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ABDOMINAL AORTIC ANEURYSM
285
surgical procedure; it’s been 20 years since I’ve worked
with a surgeon who was willing to take a patient like
this directly to the operating room. Frankly, it’s not
easy to repair a leaking aneurysm surgically, and if
it can be done endovascularly, there is a tremendous
advantage to the patient in terms of morbidity and
mortality. With this in mind, it may make sense to
get more imaging information before you go to the
operating room.
We have a patient who’s been a long-term smoker.
We know that there is an association between periph-
eral vascular disease and smoking, and a lesser asso-
ciation between smoking and aortic aneurysmal
development. It has been my experience that patients
who have Buerger’s disease have distal vascular prob-
lems usually without aneurysms. In contrast, with
aneurysmal disease, while there may be downstream
atherosclerotic plaques, for the most part have the
disease is primarily confi ned to the aorta. This is one
of the reasons that bypass works so successfully for
them. Can you tell the difference in the ED?
DB: Buerger’s disease, or thomboangitis obliterans
as it’s also known, generally presents with limb isch-
emia. It is a peripheral vascular disease problem with
thrombosis and distal embolization. It is strongly
associated with smoking, and the only treatment
I know of, short of bypass and amputation, which
are often not very successful, is smoking cessation.
In contrast to abdominal aortic aneurysm, Buerger’s
disease tends not to rupture. We don’t encounter
these patients presenting with hemorrhagic shock,
but rather with ischemia of a distal limb. Buerger’s
disease may overlap with popliteal artery aneurysms,
which tend to thrombose and embolize, and may
present with distal extremity ischemia. There also
may be some overlap with Buerger’s disease, smok-
ing, and other atherosclerotic aneurysms of the aorta
or popliteal arteries.
PR: Many patients who have emergent repair of
abdominal aneurysms will sustain non-ST-segment
elevated myocardial infarctions (NSTEMIs) dur-
ing surgery. Is there any point in obtaining a set of
enzymes on this patient before he goes to the OR?
SG: Are you considering enzymes before he goes to
the OR because you are hoping to ascertain whether
he is having a concomitant infarct preoperatively
rather than peri- or postoperatively?
patient who needs to go directly to the operating
room (OR).
PR: I couldn’t agree more, but I think we have to be
somewhat realistic here. When we fi rst started doing
vascular surgery, we were in a surgical climate where
there was much less reluctance to go the OR with-
out precise diagnoses. Over the past 20 years, we’ve
seen increasing reluctance to take patients to the OR
without imaging information. We can ask our surgical
colleagues to go directly to the OR, and there seems
to be a literature to suggest that outcomes, especially
for leaking aneurysms, can be improved by not delay-
ing for further imaging studies, but I would say that it
would be rare to fi nd a vascular surgeon who would
take this patient based on an ultrasound image alone.
I think it is unfortunate, because I think this is precisely
the kind of patient who needs to be in an operating
room instead of a CT scanner. My guess is that he is
going to get a CT scan before he goes to the OR.
One of the reasons so many of these aneurysms are
amenable to endovascular repair is because the vast
majority are not thoraco-abdominal, as 95% of them
originate in the abdomen distal to the renal arteries. It
is very rare for them to involve the renal arteries, and
it is very rare for them to be two separate aneurysms.
For the most part, thoracic aortic aneurysms are vis-
ible on a chest X-ray study, if not on an ultrasound,
by sliding your probe up into the chest, rather than
just looking into the abdomen. So I think that is kind
of a weak argument for a CT scan. However, I don’t
think it matters whether we think the patient should
go directly to the operating room or not; we are not
the ones doing the surgery, and I think it is important
for the person who has that responsibility to feel com-
fortable about what the patient requires for surgery.
SG: I’ve seen quite a number of these patients dete-
riorate rapidly. To better defi ne the anatomy expedi-
tiously, one can bring them to the operating room
where they can perform transesophageal echocar-
diography in the OR; while we have the patient
draped, you can better defi ne the anatomy in a setting
where if you need to open up the abdomen immedi-
ately, you can.
PR: For the thoracic aneurysm that is probably sen-
sible. I don’t think you need it for the abdominal
aneurysm, but again, I think we are dependent on the
person who has the skill set and responsibility for the
CHAPTER 20
286
PR: How high would you want his blood pressure
during transfer?
DB: This is a somewhat controversial area. Most of
the data about fl uid resuscitation and hemorrhagic
shock are from the trauma model, using pigs, so we
don’t know as much about this as we would like to. I
would keep blood pressures as low as the patient can
tolerate, meaning I would not over-resuscitate with
crystalloid and blood if the patient had a normal men-
tal status, was making urine, and not complaining of
chest pain or stroke symptoms. Even if the systolic
blood pressure is 100 mmHg or a little less, there is a
theoretical concern that by giving fl uid or blood, we
could increase the perfusion pressure and the bleed-
ing that has been tamponaded in the retroperitoneum
will restart and cause fatal hemorrhage. We also may
dilute out clotting factors and disrupt the body’s abil-
ity to create thrombus in the area of rupture that in
the same way could cause a fatal hemorrhage.
PR: We used to use medical antishock trouser (MAST)
suits in the fi eld and perhaps in the ED before bring-
ing patients we thought might have a leaking aneu-
rysm to the operating room. Would you consider that
as a therapy in a patient who had to be transferred?
SG: Today MAST suits aren’t readily available, and
we aren’t accustomed to using them. I think we would
waste too much precious time trying to locate one and
getting it on the patient, and lose a fair amount of the
benefi t of arranging for the patient to be transferred.
PR: The data on whether or not it helped was also
pretty muddy. I remember seeing a few patients in
whom I thought the MAST suit actually increased
hemorrhage when it was infl ated. When one uses a
MAST suit, you have to take it down compartment
by compartment, starting with the abdomen, and you
have to make sure you are giving fl uid resuscitation
simultaneously, otherwise you will have an acute pre-
cipitous drop in blood pressure leading to the develop-
ment of an acute lethal dysrhythmia. There isn’t much
you can do to make this patient safe during transfer; it
is worth transferring the patient if you don’t have crit-
ical care or vascular surgery capacity, but it is much
better if you can go from the ED directly to the OR
rather than to another ED.
PR: Many of these patients are misdiagnosed as spinal
arthritis, as the symptoms of spinal stenosis and vascular
PR: Although you would still need to go to the OR
even if the patient was in the process of evolving an
infarct, would you be able to defi ne a change in tro-
ponin level more rapidly if you had a baseline?
SG: Unfortunately, cardiac enzymes tend not to
elevate until 6–8 hours after the event. Were you to
send preoperative cardiac enzymes, they would very
likely be normal and fail to indicate ischemia. How
important is it to actually recognize ischemia as pre-
operative vs. perioperative? I don’t believe it makes
much difference when the patient became ischemic,
as ultimately he will need to be cared for in much
the same way, whether it was from a preoperative or
perioperative event. In addition, enzymes may elevate
anyhow from some myocardial leak connected with
the surgery.
PR: The proposed mechanism of the myocardial
infarction during surgery is the hypoxia produced by
the low blood pressure from the leak, which he already
has. Additionally, during surgery when you take the
clamps off to start reperfusing the graft, there is often
a drop in blood pressure. While there are great efforts
made to prevent this using blood transfusion or pres-
sors right before you unclamp, there frequently is a
drop in blood pressure. Unfortunately, this can cause
diminished fl ow in a coronary artery that is already
stenosed, or even in the carotid arteries. This reminds
us that as much as we would hope that it is, vascular
disease is not a localized problem.
Often one has access to vascular surgeons fairly
ubiquitously, but there are institutions that are reluc-
tant to take care of critical postoperative patients, and
that often might be a reason for transfer. What would
you do with this patient if you had to transfer him
before you could arrange a surgery for him?
DB: I would call the local helicopter and tertiary care
center immediately after the results of my bedside
ultrasound, even if I decided to proceed with a CT
scan. I wouldn’t feel compelled to keep the patient in
a community hospital ED if I had a reliably positive
fi nding on ultrasound, and a CT scan would delay
moving the patient to a center where defi nitive care
could be given. In reality, usually one can get a CT
scan in a community hospital before the tertiary cen-
ter has agreed to accept the patient and transport has
been arranged, so most of the time I think the CT scan
is done at the referring hospital.
ABDOMINAL AORTIC ANEURYSM
287
fl ank pain is really pleuritic chest pain and rethink
the differential, but with this patient’s presentation, I
would not consider a PE.
What if the patient presented without syncope, but
with fl ank pain and dizziness, and a CT scan showed an
unruptured 5–6 cm AAA. What should one do then?
DB: This is a symptomatic AAA until proven other-
wise, and needs to be treated in much the same way as
a ruptured AAA, with urgent vascular surgery refer-
ral. Telling patients that less than 5 cm aneurysms
tend not to rupture and putting off an evaluation to
the outpatient setting, I think, is a mistake.
PR: If the aneurysm is ⬍5 cm, I would have a hard
time believing that it is the cause of his symptoms,
but that doesn’t mean he isn’t having a vascular catas-
trophe. He could have a mesenteric artery occlusion
obstructing his renal blood fl ow, causing pain in the
groin and kidney region. Thus, I would still consider
this a vascular emergency and regardless of whether it
requires immediate operative repair, it requires imme-
diate consultation.
To conclude, I would emphasize the confusion we
create by treating aortic dissection and aortic thoracic
aneurysm as the same diseases. A dissection is a dis-
ease of the lining of the aorta, probably caused by
hypertension, and it is not an aneurysm; it’s a totally
different pathology than atherosclerosis of the tho-
racic aorta that can behave like an abdominal aneu-
rysm. Atherosclerosis of the thoracic aorta is less
common, can also rupture, and needs to be evaluated
and treated as if it were an abdominal aneurysm. The
treatment is totally different and the course is totally
different than a dissection of the aorta. The distinc-
tion can be made by imaging studies, as a thoracic
aortic atherosclerotic aneurysm will be demonstrated
as enlargement of the aorta. It has the same kind of
deformity of the entire wall of the vessel as does the
abdominal aneurysm, and it requires either stenting
endovascularly, or resection and replacement with an
artifi cial graft. We need to stop talking about dissect-
ing aneurysms, refer to them as dissecting aortas, and
confi ne the term aneurysm to atherosclerotic disease.
Case resolution
A stat vascular surgery consult was called, and a sec-
ond large bore IV was placed. Uncrossmatched blood
was sent for from the blood bank, while a blood sample
disease overlap; both have claudication. It may require
imaging studies to differentiate the two, or even an
MRI of the spine. Our patient, who presents with syn-
cope, moves us away from spinal disease; however, in a
patient with known spinal disease, it makes it harder to
jump to a vascular diagnosis. Does this patient need any
additional workup besides the ultrasound and a type
and cross before going to the OR?
DB: I don’t think so; if you only have one vial of blood
to send to the laboratory it ought to be a type and cross.
I don’t think it matters what the initial hematocrit is,
but it is very likely that the patient will need blood.
SG: It would be useful to know the patient’s baseline
renal function, especially if this turns out to have
some involvement of the renal artery.
PR: I would also forgo preoperative imaging studies
such as carotid duplex studies in a patient who might
have a bruit, as this is a patient who needs to go to the
OR, and needs to go there very quickly.
DB: I would argue to do a noncontrast CT. You can
get enough information from a noncontrast CT scan to
know whether there an aneurysm, and if it is ruptur-
ing. Some emergency physicians may prefer a contrast-
enhanced CT for better delineation of pathology, but I
think the time that it takes to wait for the creatinine to
come back, convince the radiologist to push the con-
trast, and then give the contrast is time poorly spent.
PR: Some institutions have a protocol that mandates
oral and rectal contrast as well; a bowel full of con-
trast is the last thing you need in a surgical patient.
SG: The only test I would do on this patient in addi-
tion would be a 12-lead EKG, particularly with con-
cern for concomitant cardiac dysrhythmia after this
patient’s syncopal event.
PR: Our biggest responsibility in emergency medicine
is the recognition of the aneurysm, and the expedi-
tious involvement of the service that can give defi n-
itive care. I think where we fall into error is going
down the pathway of renal colic or spinal disease, and
overlooking the time constraints of a vascular repair.
When would you pursue a pulmonary embolism (PE)
as the cause of the syncopal episode?
SG: If the physical examination was less compelling
for an aortic aneurysm, and the ultrasound and CT
were negative, then you’d have to ask yourself if this
CHAPTER 20
288
most die before presenting for care, and only half will
survive emergency surgery.
5
The prevalence of AAA
is negligible in persons under age 60, and then rises
dramatically with advancing age. By age 65, approxi-
mately 1.7% of women and 5% of men will have an
abdominal aortic diameter ⱖ3 cm.
6
Clinically impor-
tant aneurysms (over 4 cm diameter) occur in about
1% of men between the ages of 55 and 64, and the
incidence increases approximately 2–6% per decade
thereafter.
7–9
There is a male predominance of at least
three-fold, with white men being the most highly repre-
sented group. Studies that use a defi nition of maximum
external diameter (e.g., ⱖ3cm) may underestimate the
prevalence of AAA in women.
While age and male gender are obviously epidemio-
logic risk factors, there are many others. Smoking is
the strongest risk factor for the presence of AAA, and
is a major risk for growth and rupture of an exist-
ing AAA.
8–10
More than 90% of patients with AAA
have been smokers.
11
Current American College of
Cardiology/American Heart Association (ACC/AHA)
guidelines recommend smoking cessation for all
patients with an AAA or a family history of an AAA.
1
Other, lesser identifi ed risks include a family history
of an AAA, hypertension, claudication, hypercholes-
terolemia, cerebral vascular disease, and increased
height.
1,9–13
Decreased risk factors include female gen-
der, diabetes mellitus, and black race.
The true pathogenesis of an AAA is currently
unknown, it is probably multifactorial and systemic,
and is being actively studied. A genome scan of fami-
lies with an AAA identifi es a possible gene locus on
chromosome 19q13.
14
Multiple studies have focused
on vascular structural proteins, especially elastin and
collagen, degradation by various proteases, includ-
ing metalloproteinases derived from endovascular
and smooth muscle cells, and infl ammatory cells that
infi ltrate the media and adventitia. These studies hold
promise for better understanding the pathogenesis of
an AAA, and potentially earlier therapeutic possibili-
ties in the future.
Over the fi nal few decades of the 20th century,
much has been learned about the natural history of
an AAA that, when coupled with advances in surgical
modalities, has changed management for an unrup-
tured AAA. Although some aneurysms may become
symptomatic with back or abdominal discomfort,
many remain asymptomatic until rupture.
5
Given the
high incidence of death from a ruptured AAA, and
was sent for type and cross matching. The patient was
brought to the CT scanner and underwent a noncontrast
scan that showed a ruptured AAA with a right retroperi-
toneal hemorrhage. He was taken directly to the OR
from the CT scanner for repair. He underwent an open
procedure with aortic graft placement. Postoperatively
he developed transient renal failure that resolved over
several weeks. He was discharged on hospital day seven
and was doing well at 6 month follow-up.
Section III: Concepts
Introduction
The defi nition of an aneurysm is a focal dilatation
of the blood vessel compared to the normal state or
adjacent blood vessel. The defi nition of an abdomi-
nal aortic aneurysm (AAA) is an aortic diameter at
least 1.5 times the diameter measured at the level of
the renal arteries. The normal value at this level is
approximately 2.0 cm with a range of 1.4 to 3.0 cm.
1,2
A diameter greater than 3.0 cm is usually considered
aneurysmal. Abdominal aortic aneurysms involve all
the layers of the aorta and do not create intimal fl aps
or false lumens. Most (75%) AAAs are infrarenal.
An abdominal aortic aneurysm is the most common
site of an arterial aneurysm. The aorta, like most arte-
rial vessels, is made up of the intima, the media, and
the adventia. The intima is a single layer of endothelial
cells resting on a subendothelial tissue composed of
collagen, elastin, fi broblasts, and mucoid ground sub-
stance. The media provides strength and elasticity, and
is composed of smooth muscle cells within a matrix
of elastin, collagen, and ground substance arranged in
complex lamellar units. Degenerative changes within
the media are thought to be the etiology of abdomi-
nal aortic aneurysms. The abdominal aortic media is
composed of 28 lamellar units, compared to 45–56 in
the thoracic aorta. The human abdominal aortic media
lacks a vasa vasorum and has relatively fewer lamel-
lar units for its diameter than abdominal (or thoracic)
aortas of other species, resulting in a relatively elevated
estimated mean tension per lamellar unit.
3
Finally, the
adventia is a loose connective tissue around the outer
diameter and contains the nerve supply.
Approximately 15,000 deaths per year in the United
States are attributed to abdominal aortic aneurysm
rupture, making it a leading cause of death.
4
Only
10–15% of patients will survive a rupture of an AAA;
ABDOMINAL AORTIC ANEURYSM
289
rupture using these techniques has been minimal.
26
Asymmetrical bulges compared to more uniform cylin-
drical aneurysms seem to increase local wall stress,
and likely increase the risk of rupture.
27,28
Computer
generated calculated wall stress may become a valu-
able predictor of an individual AAA rupture risk as
these techniques become more widely adopted.
The best predictor of an AAA rupture is size. The
risk of rupture up to a diameter of 5.5 cm in men is
low, but substantially increases above this threshold.
29
In men, the estimated annual rupture risk is almost
zero for aneurysms less than 4 cm and increases from
0.5% to 5% percent per year between a diameter of 4
and 5 cm. With a diameter of 5–6 cm, the risk increases
to 3–15%/year. The annual risk of rupture becomes
10–20% per year for aneurysms 6–7 cm diameter,
20–40% per year for aneurysms 7–8 cm diameter,
and 30–50% per year for aneurysms greater than 8
cm diameter.
5,19,29–33
Women are more likely to rup-
ture at any given AAA diameter.
5,34
Continued smok-
ing, chronic obstructive pulmonary disease (COPD),
bronchiectasis, hypertension, a family history of an
AAA, and a larger initial diameter of an AAA, all seem
to increase the relative risk of an AAA rupture.
5,34–38
Localized blisters/blebs where the medial elastin is
diminished likely increase the risk of rupture, whereas
intraluminal thrombus does not appear to affect rup-
ture rates.
39–41
Intraluminal thrombus does, however,
seem to be associated with a rapid expansion rate
of an AAA, as does continued smoking, poorly con-
trolled hypertension, advanced cardiac disease, stroke,
advanced age, and a large initial AAA diameter.
37,42–47
Perioperative risk
Perioperative risk is an important consideration when
discussing an individual management plan, and depends
on patient factors, surgical training, and experience as
well as the anatomy of the AAA itself. A review of mul-
tiple studies reveals an average operative mortality for
open elective AAA repair of approximately 5.5%, with
a range from less than 1% to over 50%.
47–59
Cardiac
complications are the primary cause of perioperative
death, and thus existing cardiac disease is thought to
be a major risk factor. Individual risk factors for a poor
outcome include electrocardiographic evidence of isch-
emia, COPD, an elevated creatinine, low FEV
1
(forced
expiratory volume in 1 second), congestive heart fail-
ure, advanced age, and female gender.
48,50,60–65
Predictive
the fact that most patients (⬎75%) are unaware they
have an aneurysm prior to complications, there has
been a major push for screening.
15
In 2005, the United
States Preventive Services Task Force published a rec-
ommendation for one-time screening with an ultra-
sound imaging study for men aged 65–75 who have
ever smoked at least 100 cigarettes in their lifetime.
16
In 2007, Medicare started offering a one-time screen-
ing AAA ultrasound study to men ages 65–75 who
have smoked or have a family history of an AAA as
part of their covered initial preventive physical exami-
nation.
17
Ultrasound screening approaches a sensitiv-
ity and specifi city of 100% and 95%, respectively, for
the detection of an infrarenal AAA.
18
An asymptomatic, unruptured AAA is not an emer-
gency, but should invoke a thoughtful discussion with
a qualifi ed physician, preferably a vascular surgeon.
Individualized decision-making for an AAA is complex,
and requires careful assessment of factors that affect
the risk of rupture, as well as perioperative mortal-
ity, life expectancy, and patient preference.
19
The goals
of management are to prevent rupture and to prolong
life. Current guidelines suggest surveillance of an AAA
up to 5.5 cm is acceptable in men unless symptoms or
tenderness develop or rapid expansion (⬎1 cm/year)
occurs.
1,8,19
Selective repair should be effective when
the risk of rupture exceeds the risks of perioperative
mortality. Optimal surveillance interval recommen-
dations have varied, but the 2005 American College
of Cardiology/American Heart Association published
guidelines recommend surveillance with ultrasound
or computed tomography for 3–4 cm diameter AAAs
every 2–3 years, and every 6 months to 1 year for
an AAA with diameters of 4–5.4 cm.
1
In the largest
surveillance studies to date, 60–65% of patients ran-
domized to surveillance require surgery at 5 years and
70–75% at 8 years.
20–22
Ultimately, patient preference
is a major determinant in the decision to proceed with
early elective surgery versus surveillance.
Rupture risk
The great variability in estimates for risk of rupture
for a particular size of AAA refl ect that other factors
besides absolute size should be considered for each
individual case.
23–25
Many surgeons consider the ratio
of the aneurysm diameter compared to the native ves-
sel, or some other adjustment to account for body size
to be important, but the improvement in predicting
CHAPTER 20
290
Presentation
The majority of AAAs are asymptomatic. Symptoms
related to mass effect or compression of spatially
related structures may manifest as discomfort, or
vague gastrointestinal symptoms. An AAA may pres-
ent with complications from intraluminal thrombus
or distal embolization, and with erosion into adjacent
structures. A large AAA may also present with dis-
seminated intravascular coagulation causing bleeding
or thrombosis.
89,90
New or progressive symptoms are
worrisome for rapid expansion and impending rup-
ture. Asymptomatic patients may be inappropriately
referred to acute settings after a serendipitous diag-
nosis during studies for other conditions, a screening
radiographic study, or physical examination. Available
data suggest that approximately 50% of 4.0–4.9 cm
AAA and 76% of ⱖ5 cm AAA may be palpated with
careful physical examination close to the umbilicus.
91
Patients with a known AAA with back, abdominal,
fl ank, or groin pain or new onset of tenderness over
the AAA should be evaluated urgently.
After rupture, only one-quarter of the patients will
reach a hospital alive, and only 10% will reach the
operating room alive, with an additional 40% emer-
gent operative mortality rate.
92,93
Presenting patients
will usually complain of acute onset of back or abdom-
inal pain, may have a palpable abdominal mass, and
often have palpable tenderness on examination.
94,95
Almost half the patients will present with hypoten-
sion. Less common presentations include syncope and
vomiting. In the rare case of a partially contained rup-
ture, patients may complain of vague discomfort for
days, even weeks, prior to presentation, making the
diagnosis challenging. A vascular catastrophe such as
an AAA rupture should be considered in the differ-
ential diagnosis of every patient who presents with
shock, syncope, and abdominal or fl ank pain. The
most common misdiagnoses in patients with a proven
AAA rupture, according to one study, are renal colic,
diverticulitis, and gastrointestinal bleeding.
96
Diagnosis
Effectively making the diagnosis of a ruptured AAA,
given the grim prognostic data, is of critical impor-
tance. A delay in diagnosis or operative intervention is
expected to increase the morbidity and mortality of this
lethal condition. Rapid diagnosis in order to organize
models based on patient factors have been developed
to stratify patients into low- and high-risk categories.
Perioperative mortality is markedly higher with emer-
gency surgery as compared to elective surgery.
66
Operator training and experience also play a role in
risk assessment, with subspecialty training in vascular
surgery along with high volume surgeons and centers
portending a better prognosis.
49,53–55,60,61,67
Adjusted
inhospital and 30-day mortality for elective open AAA
repair has been found to be inversely proportional to
volume.
68
Finally, less quantitative pathologic factors
of the aneurysm itself, such as extensive atheroma-
tous disease, thrombus formation, calcifi cations at the
anastomosis or clamp sites, extension to the juxtarenal
level, and adhesion of the AAA to surrounding struc-
tures, make surgery more technically challenging, and
would be expected to increase morbidity/mortality.
69–74
Previous abdominal surgeries may make also make
AAA repair technically more diffi cult.
Lastly, endovascular aneurysm repair (EVAR) has
changed the landscape of both elective and emer-
gency repair of AAA. EVAR has demonstrated equal
or better early safety and effi cacy, as well as reduced
intensive-care and hospital length of stays, fewer major
complications, more rapid recovery, and less blood
loss during the procedure compared with traditional
open techniques.
75–81
Because of the lower periopera-
tive complication rate and faster recovery, EVAR may
be particularly well suited for older, high-risk patients
compared to open repair.
82–84
Anatomic eligibility for
EVAR varies from 14–54%.
85,86
Factors that infl uence
eligibility include the axial length of the aortic neck, the
diameter and condition of the iliac and femoral arteries,
and the degree of calcifi cation, tortuosity, angulation,
as well as the degree of thrombosis that exists, all of
which can infl uence the seal of the endoluminal device.
EVAR requires preoperative CT angiography with
three-dimensional reconstruction, which is repeated
immediately postprocedure, at 1 month postopera-
tively, 6 months, and then yearly thereafter. The cost of
an endoluminal device is also signifi cant. The durabil-
ity of EVAR has also been questioned. Secondary pro-
cedures are required in 10–27% of patients at 2 years
as reported in 2 large series.
87,88
More long-term studies
of newer endoluminal devices are needed to make con-
clusions about the durability of EVAR. For now, EVAR
is an option for elective surgery when anatomically fea-
sible, and may provide an alternative for patients at a
very high risk for an open repair.
ABDOMINAL AORTIC ANEURYSM
291
prompt surgical repair is the patient’s only chance for
success. In the last few decades, bedside ultrasound
imaging study has proven useful in this regard. In one
study, the time to an AAA rupture diagnosis is reduced
from 83 minutes to 5 minutes, and time from presen-
tation to reaching the operating room is reduced from
90 minutes to 12 minutes.
97
Even emergency providers
with limited ultrasound experience are able to visual-
ize large (ⱖ4 cm) AAAs more than 85% of the time.
98
The goal in a symptomatic patient is simply to visu-
alize an AAA by measuring the anteroposterior, lon-
gitudinal, and transverse dimensions (Figure 20-1).
Intramural thrombus and calcifi cations may also be
appreciated. Most of the AAA ruptures are retroperi-
toneal, and will not result in intraperitoneal abdomi-
nal free fl uid. Visualizing an AAA in a symptomatic
patient should prompt immediate vascular surgery
consultation along with other emergent management.
Signs of an AAA on a plain abdominal radiograph,
including calcifi cation of the aortic wall, paravertebral
mass, and loss of psoas or renal outlines, can be seen
in approximately 75% of patients, and may prompt
vascular surgical consultation and emergent manage-
ment in a symptomatic patient.
94
Both ultrasound and
plain X-ray studies can be done rapidly and portably
with minimal interruption in assessment and treat-
ment of these gravely ill patients.
Computed tomography (CT) scan offers advantages
including the detection of real or impending rupture,
Figure 20.2 Unenhanced CT scan, transverse view, of
the abdomen shows a large unruptured abdominal aortic
aneurysm. Note the calcifi ed aortic wall.
and providing anatomic detail useful in preoperative
planning (Figures 20-2, 20-3A–C). Disadvantages
include time, availability, and the need for an inter-
ruption in assessment and management of the patient,
and often a transfer to a site outside of the ED.
Contrast is not required to make the diagnosis, but
may be preferred by some (Figure 20-4). Angiography
and MRI are generally not used in the acute setting.
Figure 20.1 Ultrasound, transverse
view, of the abdomen shows an
abdominal aortic aneurysm measuring
8 cm in anteroposterior diameter. Note
the laminated thrombus along the
posterior wall.
CHAPTER 20
292
facilitate counseling regarding smoking cessation, as
well as appropriate hypertension and hypercholester-
olemia control as per current ACC/AHA guidelines.
1
Current guidelines also recommend beta-blocker
therapy for patients being followed nonoperatively.
Elective or urgent repair should be considered at an
Treatment
For asymptomatic, unruptured AAA patients, diagnosis
prompting risk modifi cation and surveillance or elec-
tive surgery is essential. Timely diagnosis can prompt
surgical consultation to discuss surgical options and
Figure 20.3 Unenhanced CT scan, transverse view, of the
abdomen shows a ruptured abdominal aortic aneurysm
with extensive blood in the right retroperitoneum.
Figure 20.4 Contrast-enhanced abdominal CT scan,
transverse view, shows a ruptured abdominal aortic
aneurysm with active extravasation into the left
retroperitoneum.
ABDOMINAL AORTIC ANEURYSM
293
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.
Ouriel, K, Green, RM, Donayre, C, et al. An evaluation 2
of new methods of expressing aortic aneurysm size: rela-
tionship to rupture. J Vasc Surg. 1992;15:12.
Wolinsky H, Glagov S. Comparison of abdominal and 3
thoracic aortic medial structure in mammals: deviation
of man from usual pattern. Circ Res. 1969;25:677–686.
Creager, MA, Halperin, JL, Whittemore AD. Aneurysmal 4
disease of the aorta and its branches. In: Loscalzo, J,
Creager, MA, Dzau, VJ, eds. Vascular Medicine. New
York: Little, Brown; 1996:901.
Brown LC, Powell JT. Risk factors for aneurysm rupture 5
in patients kept under ultrasound surveillance. Ann Surg.
1999:230:289.
Scott RA, Ashton HA, Kay DN. Abdominal aortic aneu-6
rysm in 4237 screened patients: prevalence, development
and management over 6 years. Br J Surg. 1991;78:1122.
Singh K, Bonaa KH, Jacobsen BK, et al. Prevalence 7
of and risk factors for abdominal aortic aneurysms in
a population-based study: The Tromso Study. Am J
Epidemiol. 2001;154:236.
Powell JT, Greenhalgh RM. Small abdominal aortic 8
aneurysms. N Engl J Med. 2003;348:1895.
Lederle FA, Johnson GR, Wilson SE, et al. Prevalence 9
and association of abdominal aortic aneurysm detected
through screening. Ann Intern Med. 1997;126:441.
Lederle FA, Johnson GR, Wilson SE, et al. The aneurysm 10
detection and management study screening program:
validation cohort and fi nal results. Aneurysm Detection
and Management Veterans Affairs Cooperative Study
Investigators. Arch Intern Med. 2000;160:1425.
Greenhalgh RM, Powell JT. Endovascular repair of abdo-11
minal aortic aneurysm. N Engl J Med. 2008;358:494.
Salo JA, Soisalon-Soininen S, Bondestam S, et al. Familial 12
occurrence of abdominal aortic aneurysm. Ann Intern
Med. 1999;130:637.
Fleming C. Whitlock EP, Beil T, Lederle F. 13 Primary care
screening for abdominal aortic aneurysm. Evidence
Synthesis No. 35. Rockville, MD: Agency for Healthcare
Research and Quality; February 2005.
Shibamura H, Olson JM, van Vlijmen-Van Keulen C, et 14
al. Genome scan for familial abdominal aortic aneurysm
using sex and family history as covariates suggests genetic
AAA diameter of 5.5 cm, or with rapid expansion
(⬎0.5cm in 6 months) of the AAA.
1
For ruptured AAA patients, the goal is rapid trans-
fer to the operating room. Any factors that may delay
going to the operating room should be omitted. In set-
tings without surgical capability, time should not be
wasted to confi rm the diagnosis when the clinical pre-
sentation is that of a leaking or ruptured AAA. Once
the diagnosis is entertained, prompt consultation (or
referral to a site with surgical capabilities) is essential
in concert with stabilization. Large-bore intravenous
access should be obtained, and preoperative labora-
tory studies sent stat.
Symptomatic but unruptured AAA patients should
be treated like those with contained rupture: immedi-
ate surgical consultation is mandated along with rapid
standard preoperative testing. The use of blood pres-
sure agents (beta-blockers) for blood pressure control
prior to surgery should be decided in conjunction with
vascular surgery on a case-by-case basis, and adminis-
tered in a well-monitored setting.
Section IV: Decision making
Most AAAs are asymptomatic.•
Screening protocols may assist in identifying •
an AAA, allowing discussion about the risks or
benefi ts of elective repair.
In symptomatic patients, fl ank pain and back pain •
may suggest less dangerous diagnoses.
Avoid narrowing the differential diagnosis too •
early, and discounting the possibility of an AAA.
With a ruptured AAA, the goal is prompt control •
of the bleeding vessel in the operating room as soon
as possible.
In an unruptured symptomatic AAA, immediate •
surgical consultation is also mandatory—here,
the emergency physician can make the biggest
difference.
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