Official reprint from UpToDate®

www.uptodate.com ©2019 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
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: Feb 2019. | This topic last updated: Sep 25, 2018.

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 abdominal aortic aneurysm 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, gender, 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 ≤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 scaling index (ASI), calculated as diameter
(cm)/body surface area (m2), is more predictive of clinical events than absolute aortic diameter in women
[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 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-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 men (4 to 8 percent in those older than 50) compared with women (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]. These 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'.)

The risk factors associated with aneurysmal disease include:

● Older age
● Male gender
● Cigarette smoking
● Caucasian race
● Atherosclerosis
● Hypertension
● Family history of AAA
● Other large artery aneurysms (eg, iliac, femoral, popliteal)

A decreased risk of AAA is associated with:

● Female gender
● Non-Caucasian race
● Diabetes
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.
Abdominal aortic aneurysms 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, 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 (do not enlarge
significantly) [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. A one-time
screening for AAA is recommended for men ages 65 to 75 who have smoked, and in men ages 65 to 75
who have never smoked but who have a first-degree relative who required repair of an AAA or died from
a ruptured AAA. Screening for other subsets should be individualized. (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 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 his/her 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 — Abdominal aortic aneurysm 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 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 surveillance'.)

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 rAAA [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'.)

Computed tomography 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 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
'Emergent 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".)

Asymptomatic aneurysm — The management of asymptomatic abdominal aortic aneurysm 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 be taken
into account include the patient's age and gender, 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 surveillance'.)

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 abdominal
aortic aneurysm. 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
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 5th to 6th grade reading 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 10th to 12th grade reading level and are best for 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

● For most adults, an aortic diameter >3.0 cm is generally considered aneurysmal. Important risk
factors for the development of abdominal aortic aneurysm (AAA) include older age, male gender,
smoking, family history, and the presence of other large artery aneurysms. The most important
negative risk factors include non-Caucasian ethnicity, female gender, and diabetes. (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 recommend one-time screening for AAA with abdominal ultrasonography in men ages 65 to 75
who have ever smoked (Grade 1A). We also suggest one-time screening with abdominal
ultrasonography in men ages 65 to 75 who have a first-degree relative who required AAA repair or
died from AAA rupture (Grade 2C). We offer screening to women who have a strong family history
of either AAA repair or death due to AAA rupture, basing the decision to screen upon their values
and preferences. Screening generally is not indicated for other women, although data are limited.
Screening for other subsets should be individualized. (See 'Screening' above and "Screening for
abdominal aortic aneurysm", section on 'Summary and recommendations'.)

● 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'.)

● Abdominal aortic aneurysms 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'.)

• When ruptured AAA is identified, repair should be undertaken emergently to give the patient the
best chance for survival.

• 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).

● For most patients with asymptomatic infrarenal AAA <5.5 cm, we recommend conservative
management (watchful waiting) rather than elective AAA repair (Grade 1A). The risk of aneurysm
rupture does not exceed the risk of repair until the aneurysm diameter reaches 5.5 cm. For patients
under observation, we generally obtain annual ultrasound; however, a more frequent interval (eg,
every six months) may be used depending upon the characteristics of the aneurysm, or other
factors. (See 'Asymptomatic aneurysm' above and "Management of asymptomatic abdominal aortic
aneurysm", section on 'Aneurysm repair versus conservative management' and "Management of
asymptomatic abdominal aortic aneurysm", section on 'Aneurysm surveillance'.)

● For good-risk surgical candidates with AAA >5.5 cm, we recommend elective AAA repair (open or
endovascular) (Grade 1A). Other situations in which elective repair of AAA <5.5 cm may be
appropriate include rapid aortic expansion, coexisting peripheral aneurysm or peripheral artery
disease, and female gender. (See 'Asymptomatic aneurysm' above and "Management of
asymptomatic abdominal aortic aneurysm", section on 'Summary of indications for elective AAA
repair'.)

● For patients with AAA >5.5 cm who have a short life expectancy (<2 years) due to advanced
comorbidities, particularly cardiopulmonary disease or malignancy, we suggest no repair over
endovascular aneurysm repair (Grade 2B). (See 'Asymptomatic aneurysm' above and
"Management of asymptomatic abdominal aortic aneurysm", section on 'Counseling the high-risk
patient'.)

● Aneurysm repair can be accomplished using open surgical or endovascular techniques. The choice
between open and endovascular AAA repair should be individualized, taking into account the
patient's age, risk factors for perioperative morbidity and mortality, anatomic factors, and the
experience of the surgeon. Endovascular aneurysm repair is associated with a lower risk of
perioperative morbidity compared with open repair for asymptomatic, symptomatic, and ruptured
AAA. Long-term mortality following elective AAA repair is not significantly different between the
techniques. (See 'AAA repair' above and "Management of symptomatic (non-ruptured) and ruptured
abdominal aortic aneurysm", section on 'Summary and recommendations' and "Management of
asymptomatic abdominal aortic aneurysm", section on 'Summary and recommendations'.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Stather PW, Sidloff DA, Rhema IA, et al. A review of current reporting of abdominal aortic
aneurysm mortality and prevalence in the literature. Eur J Vasc Endovasc Surg 2014; 47:240.

2. Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular Surgery practice guidelines
on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018; 67:2.

3. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards for reporting on arterial
aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on
Reporting Standards, Society for Vascular Surgery and North American Chapter, International
Society for Cardiovascular Surgery. J Vasc Surg 1991; 13:452.

4. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management
of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal
aortic): a collaborative report from the American Association for Vascular Surgery/Society for
Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular
Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on
Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients
With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and
Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing;
TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006;
113:e463.

5. Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic
aneurysm: the Society for Vascular Surgery practice guidelines. J Vasc Surg 2009; 50:S2.

6. Lo RC, Lu B, Fokkema MT, et al. Relative importance of aneurysm diameter and body size for
predicting abdominal aortic aneurysm rupture in men and women. J Vasc Surg 2014; 59:1209.

7. Sweeting MJ, Thompson SG, Brown LC, et al. Meta-analysis of individual patient data to examine
factors affecting growth and rupture of small abdominal aortic aneurysms. Br J Surg 2012; 99:655.

8. Evans GH, Stansby G, Hamilton G. Suggested standards for reporting on arterial aneurysms. J
Vasc Surg 1992; 15:456.

9. Chiesa R, Tshomba Y, Mascia D, et al. Open repair for juxtarenal aortic aneurysms. J Cardiovasc
Surg (Torino) 2013; 54:35.

10. Chaikof EL, Blankensteijn JD, Harris PL, et al. Reporting standards for endovascular aortic
aneurysm repair. J Vasc Surg 2002; 35:1048.

11. Stanley, J. Open surgical treatment of pararenal abdominal aortic aneurysms. In: Aortic Aneurysm
s, Contemporary Cardiology, Upchurch, G, Criado, E (Eds), Humana Press, 2009. p.159.

12. Chaikof EL, Brewster DC, Dalman RL, et al. SVS practice guidelines for the care of patients with an
abdominal aortic aneurysm: executive summary. J Vasc Surg 2009; 50:880.
13. Sandhu RS, Pipinos II. Isolated iliac artery aneurysms. Semin Vasc Surg 2005; 18:209.

14. Kent KC, Zwolak RM, Egorova NN, et al. Analysis of risk factors for abdominal aortic aneurysm in a
cohort of more than 3 million individuals. J Vasc Surg 2010; 52:539.

15. Mussa FF. Screening for abdominal aortic aneurysm. J Vasc Surg 2015; 62:774.

16. Singh K, Bønaa KH, Jacobsen BK, et al. Prevalence of and risk factors for abdominal aortic
aneurysms in a population-based study : The Tromsø Study. Am J Epidemiol 2001; 154:236.

17. Powell JT, Greenhalgh RM. Clinical practice. Small abdominal aortic aneurysms. N Engl J Med
2003; 348:1895.

18. Scott RA, Ashton HA, Kay DN. Abdominal aortic aneurysm in 4237 screened patients: prevalence,
development and management over 6 years. Br J Surg 1991; 78:1122.

19. Lederle FA, Johnson GR, Wilson SE, et al. Prevalence and associations of abdominal aortic
aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans
Affairs Cooperative Study Group. Ann Intern Med 1997; 126:441.

20. Boll AP, Verbeek AL, van de Lisdonk EH, van der Vliet JA. High prevalence of abdominal aortic
aneurysm in a primary care screening programme. Br J Surg 1998; 85:1090.

21. Svensjö S, Björck M, Gürtelschmid M, et al. Low prevalence of abdominal aortic aneurysm among
65-year-old Swedish men indicates a change in the epidemiology of the disease. Circulation 2011;
124:1118.

22. Lederle FA. The rise and fall of abdominal aortic aneurysm. Circulation 2011; 124:1097.

23. Schermerhorn ML, Buck DB, O'Malley AJ, et al. Long-Term Outcomes of Abdominal Aortic
Aneurysm in the Medicare Population. N Engl J Med 2015; 373:328.

24. Gadowski GR, Pilcher DB, Ricci MA. Abdominal aortic aneurysm expansion rate: effect of size and
beta-adrenergic blockade. J Vasc Surg 1994; 19:727.

25. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic
surveillance for small abdominal aortic aneurysms. The UK Small Aneurysm Trial Participants.
Lancet 1998; 352:1649.

26. Brady AR, Thompson SG, Fowkes FG, et al. Abdominal aortic aneurysm expansion: risk factors
and time intervals for surveillance. Circulation 2004; 110:16.

27. Vega de Céniga M, Gómez R, Estallo L, et al. Growth rate and associated factors in small
abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2006; 31:231.

28. Lederle FA, Johnson GR, Wilson SE, et al. Relationship of age, gender, race, and body size to
infrarenal aortic diameter. The Aneurysm Detection and Management (ADAM) Veterans Affairs
Cooperative Study Investigators. J Vasc Surg 1997; 26:595.
29. Brewster DC, Cronenwett JL, Hallett JW Jr, et al. Guidelines for the treatment of abdominal aortic
aneurysms. Report of a subcommittee of the Joint Council of the American Association for
Vascular Surgery and Society for Vascular Surgery. J Vasc Surg 2003; 37:1106.

30. Newman AB, Arnold AM, Burke GL, et al. Cardiovascular disease and mortality in older adults with
small abdominal aortic aneurysms detected by ultrasonography: the cardiovascular health study.
Ann Intern Med 2001; 134:182.

31. Collin J, Araujo L, Walton J, Lindsell D. Oxford screening programme for abdominal aortic
aneurysm in men aged 65 to 74 years. Lancet 1988; 2:613.

32. Thompson AR, Cooper JA, Ashton HA, Hafez H. Growth rates of small abdominal aortic
aneurysms correlate with clinical events. Br J Surg 2010; 97:37.

33. Scott RA, Wilson NM, Ashton HA, Kay DN. Influence of screening on the incidence of ruptured
abdominal aortic aneurysm: 5-year results of a randomized controlled study. Br J Surg 1995;
82:1066.

34. Fleming C, Whitlock EP, Beil TL, Lederle FA. Screening for abdominal aortic aneurysm: a best-
evidence systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2005;
142:203.

35. Ashton HA, Buxton MJ, Day NE, et al. The Multicentre Aneurysm Screening Study (MASS) into the
effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial.
Lancet 2002; 360:1531.

36. Norman PE, Jamrozik K, Lawrence-Brown MM, et al. Population based randomised controlled trial
on impact of screening on mortality from abdominal aortic aneurysm. BMJ 2004; 329:1259.

37. Lindholt JS, Juul S, Fasting H, Henneberg EW. Hospital costs and benefits of screening for
abdominal aortic aneurysms. Results from a randomised population screening trial. Eur J Vasc
Endovasc Surg 2002; 23:55.

38. Lindholt JS, Juul S, Fasting H, Henneberg EW. Screening for abdominal aortic aneurysms: single
centre randomised controlled trial. BMJ 2005; 330:750.

39. Cosford PA, Leng GC. Screening for abdominal aortic aneurysm. Cochrane Database Syst Rev
2007; :CD002945.

40. Scott RA. Priorities in the management of abdominal aortic aneurysm. Br J Surg 2007; 94:653.

41. Fink HA, Lederle FA, Roth CS, et al. The accuracy of physical examination to detect abdominal
aortic aneurysm. Arch Intern Med 2000; 160:833.

42. Akkersdijk GJ, van Bockel JH. Ruptured abdominal aortic aneurysm: initial misdiagnosis and the
effect on treatment. Eur J Surg 1998; 164:29.

43. Gloviczki P, Pairolero PC, Mucha P Jr, et al. Ruptured abdominal aortic aneurysms: repair should
not be denied. J Vasc Surg 1992; 15:851.
44. Rinckenbach S, Albertini JN, Thaveau F, et al. Prehospital treatment of infrarenal ruptured
abdominal aortic aneurysms: a multicentric analysis. Ann Vasc Surg 2010; 24:308.

45. Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic
aneurysms. J Vasc Surg 1992; 16:17.

46. LaRoy LL, Cormier PJ, Matalon TA, et al. Imaging of abdominal aortic aneurysms. AJR Am J
Roentgenol 1989; 152:785.

47. Mehta M, Taggert J, Darling RC 3rd, et al. Establishing a protocol for endovascular treatment of
ruptured abdominal aortic aneurysms: outcomes of a prospective analysis. J Vasc Surg 2006; 44:1.

48. Chien DK, Chang WH, Yeh YH. Radiographic findings of a ruptured abdominal aortic aneurysm.
Circulation 2010; 122:1880.

49. Boules TN, Compton CN, Stanziale SF, et al. Can computed tomography scan findings predict
"impending'' aneurysm rupture? Vasc Endovascular Surg 2006; 40:41.

50. Siegel CL, Cohan RH, Korobkin M, et al. Abdominal aortic aneurysm morphology: CT features in
patients with ruptured and nonruptured aneurysms. AJR Am J Roentgenol 1994; 163:1123.

51. Arita T, Matsunaga N, Takano K, et al. Abdominal aortic aneurysm: rupture associated with the
high-attenuating crescent sign. Radiology 1997; 204:765.

52. Mehard WB, Heiken JP, Sicard GA. High-attenuating crescent in abdominal aortic aneurysm wall at
CT: a sign of acute or impending rupture. Radiology 1994; 192:359.

53. Welch HG, Albertsen PC, Nease RF, et al. Estimating treatment benefits for the elderly: the effect
of competing risks. Ann Intern Med 1996; 124:577.

54. Lederle FA, Wilson SE, Johnson GR, et al. Immediate repair compared with surveillance of small
abdominal aortic aneurysms. N Engl J Med 2002; 346:1437.

55. Cao P, De Rango P, Verzini F, et al. Comparison of surveillance versus aortic endografting for
small aneurysm repair (CAESAR): results from a randomised trial. Eur J Vasc Endovasc Surg
2011; 41:13.

56. Ouriel K, Clair DG, Kent KC, et al. Endovascular repair compared with surveillance for patients with
small abdominal aortic aneurysms. J Vasc Surg 2010; 51:1081.

57. United Kingdom EVAR Trial Investigators, Greenhalgh RM, Brown LC, et al. Endovascular repair of
aortic aneurysm in patients physically ineligible for open repair. N Engl J Med 2010; 362:1872.

58. http://content.onlinejacc.org/cgi/reprint/47/6/e1.pdf (Accessed on March 23, 2010).

59. Sieunarine K, Lawrence-Brown MM, Goodman MA. Comparison of transperitoneal and

retroperitoneal approaches for infrarenal aortic surgery: early and late results. Cardiovasc Surg
1997; 5:71.
Topic 87283 Version 13.0
GRAPHICS

Anatomy abdominal aortic aneurysm

Graphic 60682 Version 13.0

Classification of abdominal aortic aneurysm

Abdominal aortic aneurysms (AAAs) are commonly described based on the relation to the renal
arteries.
◾ Suprarenal AAA: The aneurysm involves the origins of one or more visceral arteries but
does not extend into the chest.
◾ Pararenal AAA: The renal arteries arise from the aneurysmal aorta but the aorta at the level
of the superior mesenteric artery is not aneurysmal.
◾ Juxtarenal AAA: 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 AAA: 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.

Graphic 90459 Version 2.0

Safi modification of Crawford TAA classification

The Crawford classification of thoracoabdominal aortic aneurysm is based upon the extent of
aortic involvement.
◾ Type I arises from above the sixth intercostal space, usually near the left subclavian
artery, and extends to include the origins of the celiac axis and superior mesenteric
arteries. Although the renal arteries can also be involved, the aneurysm does not
extend into the infrarenal aortic segment.
◾ Type II aneurysm also arises above the sixth intercostal space, and may include the
ascending aorta, but extends distal to include the infrarenal aortic segment, often to
the level of the aortic bifurcation.
◾ Type III aneurysm arises in the distal half of the descending thoracic aorta, below the
sixth intercostal space, and extends into the abdominal aorta.
◾ Type IV aneurysm generally involves the entire abdominal aorta from the level of the
diaphragm to the aortic bifurcation.
◾ Type V aneurysm arises in the distal half of the descending thoracic aorta, below the
sixth intercostal space, and extends into the abdominal aorta, but is limited to the
visceral segment.

Adapted from: Safi HJ, Winnerkvist A, Miller CC 3rd, et al. Effect of extended cross-clamp time
during thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 1998; 66:1204.

Graphic 66037 Version 8.0

Normal abdominal aorta

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 the fourth lumbar vertebra.
The branches of the abdominal aorta include (superior to inferior) the left and
right inferior phrenic arteries, the celiac axis, left and right middle suprarenal
arteries, superior mesenteric artery, left and right renal arteries, left and right
gonadal arteries, inferior mesenteric artery, left and right common iliac artery,
and middle sacral artery. The paired lumbar arteries (L1-L4) branch from the
aorta at mid vertebral body.

Graphic 51087 Version 3.0

Pelvic circulation

Illustration modified with permission from: Uflacker R. Atlas Of Vascular Anatomy: An Angiographic
Approach, Second Edition. Philadelphia: Lippincott Williams & Wilkins. Copyright © 2006 Lippincott
Williams & Wilkins.

Graphic 60420 Version 1.0

Algorithm for the diagnosis of abdominal aortic aneurysm

AAA: abdominal aortic aneurysm; H/P: history and physical; CT: computed tomography; OR: operating room; MRI: magnetic
resonance imaging.
* Systolic BP persists <90 mmHg, in spite of resuscitation.
¶ Intravenous contrast is not absolutely required to diagnose rupture, but is highly desired if endovascular repair is an option.
Δ Unrepaired, or prior open or endovascular repair.
◊ Ultrasound, abdominal CT, or MRI may be appropriate.
§ Can be performed at the bedside or in the operating room.

Graphic 86821 Version 3.0

Ruptured abdominal aortic aneurysm on computed tomography

Aortic calcification identifies the intact wall of the aorta. A large heterogenous
retroperitoneal hematoma is present adjacent the left kidney at the site of rupture.

Graphic 72201 Version 2.0

 Abdominal aortic aneurysm repair

(Top) For open surgical repair of abdominal aortic aneurysm, the aorta is clamped
and the aneurysm sac opened. A graft is sutured into the aorta proximally and
distally. A tube graft (illustrated) or a bifurcated graft is used depending upon the
extent of iliac artery disease (aneurysm or stenosis). Once the graft is in place,
the aneurysm sac and retroperitoneum are closed over the graft.
(Bottom) For endovascular repair, the folded endograft is introduced through the
femoral (or iliac) artery and, once it is properly posititioned, the self-expanding
endograft is deployed. Iliac artery extensions are positioned and deployed to
complete the repair.

Graphic 56289 Version 1.0

Contributor Disclosures
Ronald L Dalman, MD Nothing to disclose Matthew Mell, MD, MS, FACS Nothing to disclose John F Eidt,
MD Nothing to disclose Joseph L Mills, Sr, MD Grant/Research/Clinical Trial Support: Voyager Trial [Peripheral
artery disease (Rivoxaraban)]. Consultant/Advisory Boards: Innomed [Peripheral artery disease (Femoral artery
stent)]. Equity Ownership/Stock Options: NangioTx [Peripheral artery disease (Self-assembling nanotubules)]. Other
Financial Interest: Elsevier; Rutherford [Vascular surgery (Rutherford and Comprehensive Vascular and
Endovascular Surgery textbooks)]. Mark A Creager, MD, FAHA Nothing to disclose Kathryn A Collins, MD, PhD,
FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed
by vetting through a multi-level review process, and through requirements for references to be provided to support
the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of
evidence.

Conflict of interest policy