Official reprint from UpToDate
`®
`www.uptodate.com © 2022 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
`
`Overview of abdominal aortic aneurysm
`Authors: Ronald L Dalman, MD, Matthew Mell, MD, MS, FACS
`Section Editors: John F Eidt, MD, Joseph L Mills, Sr, MD, Mark A Creager, MD, FAHA, FACC, MSVM
`Deputy Editor: Kathryn A Collins, MD, PhD, FACS
`All topics are updated as new evidence becomes available and our peer review process is complete.
`
`Literature review current through: Apr 2022. | This topic last updated: Oct 28, 2021.
`
`INTRODUCTION
`
`Mortality remains high for patients who experience rupture of an abdominal aortic aneurysm
`(AAA), but it has dropped considerably in the past 20 years due to a variety of factors [1]. Elective
`AAA repair prior to the development of symptoms is the most effective means to prevent rupture
`and aneurysm-related sudden death.
`
`The definition of AAA and aortic anatomy will be reviewed here together with an overview of the
`epidemiology, risk factors, pathogenesis, natural history, screening, clinical features and diagnosis,
`management, and surgical repair, with links to more detailed topics. Our recommendations for the
`care of the patient with AAA are consistent with those provided by the Society for Vascular Surgery
`guidelines, which were updated in 2018 [2]. Other types of arterial aneurysms are discussed
`separately. (See "Iliac artery aneurysm" and "Femoral artery aneurysm" and "Popliteal artery
`aneurysm".)
`
`DEFINITIONS AND AORTOILIAC ANATOMY
`
`Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm. A true aneurysm is
`defined as a segmental, full-thickness dilation of a blood vessel that is 50 percent greater than the
`normal aortic diameter (
`figure 1) [3]. False aneurysms of the abdominal aorta can also occur but
`are much less common and are usually due to a traumatic or infectious etiology.
`
`In most adults, an aortic diameter >3.0 cm is generally considered aneurysmal. Normal aortic
`diameter varies with age, sex, and body habitus, but the average diameter of the adult human
`infrarenal aorta is approximately 2.0 cm; 95 percent of the adult population has an aortic diameter
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`≤3.0 cm [3]. Thus, for the majority of patients, an infrarenal aorta with a maximum diameter ≥3.0
`cm is considered aneurysmal [3-5]. For men, diameter alone defines the presence of an AAA and
`predicts clinical events. However, for women, although the aorta is still considered aneurysmal
`when its diameter exceeds 3.0 cm, the diameter is less predictive of clinical events. An aortic size
`index (ASI), calculated as diameter (cm)/body surface area (m ), is more predictive of clinical events
`2
`than absolute aortic diameter in females [6].
`
`For the purposes of this discussion:
`
`Small aneurysms have a diameter <4.0 cm
`Medium aneurysms have a diameter between 4.0 and 5.5 cm
`Large aneurysms have a diameter >5.5 cm
`Very large aneurysms have a diameter ≥6.0 cm
`
`The natural history of AAA is one of progressive expansion, which is variable and depends upon
`aneurysm diameter and other factors, the most important of which is ongoing smoking [7].
`
`AAAs can be described relative to the involvement of the renal or visceral vessels. Several
`classification schemes have been described [8-11]. We use the following definitions to describe AAA
`(
`figure 2):
`
`Suprarenal aneurysm – The aneurysm involves the origins of one or more visceral arteries but
`does not extend into the chest.
`
`Pararenal aneurysm – The renal arteries arise from the aneurysmal aorta, but the aorta at the
`level of the superior mesenteric artery is not aneurysmal.
`
`Juxtarenal aneurysm – The aneurysm originates just beyond the origins of the renal arteries.
`There is no segment of nonaneurysmal aorta distal to the renal arteries, but the aorta at the
`level of the renal arteries is not aneurysmal.
`
`Infrarenal aneurysm – The aneurysm originates distal to the renal arteries. There is a
`segment of nonaneurysmal aorta that extends distal to the origins of the renal arteries.
`
`AAA most often affects the segment of aorta between the renal and inferior mesenteric arteries;
`approximately 5 percent involve the renal or visceral arteries. Up to 40 percent of AAAs are
`associated with iliac artery aneurysm(s) (
`figure 1) [3-5,12]. (See "Iliac artery aneurysm".)
`
`Thoracoabdominal aneurysms originate in the chest and may involve the visceral or renal vessels (
`figure 3). (See "Clinical manifestations and diagnosis of thoracic aortic aneurysm".)
`
`Anatomy — The abdominal aorta is a retroperitoneal structure that begins at the hiatus of the
`diaphragm and extends to its bifurcation into the right and left common iliac arteries at the level of
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`the fourth lumbar vertebra. The posterior abdominal peritoneum covers the abdominal aorta
`anteriorly and is reflected onto the posterolateral duodenum at its junction with the jejunum.
`
`The aorta lies slightly left of the midline to accommodate the inferior vena cava, which is adjacent
`to the aorta on its right. The branches of the aorta include (superior to inferior) (
`figure 4) the left
`and right inferior phrenic arteries, left and right middle suprarenal arteries, celiac axis, superior
`mesenteric artery, left and right renal arteries, left and right gonadal arteries, inferior mesenteric
`artery, left and right common iliac artery, middle sacral artery, and paired lumbar arteries (L1 to
`L4).
`
`The common iliac artery bifurcates into the external iliac and internal iliac arteries at the pelvic inlet
`(
`figure 5). The internal iliac artery gives rise to anterior and posterior branches to the pelvic
`viscera and also supplies the musculature of the pelvis. The external iliac artery passes underneath
`the inguinal ligament to become the common femoral artery [13].
`
`EPIDEMIOLOGY
`
`The estimated prevalence of abdominal aortic aneurysm (AAA) in developed countries is between 2
`and 8 percent and is higher in males (4 to 8 percent in those older than 50) compared with females
`(1 to 1.3 percent) [14]. Based on screening, approximately 1,000,000 individuals in the United
`States have an AAA [15]. The prevalence of AAA increases with age in both men and women,
`although the age-related increase is more pronounced in men [16,17]. Ultrasound screening
`studies have shown that 4 to 8 percent of older men have an occult AAA [18-20]. Because the
`incidence of AAA rises sharply in individuals over 60 years of age, the future prevalence of AAA
`could increase substantially in association with the aging population. Other studies suggest that a
`reduction in the prevalence of smoking may have the opposite effect [21,22]. (See "Epidemiology,
`risk factors, pathogenesis, and natural history of abdominal aortic aneurysm", section on
`'Epidemiology'.)
`
`In the 2010s, death from rupture of an AAA was estimated to occur in approximately 7000 patients
`per year in the United States. AAA-associated mortality has decreased by nearly 50 percent since
`the early 1990s. Although the specific reasons for this decline are unknown, the declining
`prevalence of cigarette smoking in the adult population, the increasing awareness and impact of
`government-sponsored screening programs for identifying early disease, and an increase in the
`use of endovascular repair of AAA, particularly in the older patients, all may have played a role in
`this decline [1,23]. (See "Epidemiology, risk factors, pathogenesis, and natural history of abdominal
`aortic aneurysm", section on 'Epidemiology of AAA rupture'.)
`
`

`

`RISK FACTORS
`
`Well-defined clinical risk factors are associated with the pathogenesis of abdominal aortic
`aneurysm (AAA) [14]. The most important risk factors are listed below and discussed in detail
`elsewhere. (See "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic
`aneurysm", section on 'Risk factors for the development of AAA'.)
`
`Risk factors associated with aneurysmal disease include:
`
`Older age
`Male sex
`Cigarette smoking
`Positive family history of AAA
`Other large artery aneurysms (eg, iliac, femoral, popliteal)
`Atherosclerosis
`Hypertension
`
`PATHOGENESIS AND NATURAL HISTORY
`
`Aneurysmal degeneration of the abdominal aorta is a multifactorial, systemic process generally felt
`to be due to alterations in vascular wall biology leading to a loss of vascular structural proteins and
`wall strength. A common systemic etiology for large vessel (eg, aorta, femoral, iliac, popliteal)
`aneurysm formation is supported by the occurrence of multiple aneurysms in the same patient.
`Etiologic factors felt to be important in the development and progression of abdominal aortic
`aneurysm (AAA) include proteases, inflammatory mediators, and genetic factors. Biomechanical
`forces, including stresses across the arterial wall, are also felt to play a role. (See "Epidemiology,
`risk factors, pathogenesis, and natural history of abdominal aortic aneurysm", section on
`'Pathophysiology of AAA'.)
`
`An understanding of the management of patients with an AAA requires knowledge of the natural
`history of this disorder. The natural history of AAA is one of progressive expansion, the rate of
`which is variable. AAAs expand, on average, at a rate of 0.3 to 0.4 cm per year [24-28]. Expansion
`tends to be more rapid in smokers and less rapid in patients with diabetes mellitus or peripheral
`artery disease [26]. Some aneurysms, for unclear reasons, remain relatively fixed in size for a
`period of time but then undergo rapid expansion. (See "Epidemiology, risk factors, pathogenesis,
`and natural history of abdominal aortic aneurysm", section on 'Expansion and rupture of AAA'.)
`
`The likelihood that an aneurysm will rupture is increased for those with aneurysm diameter >5.5
`cm, a faster rate of expansion (>0.5 cm over a six-month period), those who continue to smoke,
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`and in females. In addition to these, other factors that increase the risk of rupture include recent
`surgery; medical factors such as uncontrolled hypertension, which may increase aortic wall stress;
`and, possibly, aneurysm contour [29].
`
`SCREENING
`
`Screening studies show that abdominal aortic aneurysm (AAA) occurs in up to 7 percent of
`individuals over the age of 50 [18,19,30,31]. However, the majority of AAAs identified at screening
`are small, and up to 50 percent of those ≤3.5 cm in diameter remain stable throughout follow-up
`(ie, do not enlarge significantly to warrant treatment) [32]. The effectiveness of population-based
`screening for AAAs with abdominal ultrasonography has been evaluated in large randomized trials
`and systematic reviews [33-40]. Screening for AAA in men over age 65 results in a decreased risk of
`AAA-related mortality; however, for people with a low risk for AAA, any absolute benefit on overall
`mortality is likely to be small.
`
`We screen men ages 65 to 75 who have ever smoked and suggest screening men aged 65 to 75
`who have a first-degree relative who has been diagnosed with AAA. We offer screening to females
`who have a first-degree relative who has been diagnosed with AAA; screening is not otherwise
`indicated for women. The Society for Vascular Surgery (SVS) and European Society for Vascular
`Surgery (ESVS) guidelines also suggest rescreening individuals at the 10-year time point if their
`original aortic diameter is between 2.5 and 3.0 cm [2]. (See "Screening for abdominal aortic
`aneurysm".)
`
`CLINICAL PRESENTATIONS
`
`Patients with intact abdominal aortic aneurysm (AAA) may present with or without symptoms.
`
`Asymptomatic – The majority of patients are asymptomatic. A previously unknown AAA may
`also become apparent as a result of screening or be discovered incidentally on routine
`physical examination, on imaging studies performed for other indications, or in the course of
`evaluating other unrelated conditions. Asymptomatic AAAs are difficult to exclude based on
`physical examination alone in most patients, even when attempted by experienced examiners
`[41]. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on
`'Asymptomatic AAA'.)
`
`Symptomatic but not ruptured – Symptomatic AAA refers to any of a number of symptoms
`that can be attributed to the aneurysm. The development of symptoms may be a sign that
`AAA configuration is rapidly expanding, has become large enough to compress surrounding
`structures, or is an inflammatory or infectious aneurysm. Patients with symptomatic AAA
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`most commonly present with abdominal, back, or flank pain, which may or may not be
`associated with AAA rupture. AAA can also present with other clinical manifestations, such as
`limb ischemia (acute or chronic), or other systemic manifestations (fever, malaise). In patients
`with abdominal pain, rupture of the aneurysm must be excluded. (See "Clinical features and
`diagnosis of abdominal aortic aneurysm", section on 'Symptomatic (nonruptured) AAA'.)
`
`Symptomatic and ruptured – The clinical presentation of ruptured abdominal aortic aneurysm
`is variable with respect to symptoms and time course. The patient may or may not be aware
`of the diagnosis of AAA prior to their clinical manifestations of rupture. Only 20 to 30 percent
`of patients who present to an emergency department with rupture have a known history of
`AAA [42,43]. The classic presentation of severe pain, hypotension, and a pulsatile abdominal
`mass occurs in approximately 50 percent of patients [44]. Although the signs and symptoms
`of ruptured AAA may be obvious, some presentations make ruptured AAA difficult to
`recognize. Patients with rupture into the retroperitoneum may attribute their symptoms to
`other causes and delay seeking medical attention. Even after presenting to a physician, a
`misdiagnosis of ruptured AAA as renal colic, perforated viscus, diverticulitis, gastrointestinal
`hemorrhage, and ischemic bowel occurs approximately 30 percent of the time [45]. (See
`"Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Ruptured AAA'.)
`
`DIAGNOSIS
`
`A diagnosis of abdominal aortic aneurysm (AAA) is established with imaging studies that
`demonstrate the aneurysm in the patient suspected of having AAA on the basis of risk factors or
`on physical examination. Physical examination can reliably diagnose a large AAA (>5.5 cm), but the
`diagnosis is made using abdominal palpation in fewer than 50 percent of those with AAA. The
`physical examination should include a complete peripheral arterial vascular examination to assess
`for signs of thromboembolism or other peripheral aneurysms. (See "Clinical features and diagnosis
`of abdominal aortic aneurysm", section on 'Physical examination'.)
`
`Laboratory studies are not routinely obtained as part of the evaluation of asymptomatic AAA.
`However, a white blood cell count, blood cultures, and erythrocyte sedimentation rate should be
`performed in patients with systemic symptoms (eg, fever, weight loss) to evaluate for an infectious
`cause of AAA or inflammatory aneurysm. For patients with ruptured AAA, standard laboratory
`testing and type and crossmatch are obtained.
`
`Imaging — AAA that is suspected based upon clinical symptoms or signs, or incidentally on
`nonvascular imaging studies (eg, spine magnetic resonance [MR] imaging), should be confirmed
`with definitive vascular imaging (
`algorithm 1). For asymptomatic AAA, the imaging test of choice
`is abdominal ultrasonography, which has sensitivity and specificity approaching 100 percent for an
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`aortic diameter >3.0 cm [46]. Abdominal ultrasound is noninvasive and is ideal for serial imaging in
`patients with small- and medium-sized aneurysms who are being conservatively managed.
`However, ultrasound is technician dependent and has other limitations. (See "Clinical features and
`diagnosis of abdominal aortic aneurysm", section on 'Imaging asymptomatic patients' and
`"Management of asymptomatic abdominal aortic aneurysm", section on 'Aneurysm imaging'.)
`
`Computed tomography (CT) is the imaging test of choice for symptomatic AAA. Contrast-enhanced
`CT aortography is generally not needed to establish a diagnosis of ruptured AAA [47] but may be
`essential for planning surgical repair. In patients with symptoms of more than one hour, findings
`of rupture on CT scan are usually obvious (eg, retroperitoneal hematoma, extravasation of
`contrast) (
`image 1) [48]. Other findings on abdominal CT may be associated with unstable
`aneurysms or "impending rupture" (eg, crescent sign, breaks in aortic wall calcification, aortic
`blebs) [49-52]. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on
`'Imaging symptomatic patients'.)
`
`CT of the abdomen (and MR imaging) can also be used to diagnose and monitor asymptomatic
`AAA. However, these are generally limited to preoperative planning and to postoperative follow-up
`of aortic graft repairs. (See "Endovascular repair of abdominal aortic aneurysm", section on
`'Endograft surveillance' and "Open surgical repair of abdominal aortic aneurysm", section on
`'Follow-up'.)
`
`MANAGEMENT
`
`Abdominal aortic aneurysms (AAAs) are managed according to their diameter and the presence or
`absence of symptoms. Under most circumstances, patients with symptoms that cannot be
`definitively attributed to another etiology should be admitted for observation and further vascular
`evaluation. Asymptomatic aneurysms are evaluated on an outpatient basis, unless they are very
`large. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction'.)
`
`Ruptured AAA — Repair of ruptured abdominal aortic aneurysm (rAAA) can be offered to most
`patients, and the timing of the initial evaluation and management of the patient is guided by the
`hemodynamic status of the patient. (See "Management of symptomatic (non-ruptured) and
`ruptured abdominal aortic aneurysm", section on 'Ruptured AAA'.)
`
`The hemodynamically unstable patient (persistent in spite of resuscitation) with known AAA
`who presents with classic symptoms/signs of rupture (hypotension, flank/back pain, pulsatile
`mass) should be taken emergently to the operating room for immediate control of
`hemorrhage, resuscitation, and repair of the aneurysm. Imaging confirmation of the
`presence of AAA in hemodynamically unstable patients suspected but not known to have the
`disease is ideal prior to intervention but is not required. Preoperative management of
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`hemodynamically unstable patients, including the concept of "hypotensive hemostasis," is an
`area of active investigation. However, in most circumstances, volume resuscitation should be
`provided to the least amount necessary to maintain mentation and stabilize blood pressure
`and pulse rate.
`
`For patients with suspected ruptured AAA who are hemodynamically stable, abdominal
`imaging (preferably computed tomographic [CT] aortography) should be performed urgently
`to confirm the rupture prior to repair, rule out other potential etiologies as a cause of
`abdominal pain and hypotension, and determine if an endovascular repair is feasible.
`
`Open surgical versus endovascular repair of ruptured aneurysm — Both open and
`endovascular techniques can be successfully employed in the treatment of ruptured AAA.
`Endovascular repair of ruptured AAA may have some advantages over open repair; however, it is
`not universally available, and the selection of technique is best determined by the available
`surgical team. Open surgical or endovascular repair of ruptured AAA is accomplished in a manner
`that is similar to elective repair, with modifications for aortic hemorrhage control, and
`anticoagulation. Conversion rates from endovascular to open repair for rAAA may be higher
`compared with elective repair because of unanticipated anatomic features or device-related issues.
`(See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm".)
`
`Symptomatic (nonruptured) AAA — Aneurysm repair is indicated for patients with symptoms
`(abdominal/back/flank pain, thromboembolism) that cannot unequivocally be attributed to another
`etiology, regardless of aneurysm diameter. For patients with symptomatic AAA, the first priority is
`to determine whether there is any immediate concern that the aneurysm has ruptured or is at high
`risk for impending rupture, which may be suggested by clinical symptoms or signs, or certain
`radiologic features (eg, broken calcification, asymmetry) that may indicate instability of the
`aneurysm. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on
`'Imaging symptomatic patients'.)
`
`In the absence of overt rupture, patients with AAA who are thought to be symptomatic or who
`have possible signs of impending rupture should be admitted for observation and further
`evaluation. If the patient is a candidate, repair should be accomplished during the same
`hospitalization. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic
`aneurysm", section on 'Emergency versus delayed repair of symptomatic aneurysm'.)
`
`If the patient is a candidate for repair, a determination needs to be made about whether an open
`surgical or endovascular approach is more appropriate, primarily based upon an anatomic
`assessment of aortoiliac anatomy. (See "Endovascular repair of abdominal aortic aneurysm" and
`"Open surgical repair of abdominal aortic aneurysm".)
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`Asymptomatic aneurysm — The management of asymptomatic AAA is based upon an
`assessment of the patient's risk for rupture, compared with the expected risk of perioperative
`morbidity and mortality associated with repair [53]. When the risk of rupture exceeds the risk of
`repair, repair is recommended. Conversely, if the risk of repair is greater than the risk of rupture,
`conservative management and surveillance is recommended. (See "Management of asymptomatic
`abdominal aortic aneurysm", section on 'Aneurysm repair versus conservative management'.)
`
`The assessment of rupture risk depends primarily upon the diameter of the aneurysm at diagnosis
`and the patient's medical comorbidities. The annual risk of rupture has been found in randomized
`trials (discussed below) to be similar to, or lower than, the risk of repair in patients with small- or
`medium-sized aneurysms (<5.5 cm in diameter) [25,54-57]. This diameter threshold for AAA repair
`is not absolute and may depend on the patient's stature and location of the aneurysm.
`
`Other factors that need to account for include the patient's age and sex, faster expansion rates,
`and the presence of other peripheral aneurysms. (See "Management of asymptomatic abdominal
`aortic aneurysm", section on 'Other considerations' and "Management of asymptomatic abdominal
`aortic aneurysm", section on 'Summary of indications for elective AAA repair'.)
`
`Patients who are not candidates for repair or refuse repair should create an advanced directive
`detailing their wishes in the event of rupture. Family members should be made aware of these
`wishes, given that the patient may not be able to report these wishes at the time of aneurysm
`rupture. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Counseling
`the high-risk patient'.)
`
`Medical therapies — During the period of observation (watchful waiting), medical therapies are
`aimed at reducing the rate of aortic expansion and morbidity and mortality from cardiovascular
`disease. However, no medical therapy other than smoking cessation has proven effective at
`reducing the rate of AAA enlargement and possibly, by extrapolation, risk for rupture. (See
`"Management of asymptomatic abdominal aortic aneurysm", section on 'Therapies to limit aortic
`expansion'.)
`
`Aneurysm surveillance — During the period of observation, ultrasound surveillance is routinely
`performed on a schedule that depends primarily upon the diameter of the aneurysm. We generally
`obtain annual ultrasound; however, a more frequent interval (eg, every six months) may be used
`depending upon other characteristics of the aneurysm or patient-related factors. Factors that
`influence the aneurysm surveillance interval are discussed separately. (See "Management of
`asymptomatic abdominal aortic aneurysm", section on 'Aneurysm imaging'.)
`
`AAA REPAIR
`
`

`

`Aneurysm repair can be accomplished using open surgical or endovascular techniques.
`Endovascular aneurysm repair is associated with a lower risk of perioperative morbidity compared
`with open repair for asymptomatic, symptomatic, and ruptured abdominal aortic aneurysm (AAA).
`Long-term mortality following elective AAA repair is not significantly different between the
`techniques. Guidelines from major medical and surgical societies recommend an individualized
`approach to the patient when choosing between open and endovascular repair, taking into
`account the patient's age, risk factors for perioperative morbidity and mortality, anatomic factors,
`and experience of the surgeon [4,5,58]. Given the need for lifelong surveillance with endovascular
`repair, younger patients with low operative risk may benefit more from open surgical repair,
`whereas older patients and those with high operative risk may benefit more from endovascular
`repair, provided their aortoiliac anatomy is appropriate. (See "Management of asymptomatic
`abdominal aortic aneurysm", section on 'Open versus endovascular aneurysm repair' and "Surgical
`and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Open surgical versus
`endovascular repair'.)
`
`Open surgical repair — Open aneurysm repair involves replacement of the diseased aortic
`segment with a tube or bifurcated prosthetic graft (
`figure 6) through a midline abdominal or
`retroperitoneal incision [59]. With technical refinements for open AAA repair, complications such as
`acute renal failure, distal embolization, wound infection, colonic ischemia, false aneurysm
`formation, aortoduodenal fistula, graft infection, and perioperative bleeding have become less
`common following routine elective surgery but remain significant issues following emergent open
`AAA repair. (See "Open surgical repair of abdominal aortic aneurysm".)
`
`Endovascular repair — Endovascular aneurysm repair (EVAR) involves the placement of modular
`graft components delivered via the iliac or femoral arteries to line the aorta (
`figure 6) and
`exclude the aneurysm sac from the circulation. EVAR requires fulfillment of specific anatomic
`criteria. With contemporary techniques, including custom-made fenestrated and branched devices,
`most patients can be considered candidates for EVAR in experienced endovascular centers. (See
`"Endovascular repair of abdominal aortic aneurysm".)
`
`Some anatomic features of the aorta or iliac arteries may preclude the ability to place an aortic
`endograft. Endovascular repair may not be anatomically feasible if the aortic neck is occupied by
`thrombus, there is circumferential calcification at the level of the aortic neck, or both iliac arteries
`are too small for the intended device. Endovascular repair of juxtarenal or suprarenal aortic
`aneurysm is not possible where advanced devices and technical expertise are not available. (See
`"Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability'.)
`
`Endografts — Multiple endovascular devices are commercially available for repair of AAA.
`Currently available endovascular grafts for infrarenal aortic repair share a bifurcated, modular
`design. Endografts are chosen to meet size criteria dictated by the size and configuration of the
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`aneurysm. The anatomic measurements of interest include proximal neck length, aneurysm
`diameter, aortic neck angulation, iliac artery diameter, femoral artery diameter, and aortic length.
`Other considerations include whether there is flow in the inferior mesenteric artery and the
`location and number of accessory renal arteries. (See "Endovascular devices for abdominal aortic
`repair".)
`
`Complications of endograft repair — Complications following endograft placement include
`systemic complications (eg, myocardial infarction, contrast-induced nephropathy, end-organ
`ischemia) and complications related to the endograft, such as vascular injury (eg, iliac, femoral),
`early and late endoleaks, device migration, component separation, stent fracture, limb thrombosis,
`and endograft infection. (See "Complications of endovascular abdominal aortic repair".)
`
`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".)
`
`INFORMATION FOR PATIENTS
`
`UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
`The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading
`th
`th
`level, and they answer the four or five key questions a patient might have about a given condition.
`These articles are best for patients who want a general overview and who prefer short, easy-to-
`read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
`more detailed. These articles are written at the 10 to 12 grade reading level and are best for
`th
`th
`patients who want in-depth information and are comfortable with some medical jargon.
`
`Here are the patient education articles that are relevant to this topic. We encourage you to print or
`e-mail these topics to your patients. (You can also locate patient education articles on a variety of
`subjects by searching on "patient info" and the keyword(s) of interest.)
`
`Beyond the Basics topics (see "Patient education: Abdominal aortic aneurysm (Beyond the
`Basics)").
`
`SUMMARY AND RECOMMENDATIONS
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`

`For most adults, an aortic diameter >3.0 cm is generally considered aneurysmal. The most
`important risk factors for the development of abdominal aortic aneurysm (AAA) include older
`age, male sex, cigarette smoking, positive family history, and the presence of other large
`artery aneurysms. (See 'Definitions and aortoiliac anatomy' above and 'Epidemiology' above
`and 'Risk factors' above and 'Pathogenesis and natural history' above.)
`
`A definitive diagnosis requires abdominal imaging studies that demonstrate a focal, aortic
`dilation meeting the criteria for aneurysm (>1.5 times normal diameter, or >3.0 cm in the
`infrarenal segment). Abdominal ultrasound and computed tomography of the abdomen are
`both highly sensitive and specific for diagnosing AAA but are recommended under differing
`clinical circumstances (
`algorithm 1) depending upon the presence of symptoms and the
`hemodynamic status of the patient. (See 'Diagnosis' above and "Clinical features and
`diagnosis of abdominal aortic aneurysm", section on 'Summary and recommendations'.)
`
`We screen men ages 65 to 75 who have ever smoked and suggest screening men aged 65 to
`75 who have a first-degree relative who has been diagnosed with AAA. We offer screening to
`females who have a first-degree relative who has been diagnosed with AAA; screening is not
`otherwise indicated for women. For those in whom an aortic diameter between 2.5 and 3.0
`cm was identified, society guidelines also suggest rescreening individuals at 10 years.
`Screening for other subsets should be individualized. (See 'Screening' above and "Screening
`for abdominal aortic aneurysm".)
`
`AAA does not typically cause symptoms unless the aneurysm is expanding rapidly, has
`become large enough to compress surrounding structures, is associated with inflammation
`(inflammatory aneurysm, infected aneurysm), or has ruptured. Patients with symptomatic
`AAA most commonly present with abdominal, back, or flank pain. The classic presentation of
`severe pain, hypotension, and a pulsatile abdominal mass occurs in approximately 50 percent
`of patients with ruptured AAA. AAA can also present with other clinical manifestations such as
`limb ischemia (acute or chronic), or systemic manifestations, such as fever or malaise, that
`may indicate an inflammatory or infectious aneurysm. (See 'Clinical presentations' above and
`"Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Clinical features'.)
`
`AAAs are managed according the presence or absence of symptoms. (See 'Management'
`above and "Management of asymptomatic abdominal aortic aneurysm", section on 'Summary
`and recommendations' and "Management of symptomatic (non-ruptured) and ruptured
`abdominal aortic aneurysm", section on 'Summary and recommendations'.)
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`When ruptured AAA is identified, repair should be undertaken emergently to give the
`patient the best chance for survival.
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`For patients with symptomatic (nonruptured) AAA of any size or configuration who do not
`have a prohibitive risk for repair, we suggest urgent AAA repair (open or endovascular).
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`For most patients with asymptomatic infrarenal AAA <5.5 cm, we recommend conservative
`management (watchful waiting) rather