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AORTIC DISSECTION
275
in the descending aorta just distal to the left subcla-
vian artery.
A range of complications can result from an acute
aortic dissection, and these complications can lead to
diverse presentations of illness. Intimal fl ap formation
and distortion of the aortic and associated branch ves-
sel walls can cause critical compromise of arterial fl ow.
This can lead to myocardial infarction, cerebrovascular
accident, renal or spinal cord infarction, or ischemic
bowel. Involvement of the aortic root can cause acute
aortic valvular insuffi ciency and subsequent left heart
failure. Retrograde extension of the dissection into the
pericardial space can lead to pericardial effusion and
tamponade with syncope, hypotension, and sudden
death.
9
Rupture of the aortic wall may cause massive
internal hemorrhage and exsanguination.
The differential diagnosis of acute aortic dissec-
tion is diverse. Acute coronary syndrome may be the
most important differential diagnosis. It can some-
times be distinguished by the crescendo/decrescendo,
exertional, and pressure-like nature of pain. Acute
myocardial infarction is approximately 100 times
more common than aortic dissection, but as noted
above, it can actually be a complication of dissec-
tion. Pericarditis may also be confused with dissec-
tion, although it is associated with a slower pace of
symptom onset, positional discomfort, and character-
istic EKG abnormalities. Other relevant cardiologic
10% aortic arch, and 5% confi ned to the abdominal
aorta. It is useful for the emergency physician to appre-
ciate the distinctions between dissections involving
the ascending and descending aorta, as only ascending
dissections routinely require surgical repair.
Dissection is thought to occur most commonly
from a combination of weakening of the aortic wall,
increased shear forces, or localized and iatrogenic
trauma. Weakening of the aortic wall may be caused
by cystic medial necrosis, which is described as disor-
ganization and degeneration of the elastic and collagen
components.
Clinical factors most commonly associated with
aortic dissection include advanced age (approxi-
mately one-third of patients are over the age of 70); a
history of hypertension, which is elicited in approxi-
mately two-thirds of patients; male gender; and
atherosclerosis.
3,5,6
Dissection is also associated with
the connective tissue disorders Marfan’s Syndrome,
Ehlers-Danlos Type IV, osteogenesis imperfecta, the
congenital variant bicuspid aortic valve and coarcta-
tion of the aorta, prior cardiovascular and particu-
larly aortic or aortic valve surgery, infl ammatory or
syphilitic aortitis, third trimester or postpartum preg-
nancy, cocaine abuse, and possibly isometric exercise
such as weight lifting.
4,5,7,8
Blunt trauma, such as a
motor vehicle accident, may rarely cause aortic dis-
section or even complete transection, most commonly
Figure 19.2 Schematic diagram
of the Debakey and Stanford
classifi cation schemes of aortic
dissection. Adapted from
http://en.wikipedia.org/wiki/
Aortic_dissection.
Accessed 9/5/09.
CHAPTER 19
276
The majority of patients with type B dissection are
hypertensive on presentation. In one series, 35% and
25% of patients with type A dissection present with
hypertension and hypotension, respectively.
5
Up to
one-third of patients may have a weak pulse in an
extremity (pulse defi cit), or a greater than 20 mmHg
differential systolic blood pressure between arms.
10
Up to one-third of patients may have a diastolic mur-
mur suggestive of aortic regurgitation. These fi ndings
are generally associated with Type A dissection.
Transthoracic echocardiography demonstrates an
approximate sensitivity and specifi city of only 60%
and 80%, respectively, for acute aortic dissection.
12
Nevertheless, the technology, skill, and importance
of bedside ultrasonography performed by emergency
physicians as an extension of the physical exami-
nation have grown steadily. Identifi cation of peri-
cardial effusion can be made confi dently, and this
should suggest an ascending dissection.
13
A defi ni-
tive diagnosis of aortic dissection with identifi cation
of an intimal fl ap can even sometimes be made, and
the resulting time saved to operative repair may be
life saving.
14
EKG
The EKG has limited utility in diagnosing acute aor-
tic dissection. Approximately one-third of dissection
patients have evidence of left ventricular hypertrophy
on EKG and approximately 5% of dissection patients
have an associated acute MI. Ascending dissection
most commonly originates along the greater curvature
of the right wall of the ascending aorta, and when it
dissects in a retrograde fashion, it most commonly
involves the origin of the right coronary artery, caus-
ing an inferior myocardial infarction. Nevertheless,
left main involvement and anterior myocardial infarc-
tion can occur too.
15
Laboratory studies
Traditionally, laboratory studies have had limited
utility in diagnosing acute aortic dissection. Anemia
could suggest ongoing subacute internal hemorrhage,
and hematuria may suggest renal artery involvement,
but neither of these fi ndings is sensitive nor specifi c.
Investigators have explored the potential utility of a
number of newer markers, including smooth muscle
myosin, elastin fragments, and the serum D-dimer.
16–18
differentials include acute congestive heart failure and
aortic valvular disease or failure. Pulmonary condi-
tions including pulmonary embolism and pneumo-
nia, cerebrovascular accident, mediastinal tumor,
esophageal disease, and other gastrointestinal causes
of upper abdominal pain are also important differen-
tials. Finally, thoracic or abdominal aortic aneurysms
may present similarly to a type B dissection.
History
The history of aortic dissection is classically sudden,
severe, sharp, stabbing, tearing, or ripping pain in the
chest, back, or upper abdomen.
10
The intensity of pain
may be maximal at onset. Radiation or migration of
the pain to the interscapular region and elsewhere
often refl ects the anatomy of the disease and pro-
gressive propagation of the dissection. Consequently,
the pain of ascending dissection tends to present in
the anterior chest, while descending dissection may
cause pain in the central back or upper abdomen.
Many patients do not present with “classic” pain as
described above, and 5–10% of patients may have no
pain at all.
Approximately 10% of patients have neurologic
complaints. This includes a history of acute syncope,
which is associated with hemopericardium and cardiac
tamponade. Other complaints include the symptoms
of an acute cerebrovascular accident, usually due to
ascending dissection extension and involvement of the
origin of the cerebral vessels, or acute paraplegia from
spinal vessel involvement. Dyspnea may occur as a
result of acute aortic regurgitation and heart failure.
Any recent history of iatrogenic aortic manipulation
or trauma such as left heart catheterization is impor-
tant, as this may be the cause of the dissection. The
relation of acute dissection to recent exertion or heavy
lifting remains uncertain.
4,11
Relevant past medical history includes a survey
for the contributing causes described above. In par-
ticular, a history or phenotype suggestive of Marfan’s
Syndrome or previous cardiac or aortic surgery should
point to a possible dissection, as these are present in
approximately 5% and 15% of cases, respectively.
5
Physical examination
The blood pressure may be elevated, normal, or
depressed in the setting of acute aortic dissection.
AORTIC DISSECTION
277
Imaging studies
Emergency imaging is used to suggest and to diagnose
acute aortic dissection. A number of fi ndings on the
chest X-ray study may suggest acute dissection, includ-
ing a widened mediastinum, a widened or abnormal
(tortuous, kinking, lump appearance) aortic contour,
a blurred aortic knob, displacement of the outer sur-
face of the aortic contour from the intimal aortic cal-
cifi cation, tracheal deviation to the right or distortion
of the left main bronchus, and pleural effusion.
10,24
Attempts have been made to quantitate some of these
fi ndings. A widened mediastinum may be defi ned as a
ratio of the mediastinum to the chest of greater than
0.25–0.31, or a mediastinal width greater than 8 cm
at the level of the aortic knob.
23,24
Displacement of the
intimal aortic calcifi cation greater than 6 mm may be
considered positive.
Unfortunately, when subjected to rigorous blinded
testing, chest X-ray fi ndings have proven neither highly
reliable nor discriminatory. Von Kodolitsch and col-
leagues fi nd the overall sensitivity and specifi city of
the chest X-ray to be 64% and 86%, respectively.
24
The pooled overall sensitivity from multiple studies
appears to be approximately 90%.
10
A widened aortic
knob or contour and widened mediastinum may be the
most sensitive and reliable fi ndings.
10,24,25
The effect of
radiologic technique such as posterior-anterior (PA) or
anterior-posterior (AP) view on test characteristics is
uncertain. It is critical to appreciate the limited sensitiv-
ity of the chest X-ray study for aortic dissection, and the
potential delay in diagnosis a false negative may cause.
26
A normal chest X-ray study does not rule out disease.
Advanced imaging studies used to diagnose acute
aortic dissection include transthoracic and transesoph-
ageal echocardiography (Figure 19-3a and 19-3b),
com puted tomographic scan (CT scan) (Figure 19-4),
magnetic resonance (MR) angiography, and conven-
tional angiography. While the primary goal of these
studies is to diagnose aortic dissection if it is present,
there are a number of important secondary goals.
These include: identifying the location of the dissec-
tion (ascending, descending, arch, or combination), its
extent and size, the site of the intimal tear, evidence of
aortic regurgitation, branch vessel or coronary artery
involvement, or pericardial effusion. Methodologic
considerations of the imaging test include its diagnos-
tic accuracy, safety, speed, convenience, contraindica-
tions, and the ability to identify alternative diagnoses.
The most promising marker for the identifi cation
of acute aortic dissection appears to be the serum
D-dimer. D-dimer is a breakdown product of intra-
vascular clot destruction. It seems intuitive that this
marker may be elevated in conditions of intravascular
clot formation and destruction, such as pulmonary
embolism and acute aortic dissection. Advantages of
the test are that it is readily available, inexpensive,
and can be performed rapidly. Some disadvantages
are that there are multiple test methodologies with
differing test characteristics; it is known to have poor
specifi city in patients with malignancy, chronic dis-
ease, or advanced age; and it may be elevated in pre-
cisely the conditions that must be differentiated from
acute dissection, including pulmonary embolism and
acute myocardial infarction.
19,20
Using a threshold cutoff of 500 ng/ml, the sensitiv-
ity of the serum D-dimer for acute aortic dissection
appears to be approximately 95%, while the speci-
fi city is likely in the 40–50% range, depending on
the methods used to identify a control group; thus,
a negative D-dimer test would lower the odds of dis-
ease by a factor of approximately 9.
20,21
Analogous to
the use of serum D-dimer for pulmonary embolism,
the test may be most useful in patients with a low
pretest probability of acute aortic dissection based
on the history, physical examination, and chest X-ray
study. Patients who then have a serum D-dimer of
less than 500 ng/ml would effectively be “ruled out”
for the disease. Patients with a positive test would
require further urgent imaging studies. The negative
likelihood ratio of the test is 1 to 9, insuffi ciently
low to rule out disease in patients with a moderate
or high pretest probability of disease, and the test
would not be useful in this circumstance.
The goal of using the serum D-dimer would be
to identify more accurately the group of patients
at risk for acute dissection who require advanced
imaging, but this would not necessarily decrease the
number of advanced imaging studies performed. A
number of questions regarding this use of the serum
D-dimer remain, including: the optimal test meth-
odology and threshold value, sensitivity of the test
for intramural dissections isolated from the aortic
lumen, the test specifi city, the time dependence of
the test characteristics with respect to symptom
onset, and the independence of the test’s predictive
value from other clinical and radiologic predictors
of disease.
22,23
CHAPTER 19
278
required to perform MR angiography may be the
most important hindrances to its widespread use.
Conventional angiography has long been consid-
ered the reference standard for aortic imaging. In the
setting of ST elevation myocardial infarction and pos-
sible causative aortic dissection, it may be desirable to
perform aortography in the catheterization laboratory
prior to coronary angiography and possible percuta-
neous intervention. The sensitivity of this procedure
for dissection is presumed high, though not precisely
The technology and test characteristics of the vari-
ous imaging modalities have steadily improved over
the past two decades.
27,28
The sensitivity and specifi c-
ity of dedicated transesophageal echocardiography,
CT scan, and MR angiography are now all at 95% or
above at major centers, while transthoracic echocar-
diography remains distinctly less sensitive (59–85%).
Emergency physicians today most commonly use CT
scan, followed by transesophageal echocardiography,
to diagnose acute dissection.
29
The facilities and time
Figure 19.3a Transesophageal
echocardiogram longitudinal view of
the ascending aortic root: the long
arrow identifi es an ascending aortic
dissection fl ap that sits diagonally
along the length of the aortic root,
ending at the aortic valve inferiorly.
The short arrow identifi es the
leafl ets of the aortic valve which, in
this case, continue to demonstrate
good apposition despite mild
dilatation of the aortic root.
Figure 19.3b Transesophageal
echocardiogram transverse view
of the ascending aortic root: the
long arrow identifi es the dissection
fl ap just superior to the level of
the tricuspid aortic valve. The
short arrow identifi es thrombosis
underneath the dissection fl ap along
the wall of the aortic root. In this
patient, the thrombosed dissection
fl ap involved the origin of the left
main coronary artery, causing an
associated anteroseptal STEMI.
AORTIC DISSECTION
279
with ascending aortic dissection, EKG gating that
effectively freezes cardiac motion allows for evalua-
tion of the aortic perivalvular area and the coronary
arteries.
34
A number of challenges remain in the development
of the “triple rule out” protocol. Acquisition time with
associated breath hold in the scanner is approximately
20 seconds. Contrast dose (approximately 125 cc)
and radiation (approximately 12–30 millisievert) are
larger than conventional imaging protocols. Patient
limitations include known coronary calcifi cations or
stents, obesity, renal insuffi ciency, contrast allergy,
atrial fi brillation, or the inability to achieve a neces-
sarily slow heart rate to successfully gate image acqui-
sition. Finally, it is rare that emergency physicians
seriously entertain the possibility of all three diagnoses
in a single patient.
35
Emergency department diagnosis
Despite the array of advanced technology available
to practitioners today, the rapid and correct diagnosis
of all acute aortic dissections remains a tremendous
challenge. The correct diagnosis is still delayed or
determined postmortem in a signifi cant minority of
cases.
6,36,37
The most diffi cult cases seem to be patients
who present with isolated epigastric, abdominal, or
fl ank pain.
36
Isolated chest pain without radiation to
the back can also be diffi cult and doubly problematic.
defi ned. Alternatively, a patient with chest symptoms
and elevated serum D-dimer may be referred for pul-
monary embolism (PE) CT scan. This involves a con-
trast bolus timed to highlight the pulmonary arterial,
not the systemic arterial circulation. Approximately
0.5% of PE CTs demonstrate aortic dissection, but the
sensitivity of this alternate protocol CT angiography
for acute dissection is uncertain.
30
Multidetector CT (MDCT) coronary angiography
represents an important technological advance with
implications for aortic dissection diagnosis. Timed gat-
ing of CT image acquisition to the diastolic phase of
the EKG cycle allows for high resolution imaging of the
coronary arteries. MDCT coronary angiography can
be reliably used to assess for the presence of coronary
artery disease and the likelihood of an acute coronary
syndrome (ACS).
31
The simultaneous MDCT assessment for three of
the most dangerous and important conditions respon-
sible for chest symptoms (acute aortic dissection,
ACS, and PE) is now being explored with “triple rule
out” protocols. These protocols extend the coronary
angiography technology by using multiple timed con-
trast boluses and a larger imaging fi eld to include the
heart, lungs, and aorta.
32,33
Potential advantages of this
technique include a relatively rapid test with high diag-
nostic accuracy for all three conditions, and the ability
to identify a broad spectrum of other possible chest
and upper abdominal conditions. For those patients
Figure 19.4 Chest CT image
including the ascending and
descending aorta: the descending
aorta demonstrates a dissection fl ap
with heterogeneously decreased
contrast consistent with some
stasis in the posterior false lumen
portion of the vessel (long arrow).
The homogeneous appearance of
the ascending aorta suggests no
dissection involvement (short arrow).
CHAPTER 19
280
Hypotension can be treated with intravenous fl uid,
and an immediate search for underlying causes, includ-
ing cardiac tamponade, aortic regurgitation, acute
myocardial infarction, internal hemorrhage, or another
process. The clinician should be wary of pseudo-
hypotension due to isolated arterial insuffi ciency from
dissection fl ap compromise of a subclavian or iliac
artery takeoff. All of the complications described above
generally require urgent operative intervention. If pres-
sor medicines are required, primary vasoconstrictors
with relatively less inotropic effect, such as phenyleph-
rine and norepinephrine, are preferred.
Cardiac tamponade complicates approximately 18%
of acute aortic dissections. It is associated with syncope
and altered consciousness, and the associated mortal-
ity is approximately 50%.
40
Pericardiocentesis may be
a useful short-term temporizing measure for pericardial
tamponade, but there is some concern that relief of tam-
ponade without defi nitive repair will promote further
hemorrhage.
41
Surgical treatment
Untreated, the mortality of type A dissection is greater
than 50% within 30 days of onset. For this reason,
surgical treatment is usually indicated. Uncomplicated
type B dissections may be treated with blood pressure
control only. The following complications of type B
dissection may merit surgical intervention: vital organ
or limb ischemia, an expanding hematoma, retrograde
extension to the ascending aorta (by defi nition, this
converts to type A), Marfan’s syndrome, or uncon-
trolled hypertension or pain.
Emergent surgical treatment of acute aortic dissec-
tion may involve repair of the intimal tear and closure
of the false lumen, graft replacement of the involved
aortic segment, aortic valve repair or replacement, cor-
onary artery bypass grafting (if the coronary arteries
are involved or diseased), or endovascular stent place-
ment in the aorta or involved branches. Transfemoral
intraluminal aortic covered stent-graft placement is a
relatively new technique. The goals of stent placement
are to halt the fl ow of blood into the false lumen and
promote thrombosis, and to keep the true lumen open.
This has been used for type B and the distal portion
of type A dissections.
42,43
Other advanced endovascu-
lar techniques include balloon or scissors treatment to
widen the reentry site from the false to the true lumen,
Dissection is often misdiagnosed as cardiac ischemia
and treated with anticoagulant therapy, which may
increase hemorrhage into and expansion of the false
lumen. As noted above, some dissections may cause
secondary cardiac ischemia such that both conditions
exist simultaneously, making appropriate manage-
ment even more challenging.
To increase the proportion of aortic dissection
patients correctly diagnosed in the ED, the fi rst prior-
ity is to liberally consider the diagnosis in all patients
with pain in the torso, syncope, or focal neurologic
complaints. While all dissection patients do not have
pain, a combination of pain and neurologic complaints
should suggest this diagnosis. A second priority is to
consider dissection in all patients with isolated chest
pain, and to consider factors that differentiate dissec-
tion from ACS. The description of pain, its severity
at onset, its radiation, and suggestive physical exami-
nation fi ndings may all be helpful. It is also useful to
differentiate ascending versus descending dissection.
While emergency physician bedside transthoracic
ultrasound, EKG, chest X-ray, and serum D-dimer test
may all be helpful in assessing the likelihood of disease,
none of these studies alone is suffi ciently sensitive to
rule out disease. When in doubt, a defi nitive imaging
study must be performed.
Emergency treatment
Once the diagnosis of acute aortic dissection is sus-
pected, antiplatelet and anticoagulant therapies that
may be routinely administered for ACS or PE should
be withheld until the diagnosis is clear.
38
For hyper-
tensive patients, blood pressure control with a goal of
100-120 mmHg systolic pressure is considered essen-
tial to minimize further extension of the dissection.
Decreasing the force of cardiac contraction (inotropy)
and the heart rate may also be protective.
39
For these
reasons, medicines with beta-adrenergic receptor block-
ing activity such as labetalol, propanolol, and esmolol
are commonly used fi rst. Other choices include calcium
channel blockers such as diltiazem and verapamil, or
after heart rate control, a short acting angiotensin-con-
verting enzyme (ACE) inhibitor such as enalaprilat, or
nitroprusside. Renal artery compromise with second-
ary excessive renin excretion may particularly benefi t
from ACE inhibition. Appropriate analgesia should
also be administered.
AORTIC DISSECTION
281
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and bare metal stenting for static or dynamic obstruc-
tion of branch arteries.
7
Prognosis
The prognosis for patients who receive a timely diag-
nosis and modern therapy continues to improve.
Thirty-day survival postsurgery is approximately
70%. For patients with type B dissection treated
medically, 30-day survival is 92%.
5
Five-year sur-
vival for all groups discharged from the hospital is
75–82%.
Section IV: Decision making
Consider aortic dissection in all patients with pain in •
the torso, syncope, or focal neurologic complaints,
and in all patients with both chest and back pain.
Blood pressure control with a goal of 100–120 mmHg •
systolic pressure is essential to minimize extension
of the dissection. Decreasing the force of cardiac
contraction and heart rate are also protective.
Beta-adrenergic receptor blockers such as labetalol, •
propanolol, and esmolol should be used initially.
After heart rate control, enalaprilat or nitroprusside •
can be used.
CT scan, MRI, and transesophageal echocardio-•
graphy all have similar high sensitivities; however,
CT scan is generally the test of choice due to time
constraints.
D-dimer is a promising diagnostic tool that can be •
used to assess further the likelihood of disease in
patients at relatively low risk based on the history,
physical examination, and chest X-ray.
Type A and B dissection should both have emergent •
surgical consultation, although only Type A will
routinely require emergent surgery.
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283
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Abdominal aortic aneurysm
David A. Peak
1
& David F. M. Brown
2
1
Assistant Professor, Division of Emergency Medicine, Harvard Medical School,
Attending Physician and Assistant Residency Director, Department of Emergency
Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
2
Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital,
Associate Professor, Harvard Medical School, Boston, Massachusetts, USA
20
Section I: Case presentation
A 68-year-old man with a history of hypertension and
tobacco use presented to the emergency department
(ED) after a syncopal event. He was at home when he
abruptly developed right back, fl ank, and groin pain
that was severe in onset. Within about 30 seconds, he
developed nausea and passed out. EMS was called.
On arrival of the EMS unit, he was awake and alert in
a supine position complaining of ongoing right fl ank
and groin pain. Vital signs were: heart rate 90 beats/
min, blood pressure 110/60 mmHg, respiratory rate
18 breaths/min. A large bore IV was inserted, and the
patient was placed on a monitor that showed a sinus
rhythm. He was transported to the local ED.
On ED arrival, he still described the pain as above. The
past medical history was notable for hypertension and
prostatic hypertrophy. He smoked a pack per day for
50 years. Alcohol use was minimal. Medications were
lisinopril and proscar. On physical examination the vital
signs were unchanged. The head and neck examina-
tions were normal, the chest was clear to auscultation,
the heart sounds were a regular S1 S2 with an S4, and
no murmurs. The abdomen was soft but tender in the
epigastrium to palpation with a pulsatile mass. Carotid,
radial and femoral pulses were 2⫹. The extremities had
no edema. The back had no spinal or costovertebral
angle tenderness. The neurological examination was
normal. The EKG showed sinus rhythm with voltage
criteria for left ventricular hypertrophy. A bedside
ultrasound performed by the emergency physician (EP)
showed an abdominal aortic aneurysm.
Section II: Case discussion
Dr Peter Rosen: This is an interesting history that is
easy, in retrospect, to diagnose accurately, but pro-
spectively, I think it is much harder to focus upon a
vascular event in this patient, especially if the patient
focuses on his varied complaints. I’ve seen a number of
these patients who say “I felt a little bit dizzy, but it’s
really from the pain in my back and the back pain is
really killing me,” “I’ve never felt pain this severe,” or
just “get rid of my back pain.” I’ve also had patients
in whom the pain did not start abruptly but who had
back pain for months to years, had been treated for
spinal stenosis or spinal arthritis, and again, minimize
the vascular components of their pain. I think that the
issue that helps us the most in this case is the history
of syncope. But I believe that many patients are either
not aware of it, or dismiss it as a dizzy spell, and don’t
help us by telling us about the event. Are than any
clues that you like to use that put you in the direction
of vascular disease when you see a patient like this?
Dr Shamai Grossman: A patient who has a chief
complaint of abdominal and fl ank pain accompanied
by syncope: together these are classic symptoms that
CHAPTER 20
284
and I think it’s well worth listening for a bruit over
the carotid arteries, as these patients often have dif-
fuse vascular disease and have potential for stroke
and coronary artery disease. However, I have never
made the diagnosis of an abdominal aneurysm from
an abdominal bruit. Bruits in the abdomen are mostly
seen in women with renal artery stenosis, as they tend
to be younger and thinner. Gastrointestinal bleeding
is another important diagnosis that must be consid-
ered; this too may often be given to you historically,
but sometimes syncope can be an initial presentation.
I can remember a patient who presented exactly with
this history except that he came in somewhat confused;
had we not done a rectal on this patient we wouldn’t
have picked up that he was having both a gastroin-
testinal (GI) bleed and an aortic aneurysm. One of
the things about aneurysms that helps muddy the pre-
sentation of the disease is that abdominal aneurysms
can have anatomical proximity to the third portion
of the duodenum. Therefore, some of these patients
present with an upper GI bleed as a sign of their aortic
aneurysm erosion. Although GI bleeding doesn’t rule
out an aneurysm, this presentation may also be con-
sistent with a different disease entity, like peptic ulcer
disease, rather than aneurysmal disease.
PR: What is the utility of bedside ultrasound? In this
case it seems to have been useful, because it found
an aortic aneurysm, but in obese people who have an
ileus from an eroding aneurysm it may be very dif-
fi cult to see aortic enlargement.
DB: I think it is worth doing a bedside ultrasound as
part of the secondary survey in patients like this, and
if one sees an enlarged aorta, that’s extremely helpful.
However, unless you can see a normal aorta from the
transition through the diaphragm all the way through
the bifurcation, one cannot reliably exclude aortic
aneurysm with a bedside ultrasound. It is a common
pitfall to exclude the diagnosis simply because you
didn’t see the aorta well on ultrasound. Not seeing the
aorta well on ultrasound is a common fi nding, and
not because there is no aneurysm, but because there is
gas in the gastrointestinal tract or a lot of fat, which
makes the examination of the patient with ultrasound
diffi cult.
SG: I would make the argument that if you have a
positive ultrasound it is so helpful that at that point,
I would call the surgeon and say that you have a
go with vascular disease. If the patient had a history
of hypertension, this would further point you in this
direction. If you obtain a history of coronary or periph-
eral arterial disease, or when examining the patient you
note other signs common in vascular disease, such as
bruits or signs of peripheral vascular disease, and cer-
tainly if you have a pulsatile mass, you should be very
concerned that this patient may have a signifi cant vas-
cular problem, such as an abdominal aortic aneurysm
that at this point may be ruptured.
PR: In this case the patient was not only cooperative
in terms of historical fi ndings, but also physical fi nd-
ings. I think it is probably rare to have a palpable pul-
satile mass with an aortic aneurysm. If you have ever
palpated one of these during surgery, what you fi nd is
a large tube fi lled with soft toothpaste-like material.
The fl ow through that aneurysm may be slow enough
so that you don’t get any pulsation or any sensation
of a mass when you palpate through the abdomen.
In fact, fewer than 25% of these patients have a pal-
pable mass. We were further helped here because this
patient didn’t come in with normal vital signs, and
patients who have renal colic almost never present
with lowered blood pressures; they come in with ele-
vated blood pressures. Is the presence of a bruit over
the patient’s abdomen a helpful physical fi nding?
Dr David Brown: I fi nd the presence of bruits helpful,
but again I fi nd the absence of bruits does not help
me eliminate a vascular diagnosis. Although feeling a
palpable enlarged aorta is unusual, and certainly can’t
be considered the norm, the absence of this fi nding
on physical examination should also not reassure the
physician that this is not a symptomatic or enlarging
abdominal aortic aneurysm (AAA). In addition, a per-
son with a history of hypertension who presents with
a blood pressure in the normal range for someone
without hypertension should be a red fl ag, particu-
larly if you are considering the other major disease
on the differential list, nephrolithiasis, as this usually
presents with hypertension. Furthermore, this patient
is old for a fi rst presentation of renal colic, and doesn’t
give a history of prior renal colic, so that makes this
diagnosis unlikely. He also doesn’t give a history of
spinal disease, making this unlikely as well.
PR: Bruits over the aorta are uncommon. Occasionally
we hear bruits over the downstream circulation
because they have atherosclerotic narrowing as well,