunologic state.[3][5]

Inflammatory AAA

Inflammatory aortitis (caused by, for example, Takayasu arteritis or giant cell arteritis) is treated with high-dose corticosteroids and surgery.[5][203]

Endovascular aneurysm repair (EVAR) leak

Endoleak is persistent blood flow outside the graft and within the aneurysm sac.[204][205] It is not a complication following open repair; it is specific to endovascular aneurysm repair (EVAR).

Postoperative surveillance can detect major endoleaks and aneurysm sac expansion.

Risk of endoleak following EVAR is 24%.[204] There are five types of endoleak.[5]

Type I:

Leak at the attachment site (type IA at the proximal end of the endograft or iliac occluder; type IB at the distal end); usually immediate, but delayed leaks may occur.[Figure caption and citation for the preceding image starts]: Type I endoleak at the distal left iliac anastomosis (leak encircled)University of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends].
Every effort should be made to repair type I endoleak before completing the procedure (e.g., balloon molding of the proximal seal zone, placement of a proximal cuff, endostaples, liquid embolization).[206] Persistent type IA endoleak may necessitate conversion to open repair, provided the surgical risk is acceptable.[3][76][207][Figure caption and citation for the preceding image starts]: Extension stent graft deployed for the same type I endoleak (encircled)University of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends].[Figure caption and citation for the preceding image starts]: Resolution of the type I endoleak resolved after extension deployedUniversity of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends].

Type II:

Patent branch leak.[Figure caption and citation for the preceding image starts]: Type II endoleak (encircled) discovered on follow-up computed tomographyUniversity of Michigan/Dr G.R. Upchurch, Departments of Vascular Surgery and Radiology [Citation ends].

Spontaneous resolution may occur, although persistence may result in sac growth.[208]

If a type II endoleak or other abnormality of concern is observed on contrast-enhanced CT imaging at 1 month after EVAR, postoperative imaging at 6 months is recommended.[76] Around 50% of type II endoleaks are diagnosed before 30 day follow-up; 40% after 30 days, and 8% are diagnosed after 12 months of follow-up.[209]

Treatment remains controversial and is advocated either if persistent at 6-12 months or when aneurysm sac size increases such that proximal and/or distal sealing zones may be compromised.[210][211][212][213][214][215]
Treatment of choice is transarterial coil embolization, although laparoscopic ligation of collateral branches, direct percutaneous translumbar puncture of the sac, translumbar embolization, and transcatheter transcaval embolization have been reported.[205][210][211][212][216][217][218][219][220][221][222][223][224]

Type III:

Graft defect with leak through fabric tears, graft disconnection, or disintegration of the fabric.[204][205][225]
Repair is indicated upon discovery (endovascular stent graft extension).[3][76][211][215][226]

Type IV:

Leak from graft wall porosity.[204][205]
These leaks are uncommon with newer stent grafts and are self-limited.[76][211]

Type V (endotension):

Endotension is increased intrasac pressure after EVAR without visualized endoleak on delayed contrast CT scans.
Endotension is less common with the newer-generation grafts.[76]
There is no standardized method to measure endotension or consensus on indicated therapy in the absence of aneurysm enlargement; however, treatment of endotension to prevent aneurysm rupture is suggested in selected patients with continued aneurysm expansion.[76][205][215]

Bag-valve-mask ventilation: animated demonstration

How to use bag-valve-mask apparatus to deliver ventilatory support to adults. Video demonstrates the two-person technique.

Central venous catheter insertion: animated demonstration

Ultrasound-guided insertion of a non-tunnelled central venous catheter (CVC) into the right internal jugular vein using the Seldinger insertion technique.