media) and extends for a variable length resulting in a “true” and “false” lumen.

Interestingly, the prevalence of AAAs and the rate of expansion are both increased among heart

transplant patients.42–44 The responsible mechanisms remain unclear, but the obligatory chronic

immunosuppression may contribute. Arguments have been made to initiate screening programs as part

of pre- and posttransplant evaluations.

It is notable that the risk factors for AAA are similar to those associated with the development of

atherosclerosis with the noted exception of diabetes mellitus.45,46 Furthermore, atherosclerotic changes

are found almost universally within degenerative aneurysms at the time of repair, and the two disease

processes are likely related, but it is unclear how. The pathogenesis may be distinct and not necessarily

causative.

PRINCIPLES OF MANAGEMENT

The treatment goals for patients with AAAs are to prolong meaningful life, relieve symptoms, and

prevent rupture. Because surgical treatment is the only effective means to achieve these goals, the

crucial question that must be answered is whether the patient merits repair. The decision algorithm is

relatively straightforward for patients with ruptured or symptomatic aneurysms, but more difficult for

patients with asymptomatic, intact aneurysms in the elective setting. The decision to recommend

prophylactic intervention in the elective setting is contingent on the balance between the risk of the

procedure and the risk of expectant or nonoperative management within the context of the patient’s

desires or wishes and their meaningful life expectancy. Appropriate assessment of these risks requires an

understanding of the size-associated risk for rupture, the growth rate, and the morbidity and mortality

associated with repair, as well as the natural history of a patient with the risk factors that led to

aneurysm disease.

Understanding the natural history of untreated AAA requires knowledge of the physics associated with

the vessel wall. The tangential stress (t) of a fluid-filled cylindrical tube is determined by the following

equation:

t = Pr/d

where P is the pressure exerted by the blood (dyne/cm2), r is the internal radius (cm), and d is the

thickness (cm) of the arterial wall.47 The tangential stress of a cylinder 0.2 cm thick with an internal

radius of 0.8 cm and a fluid pressure of 150 mm Hg is 8 × 105 dyne/cm2 (Fig. 96-2). An increase in the

internal radius (diameter) of the cylinder to 2.94 cm and a concomitant decrease in the wall thickness,

as might occur with an aneurysm, would increase the tangential stress to 98 × 105 dyne/cm2. Thus, a 3-

fold increase in diameter would result in a 12-fold increase in the tangential stress. Aneurysms rupture

when the tangential stress exceeds the tensile strength of the vessel wall. It should be emphasized that

the tangential stress varies directly with the radius of the cylinder (vessel), but is independent of its

length.

3 The diameter of an AAA is the greatest predictor of rupture as would be predicted by the tangential

stress of the vessel wall. The diameter of an aneurysm is determined by measuring its greatest diameter

from outer wall to outer wall, preferably using an orthogonal image, throughout the extent of the

aneurysm. Orthogonal refers to a cross-sectional measurement perpendicular to the long axis, along the

centerline of flow to avoid overestimation due to tortuosity of the aorta. The collective annual rupture

risks per aneurysm diameter are shown (Table 96-1).48 Although there is some variability in the data, it

is generally appreciated that the rupture risk for aneurysms less than 5 cm in diameter is small, but

increases considerably for those greater than 5.5 cm in men and 5 cm in women. These data may be

simplified by using the rule of thumb that the annual rupture risk is ≤5% for a 5-cm aneurysm, ∼5%

for a 5.5-cm aneurysm, 10% for a 6-cm aneurysm, and 20% for a 7-cm aneurysm. These numbers

correspond to an estimated 5-year rupture risk of 50% for 6-cm aneurysms and 100% for those of 7 cm.

Notably, both the ADAM35 and UK Small Aneurysm Trial49 that randomized patients with small

aneurysms (4 to 5.5 cm) to open repair or surveillance reported that the rupture risk for surveillance

was ≤1%/yr.

2719

Figure 96-2. Cross-sectional view of a 2-cm-diameter cylinder that expands to a diameter of 6 cm while wall cross-sectional area

remains constant. t, wall stress; d, wall thickness; ri

, inside radius; r0

, outside radius. Expansion of a 1-cm-diameter cylinder to a

diameter of 3 cm with no change in wall cross-sectional area increases wall tensile stress 12-fold.

A variety of other factors have also been reported to increase the risk of aneurysm rupture including

female gender,50–52 chronic obstructive pulmonary disease,50,53 smoking,50 hypertension,50,53 family

history,54 and wall stress.55 The UK Small Aneurysm Trial reported that the rupture risk was increased

for female gender (hazard ratio, 3), current smoking (hazard ratio, 1.5), severe COPD (hazard ratio, 0.6

per L FEV1), and higher mean arterial pressure (hazard ratio, 1.2/mm Hg). Fillinger et al.56 used finite

element analysis to calculate the wall stress of AAAs and reported that the wall stress of

symptomatic/ruptured aneurysms exceeds those for elective aneurysms. The impact of the aneurysm

growth rate on rupture risk remains unclear and has been difficult to separate from aneurysm diameter

alone.52 However, an aneurysm expansion of ≥1 cm/yr is generally considered worrisome and a

potential risk factor for rupture.

Table 96-1 Estimated Annual Rupture Risk

4 The natural history of AAAs is to increase in size. The reported mean rate of growth has varied from

0.2 to 0.3 cm/yr in population studies

57–59 to 0.4 cm/yr from referral practices

60–62 with the latter

figure (0.4 cm/yr) generally quoted as a reasonable estimate. Several factors including female gender,

current smoking, and larger original diameter have been associated with an increased rate of growth as

might be predicted from the risk factors for rupture.57,59,63 Interestingly, early studies showed that

doxycycline and coenzyme A reductase inhibitors (i.e., statins) may inhibit aneurysm growth. More

recent literature has shown promise for statins inhibiting growth and rupture of AAA; however,

doxycycline has been proven ineffective in a randomized trial.63–67 It should be emphasized that these

growth rates are mean values and that aneurysms do not always grow in a linear fashion, as might be

predicted. The growth curve may be somewhat erratic or “staccato” with no growth detected during

consecutive 6-month intervals followed by a growth of 0.6 cm during the next follow-up interval.68

Furthermore, it should be emphasized that the past rate of growth does not predict future growth;

patients should not be lulled into a false sense of security if their aneurysm is relatively stable over

time, and should be encouraged to continue monitoring with a vascular specialist.

The mortality rate associated with repair of an AAA depends on the status of the aneurysm

(intact/asymptomatic, intact/symptomatic, ruptured), the physiologic state of the patient (age and

2720

medical comorbidities), and the method of repair (open vs. endovascular). Population studies from

Medicare and the Nationwide Inpatient Sample (NIS) have reported that operative mortality rates for

open repair of intact aneurysms in the United States range from 4.2% to 5.4% over the past decade.34

Predictably, the operative mortality rate increases with age, ranging from 2.2% among persons of 50 to

59 years of age to 9.2% among those >80. Interestingly, operative mortality rate has been shown to be

significantly higher among women (6.1% vs. 3.7%). The mortality rate for open repair in the

randomized trials comparing operative repair with surveillance for small aneurysms (UK Small

Aneurysm Trial – 5.8%, ADAM – 2.7%) and open repair with endovascular repair (DREAM – 4.6%,

EVAR Trial – 4.6%)69,70 are within the range of these nationwide series. Furthermore, a literature

review examining the mortality rate of open AAA repair encompassing 64 individual studies reported a

collective rate of 5.5%.71

The reported operative mortality rate for endovascular repair of intact AAAs has been consistently less

than those for the open approach.72–78 Schermerhorn et al.74 reported that the operative mortality after

endovascular aneurysm repair (EVAR) was 1.2% among Medicare beneficiaries during 2001 to 2004

while mortality within the NIS through 2005 was 1.3%. Results from the Dutch Randomized

Endovascular Aneurysm Management (DREAM) Trial70 and the Endovascular Aneurysm (EVAR) Trial79

comparing open and endovascular repair have reported that the perioperative mortality rate is lower for

endovascular repair and within the same range (DREAM – 1.2% vs. 4.6%; EVAR Trial – 1.7% vs. 4.7%).

The operative mortality rate for open repair of intact/symptomatic aneurysms among patients

undergoing emergent repair exceeds that for elective repair and has ranged from 9% to 19%.13,80,81

Various explanations have been proposed for this increased mortality rate relative to that for

intact/asymptomatic aneurysms including failure to maximize preoperative medical conditions,

increased incidence of inadvertent venous injuries, and less experienced operative teams, although the

true explanation remains unclear. However, in more recent data, De Martino et al.82 reported from the

Vascular Study Group of Northern New England a perioperative mortality of 2.1% and 0% for open and

endovascular repair for intact/symptomatic aneurysms, respectively. However, late mortality and inhospital adverse events were still higher comparable to the asymptomatic cohort.

5 6 The actual mortality rate for ruptured AAAs is somewhat difficult to determine because a

significant number of sudden deaths in elderly patients are likely secondary to ruptured aneurysms. It

has been estimated that 50% of all patients with ruptured AAAs die outside the hospital, and that

approximately 50% of those who actually undergo open repair do not survive.13 Indeed, a meta-analysis

spanning 50 years and 77 studies reported that the operative mortality rate for the open repair of

ruptured aneurysms was 48%.83 These figures correspond to an overall mortality rate of approximately

80% although this may be an underestimate. It is remarkable that the optimization of pre-hospital and

emergency room care including a reduction in the mean transfer time from the emergency department

to the operating room to 12 minutes did not appear to result in a decrease of the mortality rate of

ruptured aneurysms.84 Notably, the operative mortality rate for ruptured aneurysms treated with the

open approach has improved slightly over the past few decades with Bown et al.83 reporting a 3.5%

reduction per decade.

The mortality rate for the endovascular repair of ruptured AAAs is lower than associated with the open

approach, although data may be significantly skewed by selection bias.19,85–91 Rayt et al.88 reported a

collective mortality rate of 24% for the endovascular approach from 31 studies encompassing 982

patients while other meta-analyses or systematic reviews have reported comparable rates.86,89 The

potential to treat ruptured AAAs with the endovascular approach may represent the greatest

contribution or benefit of the technology. However, further validation is necessary since the reports

cited above likely reflect both patient selection and publication bias. In population data, Giles et al.91

and Schermerhorn et al.19 reported that the annual number of deaths across the country from both intact

and ruptured aneurysms has decreased significantly since the introduction of EVAR.

CLINICAL PRESENTATION AND DIAGNOSIS

7 The overwhelming majority of AAAs are asymptomatic at the time of discovery. Most aneurysms are

detected by abdominal or pelvic imaging studies, such as ultrasonography and CT, performed for other

indications (e.g., chronic back pain, renal cysts) rather than on physical examination. Indeed, it is often

difficult to palpate an AAA on physical examination because of its anatomic location in the posterior

abdomen adjacent to the spine and these difficulties are exacerbated in the presence of truncal obesity.

A literature review examining the accuracy of physical examination reported that the sensitivity ranged

2721

from 33% to 100%, the specificity ranged from 75% to 100%, and the positive predictive value ranged

from 14% to 100%.92 Given these fairly broad ranges, the authors concluded that physical examination

could not be relied upon to exclude an AAA. Predictably, the accuracy of primary care physicians for

detecting an AAA in patients with known aneurysms is only fair because of the limitations noted above

and the failure to actually palpate the aorta during the physical examination. Intact abdominal aortic

and iliac artery aneurysms may present with symptoms that lead to further investigation and the correct

diagnosis although this is the exception rather than the rule. Rarely, enlargement of the aneurysm may

cause vertebral erosion and chronic back pain. In addition, thrombosis of an AAA may cause acute

ischemia in the lower torso, and aneurysms may be a source of arterial macroemboli or microemboli

leading to acute ischemia of a lower extremity or digit, respectively.

Patients with intact/symptomatic or ruptured aneurysms present with abdominal or back pain related

to the aneurysm itself. The character of the pain is variable and ranges from dull to sharp. The pain is

usually acute in onset and persistent. It may be superimposed on more chronic abdominal or back pain,

but the presentation is usually not subtle, and the pain can be differentiated from more chronic

complaints. In addition, the pain may radiate from the abdomen to the back, flank, inguinal region, or

genitalia. Approximately 10% of patients with ruptured AAAs present with signs and symptoms similar

to those of ureteral colic or other acute urologic problems.93 For example, the diagnosis of a ruptured

aneurysm must be ruled out in a timely fashion in patients who might be at risk for AAA presenting

with testicular pain who have a normal urinalysis and testicular examination.

Patients with a ruptured AAA may present anywhere along the spectrum from hemodynamically

normal to profound shock. Their status depends on the ability of the tissues adjacent to the aorta to

tamponade the bleeding. If the adjacent tissues effectively contain the bleeding, the patient may present

in a hemodynamically stable state with essentially normal vital signs. However, it should be emphasized

that this is usually a temporary situation, and health care providers should not be lulled into a false

sense of security. A ruptured AAA is a true medical emergency that requires immediate operative repair

regardless of the patient’s hemodynamic status. Tamponade can quickly degenerate into free

intraperitoneal rupture and exsanguinating hemorrhage. Furthermore, vital signs may be misleading

because patients can lose up to 15% of their blood volume (class 1 shock) without any appreciable

change in their pulse rate or blood pressure. If the aneurysm initially ruptures freely into the peritoneal

space, patients usually exsanguinate before they can seek medical attention.

Patients with a ruptured AAA may also present with either an aortoenteric or an aortocaval fistula,

although both are relatively rare. Patients with an aortoenteric fistula may present with massive

intestinal bleeding, but often present with a “sentinel” bleed that is small volume. The aorta may

rupture through any portion of the bowel, although the duodenum and proximal small bowel are the

most common sites. The overwhelming majority of aortoenteric fistulae result from the erosion of a

prosthetic graft into the adjacent bowel (secondary aortoenteric fistula) rather than from an unrepaired

aneurysm (primary aortoenteric fistula). The diagnosis of an aortoenteric fistula must be ruled out in all

patients with gastrointestinal bleeding and either an AAA or a previous infrarenal aortic reconstruction.

Patients with an aortocaval fistula generally present with high-output congestive heart failure, a

continuous abdominal bruit, and edema of the lower extremities. The severity of the heart failure

symptoms depends on the size of the fistula and the magnitude of the systemic shunt.

8 Several imaging studies are available to establish or confirm the diagnosis of an AAA. Indeed, the

introduction of endovascular techniques for aneurysm repair has resulted in an evolution of these

modalities. The generic imaging goals for patients with an AAA are to establish the diagnosis, determine

the presence of rupture, determine the cephalad/caudal extent of the aneurysm, determine the

feasibility of endovascular repair, appropriately size the aneurysm and access vessels for endovascular

repair, screen for other visceral pathology, and screen for the presence of anatomic variants that would

complicate operative repair, such as a left-sided vena cava or a horseshoe kidney. Although no imaging

study satisfies every objective, ultrasound has emerged as the ideal screening study with CT

arteriography being the definitive diagnostic test and the preferred modality for operative planning.

Abdominal ultrasound is a safe, simple, and inexpensive means of detecting AAAs (Fig. 96-3). It is

relatively inexpensive and does not require the use of ionizing radiation or intravenous contrast.

Furthermore, ultrasound units are portable and almost universally available in the hospital setting

including the emergency room.94 The sensitivity of ultrasound for detecting AAAs is acceptable, and the

technique is reproducible within 0.3 cm in experienced hands.95 However, the technique is quite

operator-dependent and potentially confounded by the presence of bowel gas or extreme obesity.

Ultrasound can accurately image the infrarenal aorta to its bifurcation but is less reliable for imaging

2722

the portions of the aorta proximal to the renal arteries and distal to the iliac vessels. Furthermore, it is

not as reliable as CT for differentiating a ruptured from an intact aneurysm. However, ultrasound is an

excellent tool for screening patients at high risk for an AAA and for confirming the presence of an

aneurysm suspected by physical examination or clinical presentation. Further, it is a useful technique to

follow patients with small aneurysms (<4 cm) when the exact measurement is not crucial. It should not

be used to confirm the diagnosis of a ruptured aneurysm, nor should it be used as the sole imaging

study before elective repair because it does not provide a complete image of the aorta and iliac arteries.

Figure 96-3. B-mode ultrasound image showing a transverse view of an infrarenal abdominal aortic aneurysm. Note the vessel

wall and the large quantity of intraluminal clot surrounding the smaller, blood-filled center (dark circle).

CT arteriography overcomes many of the limitations of ultrasound and represents the current “gold

standard” for imaging patients with AAAs (Fig. 96-4). The downside of CT is the greater expense and

the potential harm that may be caused by the requisite ionizing radiation and intravenous contrast.

Indeed, the evolution of EVAR and the required follow-up imaging studies have focused increased

attention on the magnitude of long-term radiation injury. It is worth noting that the radiation dose

associated with an abdominopelvic CT scan is 10 to 20 mGy while that for a routine chest radiograph is

only 0.5 mGy. The incidence of allergic reactions to the contrast may be reduced by a steroid

preparation while the potential nephrotoxicity can be reduced by acetylcysteine or sodium

bicarbonate.96,97 Of course, the renal risks can be avoided altogether by not using contrast. However,

the quality of the noncontrast images is less than optimal, and is generally not useful for determining

eligibility for endovascular repair. CT is very sensitive for detecting both intact and ruptured

aneurysms, and the images are reproducible within 0.2 cm.95 The quality of the CT images has

continued to improve with each new generation of scanners, and the image acquisition times have

decreased. Currently, CT imaging of the arterial tree from the ascending aorta to the femoral arteries

can be obtained with an image acquisition time of less than 45 seconds. Given the quality and ease of

imaging, CT arteriograms have essentially replaced traditional catheter-based diagnostic arteriograms

for evaluation of aneurysms. Using axial CT images and 3D imaging software, a 3D image of the aorta

can be obtained that allows measurements along the centerline of blood flow (Fig. 96-5), and

dramatically improve the accuracy and consistency of sizing for endovascular repair.98 CT is also helpful

for detecting other intra-abdominal pathology or anatomic variants that may impact the operative

approach. Specific concerns include the location of the left renal vein and other associated venous

anomalies, the location and size of the kidneys, and the characteristics of the aneurysm wall. CT is

currently the sole diagnostic test performed before repair in the majority of cases and the imaging study

of choice to confirm or refute the diagnosis of a ruptured AAA. In addition, CT is the serial imaging

study of choice when aneurysms exceed 4 cm and approach the threshold for intervention.

2723